So Here Is This

2011-09-18T20:11:00.000-07:00

Researchers Announce a Breakthrough on HIV/AIDS Treatment
A technique that alters T cells has been shown to reduce the amount of virus in infected people.

By Deborah Erickson

For the first time, researchers have shown that a cell-based therapy for HIV/AIDS can reduce the amount of virus in infected people. The breakthrough — big news for researchers, who have struggled for decades to create vaccines and cell-based therapies for HIV — was announced on Sunday at the 51st Interscience Conference on Antimicrobial Agents and Chemotherapy in Chicago. To date, the sole treatment for HIV has been multidrug regimens that prolong life but never eliminate the virus.

Sangamo BioSciences of Richmond, California, says it has found a way to protect the T cells that HIV attacks first, so they can live to fight another day. The approach entails temporarily stopping a patient’s antiretroviral therapy and removing T cells carrying the CD4 receptor. This surface protein is the doorway by which the virus gains entry into the cell. The collected T cells are exposed to zinc finger nuclease, an enzyme designed to remove the gene for a coreceptor of CD4 called CCR5. The cells are then reinfused into the patient. Once they’re back in the body, the new study shows, the cells persist and travel in the body just like normal T cells.

Sangamo’s approach is based on the observation that some people have a naturally occurring mutation in the CCR5 gene that protects them against HIV. Ordinarily, humans have two copies of every gene. It turns out that individuals with a mutation in both copies of the CCR5 gene cannot be infected by the most common HIV strains. In people with the so-called Delta-32 mutation in just one copy of the gene, infection rarely progresses to AIDS. In the U.S., about 1 percent of the population is thought to carry the helpful mutation, which some researchers believe arose as protection against the Black Death.

Previous evidence existed showing that CCR5-negative cells could help AIDS patients. In 2007, an American man with AIDS and lymphoma received, as treatment for the cancer, a bone-marrow transplant from a person with the CCR5 mutation. The marrow recipient has been free of both AIDS and cancer since then. Sangamo’s method treats a patient’s own cells, with less risk than a marrow transplant.

“The data are very encouraging,” says Edward Lanphier, Sangamo’s founding CEO. “We are seeing a statistically significant correlation between our treatment and viral load reduction. This is a big step forward toward our goal of developing a functional cure for the disease.” Lanphier envisions that someday AIDS patients will not need to be on aggressive antiretroviral therapies because their virus will be well-controlled—or even undetectable, as happened with one subject with a mutation in one CCR5 gene.

Experts unaffiliated with Sangamo and its clinical trials agree that the scientific achievement is impressive, but they question the notion that it could yield a functional cure. Gerhard Bauer, assistant professor in the Stem Cell Program at the University of California, Davis, and director of that school’s Good Manufacturing Practice laboratory at the Institute for Regenerative Cures, says, “this is a great move forward, to demonstrate reduction of viral load by pushing in modified T cells. It has never been done before by any company, and I congratulate them 100 percent.”

However, Bauer says, he is “not so sure” the company will be able to create a functional cure. T cells don’t live forever, he points out.

“This is encouraging,” says Ellen Feigal, vice president of R&D at the California Institute for Regenerative Medicine, “and it provides supporting evidence for a study we funded that would take the work to the next step.” This study, by researchers at City of Hope, a cancer center in Duarte, California, aims to provide patients with a permanent supply of HIV-resistant T cells. The strategy calls for modifying patients’ blood-forming stem cells, which produce all future T cells as well as the macrophages and dendritic cells that can also be HIV targets.

Sangamo is also exploring the potential of stem-cell modification with City of Hope researchers, but the company does not concede that modified stem cells will be necessary or any better than T cells. “Yes, T cells turn over,” says Geoff Nichol, who joined Sangamo as executive vice president of R&D a few months ago to commercialize the platform, “but there are some very long-lasting subsets that can live for years and years and remember the epitope they came up against. We are feeling bullish about T cells because of our data.”

Sangamo’s news is “certainly scientifically interesting,” observes Warner Greene, director of the Gladstone Institute at the University of California, San Francisco. But, he points out, no cell therapy, whether it involves T cells or stem cells, is a practical approach to treating HIV/AIDS throughout the developing world, where seven out of 10 new infections are occurring. “We really need to be looking for therapies that can benefit the millions of individuals with HIV, not just a select few who might be able to afford cellular therapies.”

Copyright TechnologyReview.Com 2011

2011-07-26T15:39:00.000-07:00

Kaletra Plus Selzentry Yields Faster Response And Better Immune Recovery Than Kaletra Plus Truvada (IAS 2011)
By Courtney McQueen and April Clayton

Preliminary results from a small 48 week clinical trial indicate that previously untreated HIV-positive adults taking Kaletra plus Selzentry have better immune recovery and faster virologic response compared to participants taking the more standard regimen of Kaletra plus Truvada.

Based on their results, the researchers recommended further research into treatment regimens that do not contain nucleoside reverse transcriptase inhibitors (NRTIs) – such as Truvada – which currently form the backbone of antiretroviral therapy. They also noted that longer trials with more participants would be needed to confirm the long-term safety and efficacy of non-NRTI-based regimens.

The results were presented last week at the 6th International AIDS Society Conference on HIV Pathogenesis, Treatment, and Prevention (IAS 2011).

Traditional combination antiretroviral therapy regimens consist of two NRTIs plus at least one additional anti-HIV drug from a different class. However, due to side effects associated with NRTIs and the fact that some patients cannot take them due to allergies or other conditions, researchers have begun exploring alternative “NRTI-sparing” regimens (see related AIDS Beacon news).

In this study, researchers examined the efficacy of the non-NRTI-based regimen of Kaletra (lopinavir/ritonavir) plus Selzentry (maraviroc) versus the more traditional regimen of Kaletra plus Truvada (emtricitabine/tenofovir). Truvada is a combination of two NRTIs, while Kaletra is a protease inhibitor and Selzentry is a CCR5 inhibitor, which is a relatively new type of antiretroviral.

The trial included 38 HIV-positive adults who had not previously been treated for HIV. Half the participants were randomly assigned to receive Kaletra plus Selzentry, and the other half were assigned to take Kaletra plus Truvada. The researchers then assessed participants’ CD4 (white blood cell) counts and viral loads (amount of HIV in the blood) at 4, 12, 24, 36, and 48 weeks after starting treatment.

Results showed that after 48 weeks, participants in the non-NRTI Kaletra plus Selzentry group had significantly higher increases in CD4 counts than participants in the Kaletra plus Truvada group. The average increase in CD4 count for the Kaletra/Selzentry group was 226 cells per microliter, compared to 125 cells per microliter in the Kaletra/Truvada group.

Additionally, most participants in the non-NRTI group (83 percent) achieved undetectable viral loads by week 12, compared to less than half of patients in the Truvada group. By 48 weeks, 95 percent of participants in the Kaletra/Selzentry group had undetectable viral loads, compared to 83 percent of participants in the Kaletra/Truvada group.

The researchers also noted that three participants taking Kaletra plus Truvada had to interrupt treatment due to diarrhea. Overall one person in the Kaletra/Truvada group discontinued treatment, compared to none in the Kaletra/Selzentry group.

For more information, please see the study abstract and presentation (pdf) on the IAS 2011 conference website.

Copyright © 2011 AidsBeacon.com

2011-07-25T15:41:00.000-07:00

NanoViricides announces anti-HIV therapy could lead to functional cure
by Deborah Sterescu

NanoViricides (OTCBB:NNVC) reported Monday that its lead anti-HIV candidate achieved an efficacy level equivalent to a highly active anti-retroviral triple (HAART) drug cocktail in a recent animal study.

Treatment with the drug reduced HIV levels and protected human immune T-cells to the same extent as treatment with the cocktail did in a study of mice, said the company. The three drug-combination used for comparison is one of the current therapies recommended for patients with HIV.

NanoViricides, which uses special purpose nanomaterials to design viral therapies, also said that no evidence of drug toxicity was observed during the study, and that the investigational drug will now undergo further optimization.
The latest study verifies the company’s previous results, which found that nanoviricides had a significant therapeutic effect, equal or superior to the same three-drug cocktail in a mouse study.

The company’s nanoviricide therapy works to mimick cellular structures to which the virus binds, specifically attacking and dismantling them. By working differently than many combination therapies, the drug developer believes that the nanoviral treatment, or HIVCide, could compliment current standard-of-care, possibly achieving a “functional cure” of HIV/AIDS, NanoViricides said.

Although a functional cure is not a complete cure, it would allow an infected person to continue normal life even after discontinuation of therapy, maintaining undetectable viral load until a recurrence.

“Creating an adjunct drug that acts by a novel mechanism complementing the current HAART therapy is becoming extremely important,” said CEO, Eugene Seymour.

“The HIV virus mutates constantly resulting in failure of HAART therapy regimens. In some countries, it has now mutated to such an extent that in up to 40% of patients the standard HAART therapy has become ineffective.”

The company’s nanoviricide class of drugs are being developed against a number of viral diseases, including H1N1 swine flu, H5N1 bird flu, seasonal Influenza, oral and genital Herpes, viral Hepatitis C, and Ebola virus, among others.

A recent study of anti-flu treatment FluCide showed that the drug was better than oseltamivir, or Tamiflu, with a 1,000-fold greater viral load reduction than the standard flu therapy, after optimization.

“The results of the current study have provided important insight to guide the next cycle of chemical optimization. We clearly know now that we are on the right path,” said president Anil R. Diwan.

Copyright © 2011 Proactive Investors USA & Canada

2011-07-15T01:43:00.000-07:00

Got HPV and HIV? Don't panic

Human papillomavirus (HPV) is currently the most common sexually transmitted infection (STI), perhaps because it is so easy to spread through skin-on-skin contact. For this reason, condoms can decrease, but not preclude, transmission of the virus during sex.

Various strains of the virus may cause genital warts on your penis or your ass. Generally painless, they can be occasionally itchy. They are almost always benign, the obvious exception being the strains that cause anal cancer.

The chemical you used to burn off the warts was probably liquid nitrogen. Even with this treatment, warts can reoccur. Depending on your age, you may choose to be vaccinated with Gardasil, but it works best if received prior to exposure to the virus.

Health Canada has approved the vaccine for young men from nine to 26, but oddly, they must pay for this particular preventive medicine, at a cost of up to $300, and it is not always easy to find a dispensing source. Hopefully, one day both boys and girls will be vaccinated for HPV just as they receive polio and measles vaccines, but we are far from that state now.

Though it is true that your risk of developing anal cancer increases if you have HPV and HIV, that risk is actually fairly minimal. That said, you are wise to remain vigilant regarding your anal health. If you notice changes to your ass in the form of bleeding, significant growth of the warts or other lesions in the first inch inside your anal opening — or anything else unusual — get to your doctor. If you can access the Lower Mainland, you can go to the infectious disease clinic at St Paul’s Hospital to get an anal PAP test.

Is there a need to alter your sexual behaviour now that your serological status has changed? Not necessarily. Because condoms cover only your penis, and because HPV rarely limits itself only to this area, they are not entirely protective. However, you want to minimize transmission as much as possible, so if you are with new or multiple partners, glove up.

Because of the incomplete protection condoms afford, you will need to advise new sexual partners of your potentially infectious status even if you engage in protected sex. You may wish to forgo anal sex with casual partners when your CD4 count is less than optimal. You will learn to read your body’s cues and can act accordingly.

If you are in a sexually exclusive relationship, you probably share strains of viruses, so you can relax regarding barrier protection, but, of course, use your best judgment and continue to talk openly about your health. The strains of HPV you have may not be oncogenic (cancer-producing), and you want to keep it that way. Your goal is to prevent transmission and reception of new strains while still enjoying great sex.

If your health is good, your CD4 count is robust and you are doing well on HAART (highly active anti-retroviral therapy), your chances of developing anal cancer are reduced. As horrible as it sounds, anal cancer is less deadly and metastatic (easily spreading) than its sister cervical cancer, which women have learned to manage through routine PAP tests for years now. You guys must now be vocal and persistent in demanding the same good medical care.

HPV is primarily a cosmetic problem, providing you monitor your body for changes. Since it has become ubiquitous in the community, you needn’t fear rejection or embarrassment because of it.

So all in all, though having HIV and HPV is not good news, it is not terrible news, either. Several decades ago, these diagnoses would have threatened far more serious consequences. Now they signal a need for continued vigilance and monitoring of your health status — not such a bad thing, really.

The point is that this is not a death sentence. It is not even news about which you need to panic. You have illnesses that compromise your immune system, and luckily, medicine is catching up with necessary treatments, although, alas, cures are still unavailable.

Political pressure is needed to make Gardasil available for young men. Those in non-urban areas often still lack access to anal PAP tests and dignified treatment. We do not yet live in the world we hope for or deserve.

Still, you can have a long and satisfying life. I encourage you to do so. This is a situation where you can happily celebrate your half-full glass.

Got a question for Dr Ren? asktheexpert@xtra.ca

Copyright 2011 Xtra! Canada's Gay & Lesbian News

2011-07-15T01:36:00.000-07:00

Ultrasound May Determine Heart Attack Risk in HIV Patients

Risk 10 times higher in HIV patients with abnormal results compared with general population: study

People with HIV are at increased risk for blood vessel blockages, and new research shows heart ultrasounds can help determine if these patients are more likely to suffer a serious or fatal heart attack.

A report from the American Heart Association revealed that the risk for heart attack among people with HIV who have abnormal heart ultrasound tests or "stress echoes" is 10 times greater than in the general population and more than three times higher than in people without HIV who have abnormal heart ultrasounds.

"We looked at whether stress echo can help predict risk in a high-risk group — HIV patients with known or suspected heart disease — and determine whether they have a high or low risk of heart attack and death in the future," the study's senior author, Dr. Farooq A. Chaudhry, associate professor of medicine at Columbia University College of Physicians and Surgeons and associate chief of cardiology and director of echocardiography at St. Luke's Roosevelt Hospital Center in New York City, said in an American Heart Association news release.

In conducting stress echoes on 311 HIV patients averaging 52 years of age with known or suspected heart disease, researchers found that 26 percent had abnormal ultrasounds. Within an average of about three years, there were 14 cardiac deaths and 17 nonfatal heart attacks.

The study authors concluded that the HIV patients who had normal stress echo tests had on average a less than 1 percent per year risk for serious or fatal heart attack -- the same risk as in the general healthy population. In sharp contrast, the risk of heart attack among the HIV patients with abnormal stress echo test results was almost 12 percent per year.

The study, published in the current issue of Circulation: Cardiovascular Imaging, found that 100 percent of HIV patients with normal heart ultrasounds survived in the year following the test and 98 percent were alive at four years. Those survival rates dropped to 92 percent at one year and 62 percent at four years for people with HIV that had abnormal stress echoes, the report indicated.

"Although we did not study which treatments are most effective for these patients, HIV patients who have abnormal stress echocardiography should probably be monitored and treated more aggressively to prevent heart attack and death," said Chaudhry. "Conversely, patients with a normal stress echo might not need such aggressive interventions."

The American Heart Association provides more information on HIV and the heart.

Copyright © 2011 HealthDay. All rights reserved

2011-07-15T01:32:00.000-07:00

Pills found to be highly effective in preventing HIV transmission
By Thomas H. Maugh II, Los Angeles Times

Experts hail a pair of trials involving heterosexual couples in Africa as a breakthrough in AIDS prevention. The studies show that taking a pill containing one or two drugs each day can decrease transmission of HIV by as much as three-quarters.

Taking a daily pill containing either one or two anti-HIV drugs can reduce transmission of the virus by as much as three-quarters among heterosexual couples, two studies in Africa have shown — a breakthrough finding that promises to intensify a new focus on AIDS prevention.

The results were so compelling that the larger study was halted early and the drugs given to all the participants, researchers said Wednesday.

In the absence of a vaccine to protect against the virus, this new approach, termed pre-exposure prophylaxis, may be the best hope for slowing or even halting the spread of the deadly plague throughout the developing world. U.S. health officials are beginning to prepare guidelines for how the drugs could be used in this country to prevent new infections.

The findings "are two more nails in the coffin of HIV," said Mitchell Warren, executive director of the New York-based AIDS Vaccine Advocacy Coalition. "We are seeing similar results in different populations, and that gives us more certainty that these results are real."

A study of gay men reported in November showed that one of the drugs in the new trial could reduce the spread of HIV by as much as 70% when taken regularly by uninfected individuals. But a study released this year found that the drugs did not show a similar benefit among uninfected heterosexual women.

The strength of the new findings suggests that the study involving women may have been flawed.

"Our results provide clear evidence that this works in heterosexuals," said Dr. Jared Baeten of the University of Washington, co-chair of the new study.

The last year has brought several breakthroughs in AIDS prevention research, said Kevin Frost, chief executive of amfAR, the Foundation for AIDS Research. In addition to this latest finding and the study involving gay men, a study released last July found that microbicides could sharply reduce HIV transmission in women and a study in HIV-positive people showed that treating the infected person intensively could reduce transmission by as much as 96%.

Given those and other developments, "we find ourselves in a place where we have an extraordinary opportunity to radically alter the trajectory of the epidemic," Frost said. "The science is in place. We could do it with the tools we have available. It's no longer a question of, can we do this? The question is, will we do it?"

The new results are scheduled to be presented next week at the International AIDS Society Conference on HIV Pathogenesis, Treatment and Prevention in Rome, but were released early.

One trial enrolled 4,758 couples in Kenya and Uganda in which one partner was HIV-positive and the other was not. A third of the uninfected participants received a daily pill containing tenofovir, a third received a daily pill containing tenofovir in combination with emtricitabine, and a third received a placebo.

Tenofovir is marketed as Viread and the two-drug combination as Truvada by Gilead Sciences Inc. of Foster City, Calif. They are available generically in many countries for as little as 25 cents per pill, according to the World Health Organization

All couples also received condoms and counseling about how to prevent infection.

By the end of May, researchers had identified 18 new infections among the group receiving Viread, 13 among those receiving Truvada and 47 among those receiving the placebo. That corresponds to a 62% reduction in transmission among those receiving Viread and a 73% reduction among those receiving Truvada.

The second trial, sponsored by the U.S. Centers for Disease Control and Prevention, studied 1,200 healthy, sexually active males and females in Botswana. About half received Truvada and half a placebo. Among the 601 participants who took Truvada, there were nine new infections, compared with 24 among the 599 who received placebo. That amounts to a 62.6% reduction in new infections.

Among those participants who took the drugs regularly, researchers observed an even greater reduction — 77.9% — in new infections.

No significant side effects were observed in either trial. "The perception is that these drugs are really toxic," said Dr. Thomas J. Coates, an infectious diseases specialist at UCLA's Geffen School of Medicine. "They are not. The current generation is really quite safe."

Dr. Jonathan Mermin, director of the CDC's Division of HIV/AIDS Prevention, said the agency would immediately begin working with other public health groups to establish guidelines for using the drugs prophylactically in this country. Physicians should await those guidelines before prescribing the drugs, he said, but if they believe it is imperative to do it, they should adhere to the guidelines previously announced for using them in gay men.

Dr. Robert M. Grant of UC San Francisco's Gladstone Institute of Virology and Immunology speculated that the drugs might work even better in the United States than they did in Africa. People in this country "are more accustomed to using pills for prevention," he noted, and thus more likely to take the drugs regularly.

Copyright © 2011, Los Angeles Times

2011-07-14T09:26:00.000-07:00

Stop the ADAP Crisis!
By Sonia Rastogi

The AIDS Drug Assistance Program (ADAP), is a safety net that provides life-saving medications to people living with HIV. Due to a funding crisis, as of September 2010, 3,441 people are on waiting lists to access medication. South Carolinians, Pat Kelly, founder of A Family Affair and founding member of the PWN, and Bonetta Graves, coordinator at Wateree AIDS Task Force, discuss the need for action in their state where the ADAP waiting list is growing.

Pat and Bonetta spoke with SC Sen. Graham about the state’s growing waiting list at the ADAP Summit in D.C. but South Carolina will not invest more money. “If one-third of the HIV-positive people in South Carolina come out to rally … then the state would not be able to cut ADAP funding,” but right now legislators do not see the need, Pat said.

It is vital to think about how the ADAP crisis affects the lives of HIV-positive people’s family members and children. Bonetta emphasized that for women, “there are a lot of things [they] are going to be cut off from,” without HIV treatment, including the ability to work and take care of their family.

TAKE ACTION! Step one: EDUCATION. Find out how you or your community is affected by the ADAP crisis: does ADAP provide your life-saving medication? “Somebody is going to have to pull their heads up out of the sand… to get started,” says Bonetta. Step two: EMPOWERMENT. “We need to start looking at medication from a human rights standpoint.” Pat says “We have a right to medication. … It is a right to health!” Step three: SPEAK OUT! Contact your local ASO or e-mail the PWN at pwn@womenhiv.org.

Sonia Rastogi is the PWN’s Communications Coordinator based in Oakland, CA. Pat Kelly, based in Orangeburg, South Carolina, is the founder of A Family Affair and founding member of PWN.

This article is from PWN’s Fall 2010 Newsletter.

2011-07-13T10:14:00.003-07:00

Double Immunity

Dr. Stephen O’Brien’s work with HIV led to a discovery that could one day help scientists treat or prevent HIV infection: People from some European populations carry a genetic mutation that prevents HIV from entering their white blood cells. O’Brien hypothesizes that this mutation, dating back 700 years, may have been a selective advantage during the bubonic plague, as it is today, with the onslaught of HIV. From Evolution: “Evolutionary Arms Race.”

The genetic scripts written in DNA code constantly undergo changes, or mutations. At times, these mistakes in a gene’s message can be harmful; often, they have no significant effect. Occasionally, though, a mutation confers a survival advantage in the face of an environmental change. Most of the non-carriers of the mutation die, and those with the mutation are able to reproduce. With that powerful evolutionary selection force, the gene can become common in a population.

Recently, scientists were astonished to find that some individuals did not become infected with HIV, even after repeated exposure to the deadly virus.

For some reason, they were immune. A long and difficult scientific search, using blood samples from hundreds of HIV-resistant patients, finally teased out the genetic explanation. Resistant individuals had in their cells two copies of a mutation that disrupted the entryway through which HIV viruses entered white blood cells. People who inherited just one copy of the change could become infected, but their disease progressed more slowly.

With this being such a recent epidemic, where did peoples’ immunity come from?

Another puzzle was the way this resistance is distributed throughout the world. In some Northern European populations it is relatively common. In Southern Europeans it is more rare, and it is almost entirely absent in Africans, Asians, and Native Americans. Logically, the mutation must have occurred in the past, acting as a defense against a different, previous epidemic caused — like the AIDS epidemic — by a pathogen that also targeted white blood cells.

Reading a chronological history, biologists traced the HIV-resistance gene mutation back about 700 years. That was the time at which the Black Death — bubonic plague — swept like a deadly scythe through Europe, killing one-third of the population. Then, as now, there were individuals who survived the lethal organism, perhaps because it could not enter their white blood cells. The areas that were hardest hit by the Black Plague match those where the gene for HIV resistance is the most common today.

At present, scientists are trying to infect such resistant cells with bubonic plague bacteria to test the hypothesis that the mutation in the CCR-5 receptor gene could have thwarted the plague in the Middle Ages, as it does HIV today. If it turns out that this mutation does protect against the plague, this coincidence will be yet another illustration of what scientists are finding over and over in the human genome: Nature’s past successes often remain part of our genetic toolbox.

Copyright © 2001 WGBH Educational Foundation and Clear Blue Sky Productions, Inc. All rights reserved.

Evolutionary Arms Race [VHS]

2011-07-11T23:53:00.000-07:00

The Anal Dialogues
by Trenton Straube

Rectal microbicides-topical gels, ointments and lubricants laced with ?drugs to block HIV-could help stop the spread of the virus. So why is it taking so long to develop them? For one thing, an unwillingness to talk about sex-especially anal sex. Given the potential of microbicides' protective power, it's time we loosen our tongues in order to start saving lives.

In 1992, at a meeting of the Delaware Valley Women and AIDS Network, Anna Forbes first heard about experimental compounds called vaginal microbicides. It sparked an “A-ha!” moment for the longtime advocate for women’s health. Forbes saw right away how a microbicide—a gel, cream, lubricant or other topical agent that could be applied to the vagina to inhibit sexual transmission of HIV—would offer a much-needed method of protection to women, especially those who couldn’t get their partners to use condoms. And as an advocate for gay men’s health, Forbes also imagined how a rectal microbicide could offer a valuable prevention tool for anal sex for both men and women.

Women and gay men share the common concern of having their health needs respected and addressed, Forbes says. “A receptive partner is a receptive partner.” Effective microbicides would arm both male and female receptive partners with prevention tools that could save their lives.

But when she started talking about the notion of vaginal and rectal microbicides, Forbes found that even people on the cutting edge of women’s and gay men’s health advocacy were uncomfortable talking so specifically about sex, especially anal sex. It showed, according to Forbes, “this weird way that homophobia and sexism intersected.” And it pointed out “the well-kept secret that women have anal sex too.”

Undaunted by the reluctance of many of her peers, and inspired by the potential lifesaving power of microbicides, Forbes set out to convince the world to think similarly, working for a decade at the Global Campaign for Microbicides (she recently moved into consulting). The topic continued to be a hard sell. “The trouble with microbicides in comparison to pills and injections,” Forbes says, “is that they are applied ‘down there.’ You can’t talk about microbicides without talking about sex.”

Thanks in part to the unflagging efforts of Forbes and other visionary leaders (along with increasingly promising research data), the scientific and advocacy communities began rallying around vaginal microbicide research. Yet, very few people supported the notion of a rectal version. Forbes recalls the first time she saw the topic discussed in the print media, in a 1999 POZ article, “Beyond Condoms: Life After Latex,” in which journalist Michael Scarce presciently wrote: “The astonishing thing is, gay men raise no voice to advocate for a form of HIV prevention that maximizes pleasure and safety.” In Colorado the next year, at the second LGBTI Health Summit (the initials embrace lesbian, gay, bisexual, trans and intersex people), Forbes gave a presentation on the need for rectal microbicides. Only about five people showed up. Clearly, interest in the subject was lacking—even among the most likely benefactors, gay men.

Then, another A-ha! moment: The messenger, Forbes realized, needed to double as the message. A straight woman couldn’t draw the same attention in the gay community as a gay man could. “We needed a gay male face, somebody with a track record in the [prevention] field,” she says. She envisioned an organized group led by a gay man working to promote rectal microbicides and in the process tackling the taboos associated with anal sex. In 2005, Forbes approached some likely advocates: Marc-André LeBlanc from the Canadian AIDS Society, Julie Davids from CHAMP (Community HIV/AIDS Mobilization Project) and Jim Pickett of the AIDS Foundation of Chicago. Although all were overextended, they agreed on the need to fight for a new form of prevention. Thus, the International Rectal Microbicide Advocates (IRMA) group was formed.

IRMA began modestly. “We had a listserv, and our goal was to get people to share information [about rectal microbicides],” says Pickett, IRMA’s chair (its out, gay face). He recalls begging people at the 2005 National HIV Prevention Conference to join the email group. Many resisted, arguing that rectal microbicides were too futuristic and that advocating for them would deflect resources from the priority concern at the moment: condoms. “People would almost groan when Jim would get on stage,” says Ian McGowan, MD, a leading microbicide researcher.

People’s reluctance to talk about butts (male and female), similarly muzzled scientists. As recently as a few years ago, many researchers scoffed at the very idea of a rectal microbicide, claiming human anatomy made it impossible. Unlike the vagina, which is essentially an enclosed container, the five-foot-long colon, Pickett says, is “like the Holland Tunnel.” There was the question of how far ejaculate could travel up the colon. Would the colon’s entire surface have to be protected? How much gel would be required—and how much could a body take? Scientists didn’t know. That is, until Craig Hendrix, MD, at Johns Hopkins University, conducted experiments involving some brave volunteers, faux microbicides and a hollow dildo that squirted an “ejaculate” traceable by MRI scans. (Read one volunteer’s hilarious account, “Putting My Ass on the Line,” on the IRMA blog at irma-rectalmicrobicides.blogspot.com.)The experiments proved that the faux microbicide traveled well with the ejaculate and that to be effective, a microbicide would likely need to coat only the lowest 4 to 6 inches of the rectum and anal canal. Furthermore, researchers determined that ?humans could tolerate up to 30 milliliters (ml) of gel administered anally. However, the gel currently being studied requires only 4 ml, less than a teaspoon.

If these details make you squirm, you wouldn’t want Pickett’s job. The gregarious advocate constantly finds himself discussing anal sex and all its details—often in front of crowds. He does so as easily as most guys rattle off sports stats, employing honesty and humor that prove disarming. Equally important, he and IRMA back up their cause with something scientists recognize: cold, hard data.

Perhaps IRMA’s most visible work is three game-changing reports it published in conjunction with the biennial International Microbicides Conference. The first, Rectal Microbicides: Investments & Advocacy in 2006, compiled what research was being done and where—a tricky task. “A lot of researchers were concerned that if ‘anal’ or ‘rectal’ appeared in research proposals or reports, they wouldn’t get funded, so they’d scrub their papers so those words wouldn’t show up,” LeBlanc says. “Instead, they would refer to ‘topical use of products’ or other language.” And because of the dangers surrounding the subject—male-to-male sex is illegal in many countries, including 31 in sub-Saharan Africa—IRMA first had to gain researchers’ trust, proving they were not raging advocates who would alienate and antagonize. Their professionalism paid off, and the report was a hit. “It showed we were serious,” Pickett says, “and we got hundreds of new members.”

The next two reports, Less Silence, More Science in 2008 and From Promise to Product: Advancing Rectal Microbicide Research and Advocacy in 2010 (all the reports are available at rectalmicrobicides.org), addressed the reality that anal sex is more common than believed. The reports showed that among women anal sex remains an overlooked driver of the AIDS epidemic. (Because there are more women in the world than gay men, the overall number of women having receptive anal sex is higher than that of gay men.) By amassing data and research from across the globe, the reports argue effectively for developing rectal microbicides. A sampling from the 2010 report:

It is estimated that unprotected anal intercourse transmits HIV 10 to 20 times more effectively than unprotected vaginal intercourse.
Gay men in the developing world are 19 times more likely to be positive compared with the general population.
In the United States, men who have sex with men (MSM) represent 53 percent of new HIV infections.
Depending on the study, 20 to 75 percent of women report having engaged in receptive anal sex.
Globally, up to seven times more women than men have receptive anal sex.

To confront homophobia and varying cultural and religious belief systems that complicate HIV prevention (for example, the tendency in Africa to focus solely on vaginal transmission), IRMA launched Project ARM (Africa for Rectal Microbicides) and IRMA-ALC (IRMA-America Latina y el Caribe).

Beyond advocacy and education about anal sex, IRMA helps shape a unified research agenda, coordinating studies among disparate, often unconnected researchers across the globe. (“We herd the cats,” Pickett says.) It directs funds to needed areas (though it doesn’t directly fund research). It digests complex research into talking points for mainstream media, translates reports into other languages, asks important questions and pursues answers.

Along the way, microbicide research has produced some immediate benefits. At a 2006 Cape Town AIDS conference, biomedical scientists with the Population Council presented data on the possible link between anal lubes and HIV risk. (The same team, lead by David Phillips, PhD, reported in 2000 that the spermicide nonoxynol-9 damaged linings of the rectum and vagina, thus increasing the risk for HIV and herpes—findings that resulted in N-9 being removed from most condoms.) The lube presentation, Pickett says, sparked his own revelatory moment. “We were like, The lubes we have are not tested for safety? We have to get research on this. Yes, we want rectal microbicides, but people are using lubes today!”

At the time, little was known about the popularity, use and safety of anal lubes—in the United States, lubes must be tested for vaginal irritation (in rabbits) but not for rectal use. To build a research database, IRMA conducted a survey. “We thought we’d get a few dozen answers,” LeBlanc says, “but we had nearly 9,000 people respond from nearly 100 countries.” The survey was translated into six languages. “As far as we know, it’s the largest survey on anal sex in the world.” (IRMA is following up with a survey on douches and enemas, which might affect HIV/STI risk and offer a mode of microbicide delivery.)

The survey results have been pivotal to researchers such as Charlene Dezzutti, PhD, a lab director at the Microbicide Trials Network, who is examining the lube qualities that might affect HIV risk and be of use in microbicides. (For more on lube safety and her findings, see "Slippery Slopes," on the following page.)

IRMA’s hard work is paying off elsewhere too. The energetic listserv now includes more than 1,000 members. Pickett manages its daily conversation from his office at the AIDS Foundation of Chicago (AFC), where he is director of advocacy (IRMA is a project of AFC). “I think the overarching thing that has made us successful is that we bring together scientists and advocates,” Pickett says. “There is no other forum like this. An advocate in Thailand can post an opinion, and a researcher in Peru or London or Pittsburgh can comment all in the same hour—people find it really useful.”

Discussions range across prevention topics including study results, female condoms and Uganda’s Anti-Homosexuality Bill. One round of emails discussed a British safe-sex musical video with the problematic lyrics, “Something to remember as a rule of thumb, one up the bum and there’s no harm done…one up the bum and you won’t be a mum.” (Listserv members contacted the video’s creators to argue against promoting anal intercourse as a risk-free way to avoid getting pregnant.)

“[IRMA is] doing all the right stuff,” says Forbes, speaking like a proud momma. “They’re recognizing the importance of geographic and constituency diversities, and they’re promoting everybody having the discussion in whatever way makes sense in their own communities and encouraging people to share ownership—exactly what we need.”

This year, IRMA had good news to trumpet. A Microbicide Trials Network study, MTN-006, found that people who used a rectal gel containing 1 percent tenofovir, an HIV drug, had high concentrations of the med in rectal tissue and lower concentrations in the blood stream, which could mean fewer side effects. The downside: A single dose before sex probably won’t be effective.

Today, people no longer groan when Pickett takes the stage. “People came up to me after the CAPRISA results [a large South African microbicide study] and said, ‘For all these years, I thought you were crazy, but you’ve proven me wrong. Now I understand why you had such a belief in this.’”

Perhaps IRMA’s biggest success is simply getting people to confront the realities of anal sex and HIV. Because without honest dialogue about sex—whether at an international science conference, a sex education class or an intimate chat between lovers—we are never going to stop this epidemic. And that’s something we all need to speak up for.

Slippery Slopes

Can lubes increase the risk of HIV during anal sex?

A slew of recent studies suggest that using lubes for unprotected anal sex may increase the risk of HIV, and that some lubes may harm the rectum’s thin protective layer of cells (the epithelium). It’s premature to know which brands to avoid, says Marc-André LeBlanc, a lube advocate with the International Rectal Microbicide Advocates (IRMA). Most research has been done in laboratories, and it isn’t certain whether the findings translate to humans—or whether the products’ lubricating benefits outweigh their potential harm. But one fact is certain: “The best way to prevent acquiring HIV and STIs [sexually transmitted infections] during anal sex is still using male or female condoms,” LeBlanc says. “And we know that using lubes with condoms decreases the risk of the condom slipping or breaking—a big bonus.”

In the meantime, here’s a highlight of what scientists are investigating and how lube qualities might affect the success of microbicides:

Polyquaterniums, a class of chemicals common in cosmetics, seem to increase HIV replication by almost four times in lab tests. A Population Council study found this ingredient in three of four HIV-enhancing Astroglide brand lubes: Astroglide Liquid, Astroglide Warming Liquid, Astroglide Glyercin & Paraben Free liquid and Astroglide Silken Secret.
Osmolality refers to the concentration of salts, sugars and other substances (solutes) present in a lube. Hypo-osmolar lubes have a lower concentration of solutes than human cells and cause the cells to swell with water and burst. Hyperosmolar lubes cause cells to shrink and become brittle. Iso-osmolar lubes don’t affect cells because their concentrations are identical.
Most water-based lubes are hyperosmolar and damaging.
pH balance is acidic in the vagina and neutral in the rectum. Many lubes are designed for the vagina—does the difference in pH mean they affect the rectum differently?
Good and bad bacteria live in a delicate balance in the vagina and gut. Will disrupting this balance make the rectum more susceptible to HIV?
Viscosity is the slippery quality that gives lube its feel and texture. Glycerin, in water-based lubes, adds to viscosity. It also makes lubes hyperosmolar—and destructive to epithelium. When a rectal microbicide now in trials proved harmful to the epithelium, researchers solved the problem by lowering the glycerin content.

Charlene Dezzutti, PhD, with the Microbicide Trials Network and the University of Pittsburgh, looked at these qualities in six popular lubes. Some findings: Pré and Wet Platinum appear safest. Pré is the only water-based lube that is iso-osmolar and doesn’t damage the epithelium. KY Jelly wiped out entire colonies of good bacteria. Astroglide is the most hyperosmolar and most toxic to cells and tissue (Elbow Grease, ID Glide and KY Jelly have similar toxicity profiles). But Dezzutti also warns that more studies are needed before any official warning or suggestions can be issued.

Starting to Gel

Microbicides: Where they are now and where they are going

VAGINAL GEL: After two decades of disappointing results, a breakthrough arrived last summer with results of the CAPRISA 004 trial: Women using a gel containing 1 percent tenofovir (an HIV med found in Atripla, Viread and Truvada) had 39 percent fewer infections than those using a placebo. Women with 80 percent adherence to the two necessary applications per sex act (12 hours before, then immediately after) had even fewer infections. The gel also offered protection against herpes.

What’s Next: Studies are under-way to confirm CAPRISA 004 results and determine the most effective concentrations and doses, but the global economic crisis has depleted funding, slowing progress. On the bright side, the drug from the vaginal gel is showing up in rectal tissue, so one product might offer women protection in both areas.

RECTAL GEL: Microbicide Trials Network study MTN-006 looked at using the vaginal tenofovir gel rectally, with promising results announced in February. Although the vaginal formulation harmed the rectal lining and caused gastrointestinal distress, Charlene Dezzutti’s team developed a better version with less glycerin. And, says Ian McGowan, PhD, a co-principal study investigator, “We found that when you give the drug topically, you get very high concentrations in the rectal tissue—a hundred times the amount from a single Viread tablet.” A few caveats: Tenofovir works not by directly attacking and disarming HIV, but by accumulating in the tissue and CD4 cells HIV will attack, preventing HIV from replicating once it invades the cell. Unfortunately, this accumulation demands repeated doses. “I think MTN-006 suggests,” McGowan says, “that if you just take one dose, orally or rectally, half an hour before exposure, I would doubt you’d be protected.”

What’s Next: A Phase I study (MTN-007) on the safety and acceptability of the rectal tenofovir gel; and Project Gel, investigating the use of rectal microbicides among African-American and Latino men who have sex with men (MSM). “It’s critical,” McGowan says, “because these are the people who are getting infected and need the product.”

FUTURE IDEAS AND EXPERIMENTS:

Other HIV meds or combos—or completely new compounds—may offer better protection than tenofovir as microbicides (hint: HIV drugs that are too toxic as pills may work as topical solutions).

Different modes of delivery: How about a slowly dissolving ring instead of a vaginal gel? Or combining a microbicide with a vaccine, to help prepare the immune system for an encounter with HIV? And vaginal probiotics—living microbicides—could be created by genetically altering bacterial cultures such as the common lactobacilli.

Research is showing that HIV might lower the electrical barrier of epithelial cells, enabling infection even without surface damage. Such new knowledge could produce future strategies and modes of protection.

Copyright © 2011 Poz Magazine

2011-07-08T00:20:00.000-07:00

Maraviroc Abacavir STudy - Effect on Endothelial Recovery

HIV infected patients treated with abacavir might have a higher risk for the occurrence of cardiovascular events. At time of writing of this protocol the underlying mechanism is not yet elucidated, however some studies find impaired endothelial function and elevated markers of chronic inflammation in these patients,suggesting a higher lever of chronic inflammation. Recently maraviroc...

Brief Summary

Official Title: “Maraviroc Abacavir STudy - Effect on Endothelial Recovery”

HIV infected patients treated with abacavir might have a higher risk for the occurrence of cardiovascular events. At time of writing of this protocol the underlying mechanism is not yet elucidated, however some studies find impaired endothelial function and elevated markers of chronic inflammation in these patients,suggesting a higher lever of chronic inflammation.

Recently maraviroc (Celsentri®), a CCR5-receptor antagonist, became available for treatment of patients infected with HIV-1.

Improvement of endothelial function may be a potential beneficial side effect of treatment with maraviroc, due to the potential reduction of immune activation and chronic inflammation as a result of blocking the CCR5-coreceptor. Moreover, treatment intensification of HAART with maraviroc in patients with suppressed plasma HIV_RNA may decrease plasma HIVRNA below the cut-off of 50 copies/ml as well.

The investigators hypothesize that maraviroc intensification therapy in patients on an abacavir-containing regimen will improve endothelial function.

The objectives of this study are: First, to assess the effect of addition of maraviroc to an abacavir-containing regimen on endothelial function; second, to assess the effect of this intervention on markers of immune activation and chronic inflammation, and on plasma HIV-RNA below 50 copies/ml.

Study Type: Interventional

Study Design: Allocation: Randomized, Endpoint Classification: Efficacy Study, Intervention Model: Crossover Assignment, Masking: Open Label, Primary Purpose: Treatment

Study Primary Completion Date: September 2012

Detailed Clinical Trial Description

The MASTER study is a phase IV, randomized, open label, cross-over, intervention study.

Study subjects who are on stable abacavir-containing regimen will be randomized into two arms. In arm A maraviroc will be added to their regimen at baseline, while study subjects in arm B will continue their abacavir-containing regimen. After 8 weeks, cross-over of the study arms will be performed. Subjects in arm A will then stop maraviroc, while in subjects in arm B maraviroc will be added to their regimen (for 8 weeks again). The total duration of the study will be 16 weeks.

Intervention(s) in this Clinical Trial

Drug: Maraviroc
HAART of subjects enrolled in arm A will be intensified with maraviroc during week 1-8.

Arms, Groups and Cohorts in this Clinical Trial

Active Comparator: Arm A
HAART of subjects in arm A will be intensified with maraviroc during week 1-8.
Active Comparator: Arm B
HAART of subjects enrolled in arm B will be intensified with maraviroc during week 9-16
Outcome Measures for this Clinical Trial

Primary Measures

Change in flow-mediated dilatation (FMD) of the brachial artery after 8 weeks of maraviroc treatment as compared to the control group
Time Frame: After 8 weeks of treatment (cross-over)
Safety Issue?: No

Secondary Measures

Change in markers of chronic inflammation
Time Frame: Baseline, week 2 (A) or 10 (B), week 4 (A) or 12 (B), week 8, week 16
Safety Issue?: No
Change in markers of immune activation
Time Frame: Baseline, week 2 (A) or 10 (B), week 4 (A) or 12 (B), week 8, week 16
Safety Issue?: No
Change in markers of endothelial function
Time Frame: Baseline, week 2 (A) or 10 (B), week 4 (A) or 12 (B), week 8, week 16
Safety Issue?: No
Changes in plasma HIV-RNA below 50 copies/ml
Time Frame: Baseline, week 8, week 16
Safety Issue?: No
Change in endothelial function measured by EndoPAT
Time Frame: baseline, week 8, week 16
Safety Issue?: No

Criteria for Participation in this Clinical Trial

Inclusion Criteria:

Age > 18 years
HIV-1 infection
Treatment with antiretroviral regimen containing abacavir for at least the previous 3 months
Undetectable plasma HIV RNA (50 cp/ml) for at least 6 months (one 'blip' allowed, which is defined as a detectable plasma HIV-RNA level between 50 and 400 copies/ml, preceded and followed by undetectable (<50 copies/ml) plasma HIV-RNA measurements) CD4+ cell count > 200 cells/µL
Signed informed consent

Exclusion Criteria:

Pregnancy
Breastfeeding
Allergy for peanuts or soya
Hypersensitivity for maraviroc
Treatment of underlying malignancy
Acute infection in the preceding 30 days
Renal insufficiency requiring hemodialysis
Acute or decompensated chronic hepatitis
Modification of antiretroviral regimen in the previous 3 months
Gender Eligibility for this Clinical Trial: Both

Minimum Age for this Clinical Trial: 18 Years

Maximum Age for this Clinical Trial: N/A

Are Healthy Volunteers Accepted for this Clinical Trial?: No

Clinical Trial Investigator Information

Lead Investigator: UMC Utrecht Other

Overall Clinical Trial Officials and Contacts

A IM Hoepelman, MD, PhD Principal Investigator UMC Utrecht

Overall Contact: Steven FL van Lelyveld, MD s.f.l.vanlelyveld@umcutrecht.nl

Additional Information

Information obtained from ClinicalTrials.gov on July 06, 2011
Link to the current ClinicalTrials.gov record. http://clinicaltrials.gov/show/NCT01389063
Study ID Number: MASTER2010
ClinicalTrials.gov Identifier: NCT01389063
Health Authority: Netherlands: The Central Committee on Research Involving Human Subjects (CCMO)

Copyright © 2011 ClinicalTrials

2011-07-07T23:59:00.000-07:00

CD4s Above 500: HIV Treatment Need Still Unclear

If you’re diagnosed with HIV and have a CD4 cell count above 500, should you start antiretroviral (ARV) therapy immediately? An Australian study suggests that even though there may be some immunologic benefits to starting therapy earlier than is currently recommended—once the CD4 count drops below 500—the jury is still out on whether this translates into important clinical benefits.

Despite more than 25 years of ARV research and the successful development of more than two dozen medications, scientists have not been able to determine the ideal time to begin therapy. Several studies have concluded that HIV treatment is best started before a person’s CD4 count falls below 350.

Some studies, conducted during the past five years, suggest that starting therapy even earlier—when the CD4 count is between 350 and 500—further increases the chances of disease-free survival. Less is known about the potential benefits of initiating therapy earlier still, when the CD4 count is above 500.

A large clinical trial, called the Strategic Timing of Antiretroviral Treatment (START) study, is being conducted to explore the safety and effectiveness of beginning treatment when the CD4 count is above 350 cells. Preliminary data, however, are not expected for at least another few years.

In the meantime, HIV-positive people and their health care providers are on the lookout for smaller observational and retrospective studies, such as the one recently published online by the Journal of Acquired Immune Deficiency Syndromes and based on data from Stephen Wright and his colleagues with the Australian HIV Observational Database.

Wright’s group looked at the outcomes of 432 people living with HIV who started ARV therapy with a CD4 count above 350 and had been followed for six years (72 months). For their analysis, the researchers divided the study volunteers into three groups: those who started treatment with a CD4 count between 350 and 500, those who started treatment with a CD4 count between 501 and 650 and those who started treatment with a CD4 count above 650.

Twelve months after beginning treatment, all study volunteers had CD4s above 500. Average CD4 counts, after a year of ARV therapy, were 596 among those who started with CD4s between 250 and 500, 717 among those who started treatment with CD4s between 501 and 650, and 881 among those who started treatment with a CD4 count in excess of 650.

After six years, CD4 counts were comparable between the three groups. Among those in the lowest pre-treatment CD4 group, the average CD4 cell count was 689. In the middle- and high-pretreatment CD4 groups, the average CD4 count after three years was 746 and 742, respectively.

Wright’s team also sought to determine whether there was a survival advantage between the three groups. Comparing their Australian data with those of another study, the researchers documented a modest 8 percent expected reduction in the risk of death among those who started treatment with more than 650 CD4s and a 4 percent expected reduction in the risk of death among those who started treatment with 501 to 650 CD4s, compared with those who started treatment with CD4s between 350 and 500. It is important to note, however, that the estimated number of deaths in these three groups were very low, which translated into very small differences in the absolute risk of death between those in the two highest CD4 groups compared with those starting with CD4s between 350 and 500.

“Our analysis suggests that patients who start [ARV therapy] at CD4 counts [greater than] 650 have better preserved immune function, but only to a relatively modest degree,” the authors conclude. “Furthermore the extent to which this might be expected to result in better clinical outcomes is uncertain.”

Copyright © 2011 AIDSmeds

2011-07-06T01:16:00.001-07:00

Will you please sign this petition and leave a comment to tell Washington and States to STOP cuts to ADAP and other HIV/AIDS services; and to instead FULLY fund these programs.

2011-07-06T00:16:00.001-07:00

Physicians urge FDA not to approve Truvada
Alaric Dearment

LOS ANGELES — A group of physicians is urging the Food and Drug Administration not to approve a drug made by Gilead Sciences for the prevention of HIV infection.

Fifty-five physicians signed a letter spearheaded by the AIDS Healthcare Foundation citing concerns about the use of Gilead’s Truvada (tenofovir disoproxil fumarate and emtricitabine) for “pre-exposure prophylaxis,” or PrEP. Concerns included the risk of a decrease in condom use and a lack of information showing proper use in “real world” situations.

“As medical care providers, we strongly support continued research on the prevention of HIV, but oppose approval of a pre-exposure prophylaxis that runs the risk of contributing to the spread of HIV and drug-resistant viruses,” the physicians wrote. “Our first obligation is to do no harm to individuals and to the public health.”

Copyright © 2011 Drug Store News

2011-07-06T00:09:00.000-07:00

How Much Is a Drug-Resistance Death Worth? Less Than $600
By Maryn McKenna

So, antibiotic resistance: We care about it, right? The World Health Organization does: It made antimicrobial resistance the theme of this year’s World Health Day. The Centers for Disease Control and Prevention does. The journal Lancet Infectious Diseases says it’s a “global health concern.” The major association for infectious disease physicians has pleaded for attention. Two separate sets of legislators have introduced two bills in Congress.

You’d think, with all those calls for attention, that combating antibiotic resistance would be a priority in the United States. But if we can take how much we spend to research a problem as a gauge of how much we care about it, then antibiotic resistance is no priority at all.

As in: For every death from AIDS, the US federal research establishment awards approximately $69,000 in grant funds. And for every death from MRSA, it awards $570.

The numbers come from an analysis presented at the World HAI Forum by Dr. Eli Perencevich of the University of Iowa (and the blog Controversies in Hospital Infection Prevention) and co-authors S. Kwon and M.L. Schweizer. (As far as I can tell, their poster is not online; perhaps they’ll post on it?)

As researchers competing for grants, they noted that the research budget at the National Institutes of Health has been rising, from $13.1 billion in 1998 to $28.7 billion in 2008; within that, so has the research budget at NIH’s National Institute of Allergy and Infectious Diseases (NIAID), from $1.4 billion to $4.6 billion over that same decade. They wondered how much of that research funding was going to this resistance problem that health authorities nationally and globally have pronounced a crisis. MRSA, let’s remember, kills an estimated 19,000 Americans a year: more than HIV, and more than pneumococcal disease, meningococcal disease, H. influenzae and group A Streptococcus combined.

They found the answer to be: Not very much.

To derive that answer, they drilled down into NIH’s Research Portfolio Online Reporting Tools database, RePORT for short, looking for all the grants awarded by NIAID that went to antibiotic resistance, antimicrobial resistance or hospital-associated infections. They especially looked for grants aimed at the seven most important resistant pathogens, the ones that cause the most illness and death and for which there are few remaining drugs that work: the Enterobacter species, MRSA and other resistant staph, C. difficile, Acinetobacter baumanii, Klebsiella pneumoniae, Pseudomonas aeruginosa and Enterococcus faecium, collectively known as ESCKAPE.

What they found looked, at first, to be encouraging: From 2007 to 2009, the amount per grant and the total amount awarded for those topics and pathogens had gone up. In 2007, the total was $180 million; in 2009, it was $398 million. But then they looked at what NIH awards for other infectious diseases, and at that point the picture was much less positive. In 2007, NIAID funding for HIV/AIDS was $1.24 billion.

Plotted against the 18,000 AIDS deaths that year, that came to $69,000 per death. Breaking the antibiotic resistance funding apart by pathogen, they compared the 2007 funding for MRSA and for C. diff, and for the 18,650 deaths from invasive MRSA and 6,372 deaths from C. diff. Per death, the funding for those organisms was $570 and $560.

I asked Perencevich to help me make sense of these numbers. He replied by pointing to the utter dearth of new drugs for resistant pathogens — and to the fact that, because HIV has been a research priority for most of the 30 years of its existence, research has brought forth thousands of antiviral compounds and drug combinations for treatment.

“That’s what funding can do,” he said. “We need a renewed focus on antibacterial drug discovery and infection prevention. Our take-home point is that we ought to bring to this the same vigor that we’ve brought to HIV.”

Copyright © 2011 Wired

2011-07-06T00:04:00.000-07:00

Is a HIV vaccine a viable option and at what price? An economic evaluation of adding HIV vaccination into existing prevention programs in Thailand

This study aims to determine the maximum price at which HIV vaccination is cost-effective in the Thai healthcare setting. It also aims to identify the relative importance of vaccine characteristics and risk behavior changes among vaccine recipients to determine how they affect this cost-effectiveness.

Methods: A semi-Markov model was developed to estimate the costs and health outcomes of HIV prevention programs combined with HIV vaccination in comparison to the existing HIV prevention programs without vaccination.

The estimation was based on a lifetime horizon period (99 years) and used the government perspective. The analysis focused on both the general population and specific high-risk population groups.

The maximum price of cost-effective vaccination was defined by using threshold analysis; one-way and probabilistic sensitivity analyses were performed. The study employed an expected value of perfect information (EVPI) analysis to determine the relative importance of parameters and to prioritize future studies.

Results: The most expensive HIV vaccination which is cost-effective when given to the general population was 12,000 Thai baht (US$1=34 Thai baht in 2009).

This vaccination came with 70% vaccine efficacy and lifetime protection as long as risk behavior was unchanged post-vaccination. The vaccine would be considered cost-ineffective at any price if it demonstrated low efficacy (30%) and if post-vaccination risk behavior increased by 10% or more, especially among the high-risk population groups.

The incremental cost-effectiveness ratios were the most sensitive to change in post-vaccination risk behavior, followed by vaccine efficacy and duration of protection. The EVPI indicated the need to quantify vaccine efficacy, changed post-vaccination risk behavior, and the costs of vaccination programs.

Conclusions: The approach used in this study differentiated it from other economic evaluations and can be applied for the economic evaluation of other health interventions not available in healthcare systems.

This study is important not only for researchers conducting future HIV vaccine research but also for policy decision makers who, in the future, will consider vaccine adoption.

Author: Pattara LeelahavarongYot Teerawattananon Pitsaphun Werayingyong Chutima Akaleephan Nakorn Premsri Chawetsan Namwat Wiwat Peerapatanapokin Viroj Tangcharoensathien

Copyright © 2011 7th Space Interactive

2011-07-05T23:58:00.000-07:00

People With HIV May Be More Prone To Nervous System Problems That Affect The Heart Rate

Results from a recent Danish study indicate that otherwise healthy HIV-positive individuals may have moderate dysfunction of the nervous system that affects the heart rate, even after years of antiretroviral therapy. In particular, the researchers found that people with HIV had significantly higher resting heart rates and lower heart rate variability compared to HIV-negative individuals.

Additionally, the moderate nervous dysfunction (known as autonomic dysfunction) was associated with higher blood sugar and cholesterol levels, although this was not the case for HIV-negative study participants.

Based on their results, the study authors recommended close monitoring and maintenance of blood sugar and cholesterol levels in people with HIV. They also suggested that further studies be conducted to understand why HIV-positive individuals might be more sensitive to the effects on the nervous system of changes in blood sugar and cholesterol levels.

Autonomic dysfunction is a malfunction of the body’s autonomic nervous system, which controls automatic functions such as heart rate, digestion, and perspiration. Autonomic dysfunction is linked to an increased risk of heart problems.

In particular, heart rate and heart rate variability, or how the time interval between heart beats varies, are linked to measures of congestive heart failure, damage from diabetes, and mortality risk after a heart attack. Normally the heart rate should vary according to certain signals from the body, such as respiration rate or stress levels; lower variability can indicate problems with the autonomic nervous system.

According to the study authors, results from previous studies have shown evidence of autonomic dysfunction in people with HIV, especially individuals with advanced HIV or AIDS. However, there have been few studies investigating autonomic dysfunction in HIV-positive individuals whose HIV is well controlled with antiretroviral therapy.

Although antiretrovirals have the potential to reduce damage to the nervous system caused by HIV, they have also been implicated in high cholesterol levels and pre-diabetes, which could themselves cause autonomic nervous system damage.

In this study, the authors investigated the presence of autonomic dysfunction, as measured by heart rate and heart rate variability, in HIV-positive individuals who had been on antiretroviral therapy for at least one year.

The study included 97 HIV-positive individuals and 52 age- and gender-matched HIV-negative individuals. Participants with HIV had been HIV positive for a median of 11 years and had taken antiretrovirals for a median of seven years; all but one had viral loads (amount of HIV in the blood) of less than 400 copies per milliliter.

None of the participants had any history of heart disease, diabetes, or were taking medication for high blood pressure.

In order to measure heart rate and heart rate variability, the researchers performed an electrocardiogram on each participant for 15 minutes after an initial 10-minute resting period.

The researchers found evidence of moderate autonomic dysfunction in the HIV-positive study group compared to the HIV-negative study group. In particular, HIV-positive participants had faster heart rates than HIV-negative participants, with the time between heartbeats an average of 77 milliseconds (about 8 percent) shorter.

In addition, the heart rate variability was around 10 percent lower in HIV-positive individuals compared to HIV-negative individuals.

Results also showed that the dysfunction was linked to higher blood sugar and cholesterol levels, but only in the HIV-positive participants.

There was no link between dysfunction and duration of HIV infection, viral load, CD4 (white blood cell) count, or duration or type of antiretroviral therapy.

For more information, please see the study in PLoS One.

Copyright © 2011 The AIDS Beacon

The Autonomic Nervous System. Part II. Dysfunctions

Disorders of the Autonomic Nervous System

2011-07-04T23:59:00.001-07:00

Reyataz side effect: Mononeuritis multiplex

A study of Mononeuritis multiplex among people who take Reyataz. The study is created by eHealthMe based on reports from FDA and user community.

On Jul, 4, 2011: 3,710 people reported to have side effects when taking Reyataz. Among them, 1 people (0.03%) has Mononeuritis Multiplex.

Copyright © 2011 eHealthMe

2011-07-04T23:56:00.001-07:00

Atazanavir/r exposure is associated with an increased rate of renal stones compared with efavirenz, lopinavir/r and darunavir/r

Authors: Rockwood N, Mandalia S, Bower M, Gazzard B, Nelson M

There have been no data presented on the relative rates of the development of renal stones (RS) in those receiving ritonavir boosted atazanavir (ATZ/r) when compared with other commonly used antiretrovirals (ARVs).

We compared the rate of development of RS in a cohort of HIV infected individuals attending the Chelsea and Westminster Hospital Foundation Trust exposed to ATZ/r with those exposed to efavirenz (EFV)/lopinavir/r (LPV/r) and darunavir/r (DRV/r) over a 45 month study period.

The rate of development of RS in the ATZ/r group(n?=?1206) compared to the EFV/LPV/r/DRV/r combined group (n?=?4449) was 7.3 [95%CI: 4.7-10.8] per 1000 patient years and 1.9 [95%CI: 1.2-2.8] per 1000 patient years (p?

When choosing a boosted protease inhibitor, ATZ/r RS should be considered as a potential co-morbidity.

Copyright © 2011 MedicineJournalFeeds

2011-07-04T23:51:00.000-07:00

A glimmer of a path to an AIDS vaccine
By Michael Gerson

In the 3-D model on the computer screen, the AIDS virus resembles a deformed head of broccoli, its clustered surface constantly shifting. Researchers at the National Institutes of Health’s Vaccine Research Center attribute moral characteristics to their enemy; it is “deceptive” and “diabolical.” The virus is covered in a cloak of sugars that mimic natural proteins, making it invisible to the immune system. Its true nature is only revealed to the body when the virus needs to get into a cell — latching onto a protrusion and injecting its genetic poison with a spring-loaded harpoon. It protects itself by constantly changing its genetic sequence. A person infected by one version of the virus, in a matter of weeks, can carry a million small mutations.

During its 30-year march, the virus has infected 65 million human bodies. Thirty million men, women and children have died. There is not a single example of an infected person whose immune system cleared the virus from his or her body.

This is the largest challenge for the vaccine researcher. The immune system has effective responses to diseases such as polio, measles or smallpox. Many people recover and gain immunity. The body itself proves that a vaccine is possible. But there is no naturally protective response to the AIDS virus. Medical researchers have to do better than nature.

During the decade following the creation of the Vaccine Research Center by President Bill Clinton, scientists gained a better understanding of the virus. But their main discovery was how difficult it would be to defeat. There was not even a scientific route to a solution. “It was like the ancient Greeks looking for a path to the moon,” recalls structural biologist Peter Kwong.

An audit of the center in 2008 would have found billions of dollars spent on few answers. But scientific progress often comes fitfully. “You do the groundwork,” says Gary Nabel, director of the center, “and then it pops.” In 2009, there were two unrelated breakthroughs. A Thai vaccine trial managed to produce a small protective effect, though researchers did not know why. At about the same time, improved diagnostics found that 10 to 25 percent of people with HIV produce antibodies that neutralize the virus — though the response is too weak and too late to make a difference.

The virus, it turns out, is vulnerable in one place. There is a portion of its cloak that can’t shift and camouflage itself — the small area where the virus latches on to the target cell. An antibody with the same footprint as the cell can block the attachment.

Scientists at NIH have now cloned that antibody. Produced in large enough quantities, it can be injected. Testing is scheduled to start next year. But even if this approach works, injecting manufactured antibodies won’t be an immediately practical solution. A gram of the antibody, Nabel estimates, might cost $100 to produce. Perhaps 100 million people would need to be injected once a month. This approach would be prohibitively expensive until costs are dramatically reduced.

The greater hope is a vaccine that could be injected once or a few times, producing an immune response that gives sustained protection. “We want the body to be the manufacturing plant for the antibodies,” explains Nabel. Unlike the precedent of other vaccines, it isn’t possible to use a dead version of the virus to produce immunity. It may be necessary to break off just the vulnerable bit of the virus, then introduce it into the body to provoke the production of antibodies. “It is not a fictional idea,” Nabel assures me. But it hasn’t been done before.

In the short and medium terms, neither injected antibodies nor a vaccine will be a substitute for other forms of AIDS prevention. Large reductions in infection rates can be achieved through consistent condom use, behavior change and circumcision. The treatment of HIV-infected pregnant women with AIDS drugs can prevent transmission to their children. Microbicide gels are promising.

But researchers at NIH know that an effective vaccine would be a decisive defeat for their wily enemy. “Every day there are 7,000 new infections,” reflects Nabel. “If we do our work a day sooner, it would make a difference.”

The day that work is finished remains distant. But now, at least, there is a path to the moon.

Copyright © 2011 Washington Post

2011-07-04T23:43:00.001-07:00

HIV drugs can lead to premature ageing of mitochondrial DNA
By Mehmet Fidanboylu

New research has revealed that a group of generic anti-HIV drugs may be linked to premature ageing. The study, which was carried out by UK scientists at the Institute of Genetic Medicine at Newcastle University, could explain why people treated with this class of drugs sometimes show signs of age-related conditions, such as heart disease and dementia.

The researchers studied muscle cells taken from people with HIV who had previously taken drugs known as nucleoside analogue reverse-transcriptase inhibitors (NRTIs) and found that DNA in the mitochondria of their cells had accumulated a number of errors that was more comparable to healthy people 20 or 30 years older.

'The DNA in our mitochondria gets copied throughout our lifetimes and, as we age, naturally accumulates errors. We believe that these drugs accelerate the rate at which these errors build up', said Professor Patrick Chennery, who led the study, adding: 'Over the space of, say, ten years, a person's mitochondrial DNA may have accumulated the same amount of errors as a person who has natural aged twenty or thirty years'.

NRTIs were a major breakthrough in the battle against HIV when they were developed in the late 1980s. But side-effects such as premature ageing and frailty have meant that they have been replaced by a cocktail of more recent drugs. However, NRTIs are generally favoured over these new drugs in developing countries due to their lower costs.

Until now it has not been clear why NRTIs, which include AZT or zidovudine, have these side-effects. 'HIV clinics were seeing patients who had otherwise been successfully treated but who showed signs of being much older than their years. This was a real mystery', said Professor Chinnery, 'but colleagues recognised many similarities with patients affected by mitochondrial diseases... and referred them to our clinic'.

Defects in mitochondrial DNA are often seen in age-related conditions, although it is not yet known whether this is a cause or consequence of taking the drugs.

It was estimated in 2009 that 33.3 million people had HIV, and of these 22.5 million live in Africa. The researchers were keen to stress that while NRTIs do sometimes have side-effects, not taking them would be worse: 'These drugs may not be perfect, but we must remember that when they were introduced they gave people an extra ten or twenty years when they would otherwise have died. In Africa, where the HIV epidermis has hit hardest and where more expensive medications are not an option, they are an absolute necessity', said Dr Brendan Payne, a co-author of the study.

The researchers will now look at how the damage believed to be caused by the drugs can be repaired. The study was published in Nature Genetics.

Copyright © 2011 BioNews

2011-07-04T10:12:00.001-07:00

Maraviroc Switch Collaborative Study (MARCH)

MARCH is an international, multicentre trial planning to enroll 560 HIV-1 infected patients who are currently on 2N(t)RTI + PI/r regimen and virologically suppressed.

Participants will be randomized (1:2:2) to one of three treatment groups: to continue their current treatment regimen, maraviroc dose at 150 mg twice daily with PI/r, or maraviroc at 300 mg twice daily with 2N(t)RTI. As the participants population have HIV RNA <200 copies/mL, the phenotypic assessment of tropism cannot be used to determine tropism, instead we will employ the genotypic assessment of tropism by sequencing the V3 loop of the HIV envelope.

The main aim of this study is to investigate whether switching to maraviroc, in combination with either RTI or PI/r, is as good at keeping the HIV viral load undetectable as the combination of RTI with PI/r. The other aim is to see if switching to these combinations with maraviroc will improve some of the side effects that can be seen when people take combination therapy including RTI and PI/r.

The study hypothesis is that in stable, virologically suppressed (plasma HIV-RNA <200 copies/mL) patients with no history of prior virological failure, a switch to either MVC dosed at 300mg twice daily (bid) combined with the same 2N(t)RTI backbone regimen or MVC dosed at 150mg twice daily (bid) with the current PI/r (or 300mg bid at the discretion of the investigator if the PI/r is fosamprenavir/r) provides similar (non-inferior) antiretroviral efficacy compared to continuation of the current 2N(t)RTI + PI/r regimen.

Copyright © 2011 ClinicalTrials.gov

2011-07-03T00:08:00.001-07:00

Study Reveals Why Some HIV-Infected People can Handle the Disease Better Than Others

The mechanism of how the immune system of the infected people handles HIV, and how HIV evades the immune system’s response has been revealed in a new study.

Researchers at Case Western Reserve University School of Medicine have discovered a long-sought cellular factor that works to inhibit HIV infection of myeloid cells.

Myeloid cells are a subset of white blood cells that display antigens and hence are important for the body’s immune response against viruses and other pathogens.

The factor, a protein called SAMHD1, is part of the nucleic acid sensing machinery within the body’s own immune system. It keeps cells from activating immune responses to the cells own nucleic acids, thus preventing certain forms of autoimmunity from developing.

SAMHD1 factor, researchers have found, can also sense and interfere with infection of myeloid cells, such as macrophages and dendritic cells, with HIV-1 and related immunodeficiency viruses.

As such, SAMHD1 prevents the synthesis of virus copies in these cells, according to research led by Jacek Skowronski, PhD, a professor in the Department of Molecular Biology and Microbiology.

“The identification of SAMHD1 and its function may help to explain why some infected individuals can control HIV infection better than others,” Dr. Skowronski said.

“Ultimately, it could also provide a basis for conceiving of new therapies and treatment approaches to block HIV infection and/or its replication in infected individuals, and to stimulate body’s own immune response to HIV,” he added.

The study was recently published in the journal Nature.

Copyright © 2011 MeD India

2011-07-03T00:05:00.000-07:00

Why people with HIV suffer memory loss despite potent therapy

Researchers at Albert Einstein College of Medicine of Yeshiva University have solved a longstanding medical mystery – why so many people with HIV experience memory loss and other cognitive problems despite potent antiretroviral therapy.

Even though antiretroviral treatment suppresses HIV replication and slows the progress of HIV disease, between 40 and 60 percent of HIV-infected people eventually develop mild-to-moderate neurological deficits, and up to 5 percent develop full-blown dementia.

Until now, researchers have not been able to explain why these complications, collectively known as neuroAIDS, occur.

In a previous study, the Einstein researchers found that HIV infects about 5 percent of brain cells known as astrocytes.

These cells bolster the blood-brain barrier, a network of blood vessels that prevents harmful substances from crossing into the brain from the bloodstream.

Now, they have shown that even this low-level of astrocyte infection can profoundly damage the blood-brain barrier.

“The relatively few infected astrocytes emit toxic signals through specialized channels that kill neighboring uninfected astrocytes, ultimately weakening the blood-brain barrier and allowing harmful compounds to enter the brain,” said senior author Joan Berman, Ph.D., professor of pathology and of microbiology and immunology at Einstein.

The evidence came from a laboratory model of the blood-brain barrier constructed of human cells and from examining brain tissue of macaque monkeys infected with the simian form of HIV.

The results suggest that drugs capable of reducing the damaging signaling cascades triggered by HIV-infected astrocytes might help in preventing or treating neuroAIDS.

Their findings were published in the June 29 issue of The Journal of Neuroscience. (ANI)

Copyright © 2011 Truth Dive

2011-07-02T00:11:00.000-07:00

Who Should Consider HIV Tropism Testing for Maraviroc Response?

Experts, such as the U.S. Food and Drug Administration and the Department of Health and Human Services, agree that all people planning to start maraviroc (Selzentry®) therapy should have human immunodeficiency virus may also be considered for people taking maraviroc who are not responding as hoped.

Before starting therapy

Maraviroc drug information (approved by the US Food and Drug Administration) says that only adults with CCR5-tropic HIV should take maraviroc. Maraviroc only works in people with CCR5-tropic HIV. It does not work on those with CXCR4-tropic HIV, or HIV that uses both receptors.

The way to find out which receptor your kind of HIV infection uses is with HIV tropism testing. Everyone considering maraviroc therapy needs to have HIV tropism testing before taking the drug. In rare cases, therapy may start before these test results are available. In these rare cases, testing should be done as soon as possible.

When therapy doesn’t work

Some experts believe that HIV tropism testing should be repeated if maraviroc doesn’t work as expected. There are many reasons maraviroc may not work, including a dose that is too low, not taking the drug regularly enough, or being resistant to the drug for reasons other than HIV tropism.

Another important reason maraviroc may stop working is that HIV viral tropism can change over time. Someone who has CCR5-tropic virus at the beginning of therapy can later have CXCR4-tropic virus.

A Department of Health and Human Services Panel on Antiretroviral Guidelines for Adults and Adolescents recommends:

“Coreceptor tropism assay should be performed whenever the use of a CCR5 inhibitor is being considered.”

“Coreceptor tropism testing might also be considered for patients who exhibit virologic failure on a CCR5 inhibitor.”

Copyright © 2011 Aspirus Genetics

2011-06-30T20:26:00.000-07:00

HIV disrupts blood-brain barrier

HIV weakens the blood-brain barrier — a network of blood vessels that keeps potentially harmful chemicals and toxins out of the brain — by overtaking a small group of supporting brain cells, according to a new study in the June 29 issue of The Journal of Neuroscience. The findings may help explain why some people living with HIV experience neurological complications, despite the benefits of modern drug regimens that keep them living longer.

Standard antiretroviral treatments successfully suppress the replication of HIV and slow the progression of the disease. Yet recent studies show 40 to 60 percent of patients on such therapy continue to experience mild to moderate neurological deficits — including memory loss and learning challenges.

In the new study, Eliseo Eugenin, PhD, of Albert Einstein College of Medicine, found that HIV infection in a small number of supporting brain cells called astrocytes breaks down the blood-brain barrier, despite low to undetectable viral production. Under normal conditions astrocytes help bolster the blood vessels comprising the barrier.

Astrocytes (pictured in green) help to support blood vessels (red) that act as the blood-brain barrier - a network that keeps potentially harmful chemicals and toxins out of the brain. This image shows the close interaction between the cells in the human brain. Credit: Eugenin, et al. The Journal of Neuroscience 2011.

To test if HIV interfered with this support system, Eugenin and his colleagues built a model of the blood-brain barrier using human cells in the laboratory. In a previous study, the researchers found HIV infects around 5 percent of astrocytes. In the current study, the researchers found the presence of HIV in a similar percentage of astrocytes led to the death of nearby uninfected cells and made the barrier more permeable.

As the neighboring cells died, however, HIV-infected astrocytes survived. Astrocytes exchange chemical signals through specialized molecules called gap junctions. When they were blocked in the model, it prevented the changes to the blood-brain barrier and nearby cells, suggesting the infected astrocytes relay toxic signals to neighboring cells through the gap junctions.

“Our results suggest HIV infection of astrocytes may be important in the onset of cognitive impairment in people living with the disease,” Eugenin said. “New therapies are needed that not only target the virus, but also to stop the virus from spreading damage to other uninfected brain cells.”

Eugenin’s group also analyzed the brain tissue of macaque monkeys infected with the simian form of HIV. Similar to what they saw in the human blood-brain barrier model, the researchers found uninfected cells in contact with HIV-infected astrocytes died, while infected astrocytes remained alive as the disease progressed.

“Researchers have been stymied to explain why HIV-associated neurological complications persist, despite potent combination antiviral therapies that have dramatically improved health and survival,” said Igor Grant, an expert who studies HIV-associated neurocognitive impairment at the University of California, San Diego. “This study provides a possible explanation indicating that minute numbers of infected astrocytes can trigger a cascade of signals that could open the brain to various toxic influences.”

The findings open up the possibility of developing new therapeutic approaches that block or modify the transmission of signals from the HIV-infected astrocytes, added Grant, who was not affiliated with the study.

Copyright © 2011 Society for Neuroscience: http://www.sfn.org

2011-06-30T20:08:00.000-07:00

Gilead Sciences and Tibotec to develop combination HIV therapy

Gilead Sciences has announced a new alliance with Tibotec Pharmaceuticals that will see the companies produce a combination treatment for HIV.

The license agreement will focus on the development and commercialisation of a fixed-dose antiretroviral therapy, combining Tibotec's approved HIV drug Prezista with Gilead's investigational pharmacoenhancing agent cobicistat.

Should this treatment be approved, Tibotec would take responsibility for its global production and sales, with Gilead retaining the rights to cobicistat as a standalone product.

The companies are also in discussions over a similar collaboration to create a single-tablet HIV regimen combining Prezista with Gilead's compounds Emtriva and GS 7340, as well as cobicistat.

Dr Norbert Bischofberger, Gilead's executive vice-president for research and development and chief scientific officer, said: "This agreement represents another important step forward in our commitment to developing simplified treatment regimens that can help address the individual needs of people living with HIV."

Earlier this year, the company entered into an alliance with MicroDose Therapeutx to develop a new treatment for respiratory syncytial virus.

Copyright © 2011 Zenopa

2011-06-29T23:51:00.000-07:00

If you’re HIV positive, safe sex isn’t just about condoms
Deborah Jack

As the HIV epidemic has evolved over three decades, the “just use a condom” message has remained the cornerstone of prevention. But stubbornly high levels of new HIV infections in the UK show we’ve struggled to always translate this simple message into real life.

Most monogamous couples will decide to stop using condoms at some point, but what if one half of the couple is HIV positive? Until recently, it has been assumed there is no safe option other than condoms for life. But new research into the preventive benefits of HIV treatment (antiretroviral therapy) is set to change this, and could potentially revolutionise the way we think about HIV prevention and safer sex advice.

HIV treatment works by reducing the level of HIV in the body (the viral load) to such an extent that a person’s infectiousness is almost zero (clinically referred to as “undetectable”). A big effect of this — in addition to keeping the person healthy — is that the risk of transmitting HIV to another person is dramatically reduced.

Last month we heard the conclusive results of the first global study into HIV “treatment as prevention” — a 96% reduction in transmission risk when the HIV-positive partner received treatment and responded effectively. When put into practice, this means people living with HIV who are on treatment can, like everyone else, consider giving up condoms when their relationship is committed and monogamous.

But before we get carried away, it is not time to throw away our condoms altogether. They are still the best protection against other sexually transmitted infections, so any couple wanting to rely on treatment rather than condoms to prevent HIV transmission must be confident they are both STI free and monogamous. Other STIs in the body can make HIV levels spike upwards, which seriously compromises the effects of treatment as prevention and significantly increases risk of transmission.

The notion of ditching the condoms when one half of a couple is HIV positive also throws up other practical challenges in a relationship. A condom is visible, its use is mutual, and if it fails this is usually evident. By contrast, the level of HIV in a person’s body is invisible has been measured at some point in the past (up to four months, usually) and that information has been given to only one of the sexual partners. Very different issues of trust are involved and to rely on this method means relying in both partners’ faithfulness, or on their courage to come clean if they have sex with anyone else.

Last year, at the National Aids Trust’s seminar on HIV treatment as prevention, we heard stories from couples who were in this situation and trying to navigate their safer sex options in a way that suited them both.

Some couples were happy to rely on treatment as prevention, but for others it was a lot more complex. In some instances the negative partner was happy to rely on treatment but the positive partner was too worried about the risk (however small) of passing HIV on to the one they love. For others it was the opposite, with the HIV-negative partner anxious about risk of infection despite the HIV positive partner’s desire to no longer use condoms.

What is clear from people’s experiences is that HIV treatment as prevention is not some “quick fix”. There remain complex issues of love and trust to negotiate, as well as unlearning the internalised stigma and fear around HIV, which people have lived with for years.

This is not to say that treatment as prevention will only have benefits for those who are in long-term, monogamous relationships. Being on treatment will still reduce infectiousness even if you have more than one partner, but you could not rely on it to prevent transmission in the same way that an exclusive couple might.

Additionally, one of the biggest barriers to HIV treatment as prevention is the fact that at least a quarter of people living with HIV in the UK have not been diagnosed — and therefore are not on treatment.

So with the exception of those in completely monogamous (and honest) relationships, the message is still “use condoms”. But the fact remains that people will always make their own decisions based on the level of risk they’re prepared to live with.

What we need is clear guidance on how individuals should be advised on using “treatment as prevention” as a safer sex option and this should be combined with renewed efforts to encourage condom use. Crucially, this will require appropriate, accessible support for those people who find using condoms or negotiating their use difficult — a much larger number of people than is usually acknowledged.

Thirty years into the epidemic, an HIV prevention revolution could be upon us. But the basic need for well-resourced, appropriate HIV and sexual health support services remains the same. And while we aren’t ready to lay condoms to rest just yet, the “just use a condom” message can now be combined with a new source of encouragement for those diagnosed with HIV that if they commence and stick to their treatment, when the timing is right in their lives there will be another option available to them for safer sex.

Copyright © 2011 The Guardian

2011-06-28T23:59:00.000-07:00

Cushing’s syndrome and adrenal axis suppression in a patient treated with ritonavir and corticosteroid eye drops.
Molloy A, Matheson NJ, Meyer PAR, et al.

A 51-year-old woman with HIV presented with weight gain and a 1-month history of right hip pain. Her ART included tenofovir (300 mg once daily), emtricitabine (200 mg once daily), and atazanavir/ritonavir (300/100 mg once daily). Because of previous bilateral cytomegalovirus retinitis, complicated by immune recovery uveitis with severe, chronic, cystoid macular oedema, she was also using dexamethasone 0.1% eye drops six times daily, and betamethasone 0.1% eye ointment at night, in both eyes.

On examination, she was noted to have central adiposity and enlargement of the dorsocervical fat, but no peripheral lipoatrophy. An MRI scan of the hip showed avascular necrosis. A tetracosactide (Synacthen) stimulation test showed marked suppression of the pituitary-adrenal axis, with a baseline cortisol of less than 25 nmol/L rising to only 37 nmol/l 30 min after administration of tetracosactide 250mg (normal response at 30 min, >570 nmol/L). Adrenocorticotropic hormone (ACTH) was undetectable.

The presence of adrenal axis suppression with low ACTH, in the context of Cushingoid features and avascular necrosis of the hip, suggested ongoing exposure to high systemic levels of exogenous corticosteroids. Ritonavir and atazanavir were substituted with efavirenz (600 mg once daily), while continuing the steroid eye drops. Oral hydrocortisone 15 mg daily was added to avoid precipitating crisis due to adrenal insufficiency. Over the following year, the patient’s weight declined, with marked improvement in her adrenal function. Analysis of stored serum samples revealed elevated levels of dexamethasone at presentation (1.4-1.7 nmol/L) which fell dramatically after discontinuation of protease inhibitor therapy (undetectable to 0.181 nmol/L).

Although prior courses of oral and intravenous corticosteroids may have contributed to adrenal axis suppression, the close temporal correlation between discontinuation of ritonavir, reversal of weight gain and recovery of adrenal function, combined with detectable levels of dexamethasone in the blood, strongly suggests that co-administration of ritonavir was responsible for the accumulation of excessive systemic levels of topical ocular corticosteroids, resulting in adrenal axis suppression and Cushing’s syndrome.

Click here for the reference from PubMed.

Copyright © 2011 HIV-druginteractions.org

2011-06-28T23:52:00.000-07:00

Norvir-Free Boosted Prezista Tablet in the Works

Tibotec Therapeutics—the research and development division of Janssen Pharmaceuticals—has entered an agreement with Gilead Sciences to develop a fixed-dose combination (FDC) tablet containing its protease inhibitor Prezista (darunavir) and Gilead Sciences’ experimental boosting agent cobicistat, according to a Janssen announcement.

During the past decade, a number of different HIV drugs have been combined into single pills, both to reduce the total number of pills that people with HIV take and to extend the rights of companies to exclusively sell their drugs. The most successful of these combinations, Atripla—which contains Bristol-Myers Squibb’s Sustiva (efavirenz) and Gilead’s Truvada (tenofovir plus emtricitabine)—was the first to combine drugs from two different companies.

Aside from Kaletra, which combines Abbott Laboratories’ lopinavir and ritonavir, there are no other protease inhibitors (PIs) co-formulated with other necessary agents designed to minimize dosing requirements while at the same time boosting effectiveness. With Gilead developing an agent, cobicistat, that can be used as an alternative to Norvir (ritonavir) to boost blood levels of other PIs, some PI manufacturers have expressed interest in partnering with Gilead to develop co-formulated products that can further minimize daily pill counts.

“We are excited to be able to study and develop Prezista with an alternative boosting agent in a combination product which has the potential to reduce the number of tablets patients take,” said Johan Van Hoof, MD, of Janssen. “Prezista is one of the leading protease inhibitors, and co-formulating it with cobicistat in a new combination product demonstrates our commitment to HIV and innovations that will provide new options for patients.”

The deal to combine Prezista with cobicistat will depend on two criteria. First, the U.S. Food and Drug Administration (FDA) must approve cobicistat. This approval is anticipated sometime within the next year. The second, according to Janssen, is that negotiations between it and Gilead on another FDC tablet must also be complete.

This other FDC will combine Prezista and cobicistat with Gilead’s Emtriva (emtricitabine) and another Gilead drug that is in early stage testing. That drug, GS-7340, requires much lower doses than Viread and is expected to remain in the body for a long time before it is eliminated. This would make it ideal to combine with other drugs.

Janssen said it will have full rights and responsibilities for manufacturing and marketing the FDC of Prezista and cobicistat, while Gilead will take full responsibility for manufacturing and marketing the FDC of four drugs

Copyright © 2011 AidsMeds.com

Protease inhibitor combination sustains virologic response. (No Resistance After 4 Years).: An article from: Family Practice News

Abbott Laboratories Abbott Park, IL, July 14 (DDMAC).(DDMAC/PROMOTIONS): An article from: Warning Letter Bulletin

Combivir plus Kaletra well tolerated for HIV prophylaxis. (Compared with Combivir Plus Nelfinavir).: An article from: Family Practice News

Combivir + Kaletra is well tolerated for HIV prophylaxis. (Compared with Combivir + Nelfinavir).: An article from: Internal Medicine News

Response and resistance with Prezista versus Kaletra after earlier treatment.(Latest Studies on HIV Treatment and Prevention): An article from: HIV Treatment: ALERTS!

2011-06-28T23:46:00.000-07:00

Understanding the link between HIV and dementia

HIV can hide out in the brain, protected from the immune system and antiviral drugs, Dr Lachlan Gray and his colleagues at Monash University and the Burnet Institute have found.

Their discovery is an important step in understanding the link between HIV infection and HIV dementia, and is important for the eradication of HIV in general.

“The persistence of the virus in the brain compromises the brain’s normal function, and leads to the death of neurons and to clinical dementia,” Lachlan says.

In fact, about one in five of those infected by HIV ends up with dementia.

“We believe our findings will aid the development of novel drugs that will prevent HIV using the brain as a sanctuary, and help to shape future eradication strategies.”

Lachlan’s work is being presented for the first time in public through Fresh Science, a communication boot camp for early career scientists held at the Melbourne Museum. He was one of 16 winners from across Australia.

Lachlan has been examining the life cycle of the virus to understand better how it survives within the brain.

“We’ve identified changes in the way the virus reproduces, which allows it to keep a low profile and persist undetected in the brain.”

At present, people living with HIV must rely on the continued use of antiviral drugs to control their infection.

“Viral persistence is a major barrier to the cure of AIDS. Modern drugs are very good at controlling the virus, but they are unable to eradicate it from ‘sanctuary’ sites like the brain,” Lachlan’s supervisor, Associate Professor Melissa Churchill says.

“Unfortunately, brain infection often leads to dementia which can be very debilitating. Somewhat more concerning, HIV is now the commonest cause of dementia in people under the age of 40, and is placing an extra burden on our mental health services.”

Lachlan’s research is part of a larger project aiming to trial new drugs that could potentially eradicate or even cure HIV.

Lachlan Gray is one of 16 early-career scientists unveiling their research to the public for the first time thanks to Fresh Science, a national program sponsored by the Australian Government.

His challenges included presenting his discoveries in verse at a Melbourne pub.

For interviews, contact Lachlan Gray on 0416 148 377 or Lachlan.gray@monash.edu

For Monash University, contact Glynis Smalley on (03) 9903 4843 or glynis.smalley@monash.edu.au

For the Burnet Institute, contact Cath Somerville on (03) 8506 2404, 0422 043 498, cathsomerville@burnet.edu.au

For Fresh Science, contact AJ Epstein on 0433 339 141, aj@scienceinpublic.com.au or Sarah Brooker on 0413 332 489 or email Niall Byrne on niall@scienceinpublic.com.au

Copyright © 2011 Fresh Science

2011-06-27T21:26:00.001-07:00

Lessons from maraviroc clinical trials

Maraviroc is the first commercially available HIV chemokine receptor antagonist targeting HIV that utilizes the CCR5 chemokine receptor (R5 tropic). The Maraviroc versus Optimized Therapy in Viremic Antiretroviral Treatment-Experienced Patients (MOTIVATE) trials were two randomized, placebo-controlled studies designed to demonstrate the activity of maraviroc in triple-class-experienced HIV individuals, with a primary end point of viral load suppression at 48 weeks. Maraviroc outperformed the placebo plus optimized background (OBT) arm, and exhibited a favorable safety profile with low discontinuation rates, which equaled those of the placebo plus OBT group. The results of these trials led to maraviroc receiving regulatory approval for the treatment of HIV.

Copyright © 2011 PubMed.gov

2011-06-27T21:21:00.001-07:00

FDA panel backs HIV drug Selzentry

The Food and Drug Administration (FDA) has recommended the use of Pfizer's Selzentry as an initial treatment for HIV patients, despite continuing concerns over the level of effectiveness of the drug.

Selzentry had been approved earlier as a secondary drug for HIV-infected people who do not benefit from other antiviral treatments. But Pfizer had been seeking its use on patients who were not already under treatment to fight HIV.

In initial studies where it was compared with Sustiva, an antiviral manufactured by Bristol-Myers Squibb, Selzentry failed to prove it was at least as effective.

Of the patients who were tested, 32% given Selzentry did not show a sufficiently effective response, against 24% for Sustiva.

However, after Pfizer repeated the trials using a different method to screen participants it was able to meet the target.

Experts on the FDA panel, while voting 10-4 in favour of approving the drug as a first option for HIV patients, also raised concerns about its effectiveness.

Dr Russell Van Dyke of the Tulane University School of Medicine, said: "It's clearly an active drug, it demonstrated effectiveness. But I'm worried it's not as potent as we might like."

Copyright © Press Association 2009

2011-06-25T00:16:00.000-07:00

Selzentry is designed to prevent R5-tropic HIV from entering your T-cells

SELZENTRY was specially designed to target R5 HIV, a common type of HIV. To find out if you have R5 HIV, you can be prescreened with an HIV tropism test (sometimes called a tropism assay). This can let you see right away if SELZENTRY could be part of your personalized HIV therapy program.

A tropism test is a blood test that reveals how your HIV enters T-cells. HIV can enter T-cells via an R5 or X4 co-receptor. A tropism test reveals which of these receptors your HIV uses.

You have R5-tropic HIV if HIV uses the R5 co-receptors to enter your T-cells. You have X4-tropic HIV if HIV uses the X4 co-receptors to enter your T-cells. You have dual or mixed tropic HIV if HIV uses both the R5 and the X4 co-receptors to enter your T-cells.

SELZENTRY® (maraviroc) is a CCR5 inhibitor that is used with other HIV medicines to treat CCR5-tropic HIV. SELZENTRY is not recommended in patients with dual/mixed or CXCR4-tropic HIV. It is for adult patients with CCR5-tropic HIV only. A tropism test is needed before starting SELZENTRY. SELZENTRY does not cure HIV infection or AIDS and does not lower the risk of passing HIV to other people.

People taking SELZENTRY may still develop infections, including opportunistic infections or other conditions that happen with HIV infection. The long-term effects of SELZENTRY are not known at this time. It is very important that you stay under the care of your healthcare provider during treatment with SELZENTRY.

Copyright © 2011 ViiV Healthcare Group of Companies All Rights Reserved.

CryoCor cryoablation system, Selzentry.(New & Approved): An article from: Family Practice News

New antiretroviral helps control HIV after earlier treatment failures.(Selzentry): An article from: HIV

Selzentry.(NEW & APPROVED): An article from: Internal Medicine News Treatment: ALERTS!

2011-06-25T00:07:00.000-07:00

Tobira Launches Phase II Study of Entry Inhibitor Cenicriviroc

Tobira Therapeutics is recruiting for a Phase IIb study of its CCR5/CCR2 entry inhibitor cenicriviroc (TBR-652). It is hoped that cenicriviroc will not only offer people a new antiretroviral (ARV) option to keep HIV in check, but that it will also prove useful in reducing the cellular inflammation that scientists believe is behind a host of health problems.

Cenicriviroc is from a class of drugs that blocks the CCR5 coreceptor on CD4 cells, thus making them resistant to HIV infection. It is in the same class of drugs as Selzentry (maraviroc) but may be used once-daily instead of twice-daily.

Cenicriviroc also has another unique attribute. In addition to blocking the CCR5 coreceptor, it also blocks another coreceptor called CCR2, which is involved in inflammatory diseases such as rheumatoid arthritis. In recent years, researchers have shown that cellular inflammation, even in people whose HIV is well controlled by ARV therapy, may contribute to a number of health problems, including cardiovascular disease. It is hoped, though it will take time to prove this, that cenicriviroc will be a dual-purpose drug—fighting HIV directly while also reducing HIV-related inflammation.

According to Tobira press materials, the new study will pit cenicriviroc against Sustiva (efavirenz), both of them paired with Truvada (tenofovir plus emtricitabine). Tobira will be studying two doses of cenicriviroc, 100 milligrams (mg) and 200 mg once-daily.

“This study is based on the strength of the cenicriviroc Phase IIa proof of concept, pharmacokinetic and safety findings that were presented at key HIV/AIDS conferences and published in peer-reviewed journals,” said Melanie Thompson, MD, of the AIDS Research Consortium of Atlanta, and a lead investigator in the Phase IIb study. “The study will further explore cenicriviroc’s antiviral activity and safety as well as effects on immunologic and inflammatory biomarkers, including the effects of CCR2 receptor inhibition in HIV-1 infected patients.”

To learn more about the cenicriviroc study, visit the clinical trials database run by the National Institutes of Health (NIH).

Copyright © 2011 AidsMeds.com

Once-a-day Truvada lowers HIV risk in gays and transgender women.(Article 3): An article from: HIV Treatment: ALERTS!

Euroscreen announces CCR5 licensed to Pfizer.(Brief Article): An article from: BIOTECH Patent News

2011-06-24T23:52:00.001-07:00

GeoVax Labs Inc. (GOVX) Opens Third Site for HIV/AIDS Vaccine Testing

GeoVax Labs Inc., a biotechnology company in operation to create, develop and test innovative HIV/AIDS vaccines, today announced it has opened a third site for testing the therapeutic potential of its HIV/AIDS vaccine in conjunction with the AIDS Research Alliance, the nation’s only independent, nonprofit research institute dedicated to the search for a cure for AIDS.

The Los Angeles-based ARA will team up with two existing members of GeoVax’s clinical trial site team, the AIDS Research Consortium of Atlanta and the Alabama Vaccine Research Clinic at the University of Alabama at Birmingham.

The therapeutic trial marks the first trial designed to test GeoVax’s vaccine as a possible treatment for HIV. The upcoming clinical trial will test safety, vaccine-induced immune responses, and the ability of the vaccine to control viral replication in HIV-infected patients.

GeoVax said previous studies involving simian prototypes of the vaccine in infected non-human primates demonstrated the vaccine’s ability to control viral replication in the absence of anti-viral drugs.

“We are excited to expand our therapeutic trial team to include the AIDS Research Alliance,” Mark Newman, PhD, vice president of Research and Development at GeoVax stated in the press release. “They are a group with a mission that parallels that of GeoVax, developing a vaccine to prevent infection by HIV and developing better treatments for those who become infected.”

Dr. Stephen Brown, ARA’s medical director, said that the development of new products and approaches that springing from existing antiretroviral drugs regimens would represent a major breakthrough in AIDS research.

GeoVax’s vaccines are currently being tested in HIV-uninfected persons in a phase II clinical trial by the HIV Vaccine Trials Network (HVTN), which are funded by the National Institute of Allergy and Infectious Diseases, a division of the National Institutes of Health.

Copyright © 2011 International Business Times

2011-06-24T23:43:00.001-07:00

‘Molecular cap’ blocks processes that lead to Alzheimer’s, HIV

Scientists have designed molecular inhibitors that could delay the onset of Alzheimer’s disease and prevent the sexual transmission of HIV.

The researchers say the inhibitors target specific proteins associated with Alzheimer’s disease and HIV to prevent them from forming amyloid fibres, the elongated chains of interlocking proteins that play a key role in more than two dozen degenerative and often fatal diseases.

“By studying the structures of two key proteins that form amyloids, we were able to identify the small chain of amino acids responsible for amyloid fibre formation and engineer a ‘molecular cap’ that attaches to the end of the fibres to inhibit their growth,” research leader David Eisenberg, director of the UCLA-Department of Energy Institute of Genomics and Proteomics and a Howard Hughes Medical Institute investigator, said.

“This research is an important first step toward the development of structure-based drugs designed against amyloid diseases,” Eisenberg, who is a UCLA professor of chemistry, biochemistry and biological chemistry and a member of the California NanoSystems Institute at UCLA, said.

“Our results have opened up an avenue so that universities and industry can start creating therapeutics that could not have been produced 10 years ago,” he stated.

Eisenberg and his research team found that of the entire tau protein, a small chain of just six amino acids - abbreviated VQIVYK — was responsible for the formation of amyloid fibres.

By studying the structure of the fibres using microcrystallography, a method developed at UCLA for this research, the team was able to use the fibres as a template to design an inhibitor that could “cap” the fibre and stop it from growing.

The introduction of the inhibitor into a tau protein solution completely prevented amyloid fibre formation, validating the idea that the structure-based design of therapeutics for amyloid diseases is a plausible option.

The study has been published online June 15 in the journal Nature and will be available in an upcoming print edition.

Copyright © 2011 Asian News International/DailyIndia.com

2011-06-24T00:41:00.000-07:00

HIV study reveals double jeopardy
Sumitra Deb Roy

MUMBAI: The clever HIV virus could be present in drastically different variants in the bodily fluids — blood and semen — of the same individual. This was recently established by a study of 12 HIV-infected men whose blood and semen samples were analyzed by Parel’s National Institute for Research in Reproductive Health (NIRRH).

The finding is significant, said scientists of NIRRH, as it negates the notion that an infected person can go slow on treatment or think of starting a family once the viral load in the bloodstream becomes undetectable.

The study clearly established that the type and behaviour of the HIV virus present in the bloodstream of an infected individual could be drastically different from the type and behaviour of the virus present in the same individual’s semen. In certain cases, it could look as if the individual is infected with two different types of virus altogether.

The pathbreaking HIV study, carried out by NIRRH in collaboration with the JJ Hospital’s medicine department, was recently published in the Journal of Medical Virology.

Principal investigator Dr A H Bandivadekar told TOI that the study proves that the virus could disappear from the blood stream due to anti-retroviral therapy but still be very much present in the semen. “This difference in the virus nature influences the transmission of HIV, the progression of the ailment, the virus’ response to the host defence and also treatment,” he added.

Further, Bandivadekar added that the study pointed out that sperm-associated virus too is a huge risk factor for HIV transmission and possibly for parent child transmission. “Therefore, assisted reproductive technology where sperm washing is used may not be termed as a completely safe procedure for maternal or fetal transmission of HIV,” he said.

The study further adds to the intriguing nature of the virus as it adds to the unpredictability, given its nature of constant mutation. In several of the individuals studied, the viral count in the blood differed vastly from the count in semen. For instance, while the blood plasma in one individual had 11,284 copies of the virus, the viral presence in his semen was around 5,432 copies. Also, in two individuals, the virus load in the blood had gone below detectable levels, but there were significant quantities of the virus present in the semen. Simply put, the virus in the blood and semen infect the same individual in different ways.

Head of JJ Hospital’s ART centre and one of the investigators, Dr Alka Deshpande, said the study also means that those on anti-retroviral medication should not think that it could keep the virus in both the compartments, blood and semen, under control. “It is now clear that there could be genetic differences in virus even if they are present in the same individual’s body,” she added. “It only means that whenever a vaccine or drug is created, the variant nature of the virus has to be kept in mind so that it can attack all compartments,” she added.

Copyright © 2011 Times of India

2011-06-22T00:00:00.000-07:00

Forum explores Truvada’s use in fighting HIV
by Kate Sosin

When Gladstone Institutes released evidence that Truvada, a one-a-day HIV pill, might prevent HIV in addition to treating it, the news sparked both excitement and skepticism.

The AIDS Healthcare Foundation (AHF), the largest HIV/AIDS medical provider in the country, came out against the use of Truvada for prevention, despite the fact that Gladstone’s Iniciativa Profilaxis Preexposicion (iPrEx) trial showed the drugs to be more than 90-percent effective in preventing HIV in those who took it daily.

Experts on the study sat down with Feast of Fun podcasters Fausto Fern?”s and Marc Felion at Center on Halsted June 15 to talk about what the study means and if Truvada could signal the end of the pandemic. Present were Dr. Robert Grant of Gladstone Institute, Keith Green, director of federal affairs at AIDS Foundation of Chicago, and a youth who participated in a similar study Green conducted in Chicago.

“In our wildest dreams, we did not think [Truvada] would be more than 90-percent effective in those who took it,” Grant told the audience.

The findings also astounded Green, who halted Project PrEPare, a similar Chicago study, because he didn’t want to continue administering placebos when he knew Truvada worked.

While the effectiveness of Truvada in preventing HIV is clear, the practicality of it remains uncertain. For one, Truvada is meant to be taken daily, which could pose a challenge to many not accustomed to the routine or whose lives don’t always allow for consistency, such as youth living on the street. Additionally, Truvada is not without side effects including nausea, although that tends to go away over prolonged use, said Grant.

One barrier in getting people to use Truvada is stigma, Grant said.

“These pills, in particular, have been the one thing that folks want to avoid,” he said, adding that fear surrounding HIV/AIDS contributes to fear around taking Truvada for prevention. “It strikes people as a misuse [of the drug].”

The drug could cost as much at $10,000 a year, an impossibly high price for people without insurance. In Illinois, the AIDS Drug Assistance Program (ADAP) which provides antiretrovirals to those who cannot afford them, is already cash-strapped. Truvada used for prevention could compete with Truvada treatments, creating a kind of Catch-22 for service providers who want to end the spread of HIV but also serve those who are positive already.

“We really have an ethical dilemma,” Green said.

Still, many insurance companies are interested in Truvada for prevention because even with the cost of the drug, prevention is at least half the cost of treatment.

Rico, the youth who participated in Green’s Chicago study on Truvada said that taking the drug made him “more considerate” of his body and protecting himself. He said that he had been hesitant to participate in the study but decided to sign up when he learned of the impact it could have on his community.

Grant and Green did acknowledge that iPrEx study had its shortcomings.

“I started to look at Dr. Grant’s work, and those people didn’t look like our people,” Green said, adding that a low number of youth and African Americans had participated. Grant agreed and noted that their efforts would seek the expertise of Chicago service providers whose work included a diversity of clients. Still he added, the drug seemed to work equally well among people of every race.

As for AHF’s critiques of using Truvada for prevention, neither Grant nor Green seemed to give them much weight.

“This is a large corporation, actually that has revenues above 300 million dollars a year, so well above my pay grade,” said Grant, who went on to say that he was not certain about why AHF was working to discredit the trial results.

Truvada is awaiting FDA approval before it can be marketed for HIV prevention. Grant said that Gilead, the company that makes Truvada, will likely be hesitant to market the drug for prevention and that it will be up to AIDS service providers to make the leap in making Truvada more accessible.

For some, that leap can’t come quickly enough.

“We either pay now or we pay forever,” Grant said. “We have a chance now to stop this epidemic.”

Copyright © 2011 Windy City Times

More new non-AIDS illnesses with Epzicom than Truvada in 96-week trial.(Article 1): An article from: HIV Treatment: ALERTS!

Doubled failure risk with Epzicom vs Truvada at high starting viral load.(Article 2): An article from: HIV Treatment: ALERTS!

Once-a-day Truvada lowers HIV risk in gays and transgender women.(Article 3): An article from: HIV Treatment: ALERTS!

Differences between Epzicom and Truvada at week 48 of ASSERT trial.(Article 4): An article from: HIV Treatment: ALERTS!

2011-06-21T00:18:00.000-07:00

Some proteins can map aging process

Anabolic steroids, which are sometimes used to reverse loss of lean muscle tissue that is not only associated with disease such as HIV and cancer, but also with the normal aging process, can have unwanted side effects.

But a new research has shown that nine proteins, isolated from blood, alter with age and that the profile of some of these proteins can be reversed by testosterone treatment.

In a combined study, researchers from Boston University School of Medicine and University of Texas Medical Branch compared protein levels in serum samples from two groups of healthy men - young men aged 18-35 and older men aged 60-75.

Seven proteins, which were either growth factors (IGF-1, IL-7, IL-12p40, PDGFß), or were involved in immune response (ENA78, MIP-1ß, IP-10) and pro-collagen (PIIINP) were all reduced in older men. In contrast the monokine MIG, also involved in immune activity, was elevated.

Testosterone treatment increased lean muscle mass and levels of the appetite suppressing hormone leptin, for both groups of men. Testosterone also increased levels of PIIINP and IGF-1 in young men and the researchers saw a similar increase in a small group of older men.

Dr Monty Montano said, "The blood proteins we found that altered with healthy aging also have links to maintenance of muscle, such as IGF-1 and pro-collagen, or are involved in regulation of the immune system, possibly reducing T-cell and neutrophil responses with age. Additionally all of the proteins we found are involved with the signaling pathways controlled by AKT, NF?ß and TGFß which are known to be associated with aging."

"It is no simple matter to find a one size that fits all test for aging - our results suggest that there is a difference in response to anabolic steroids between young and older men, despite both groups increasing in muscle mass. It seems that testosterone replacement does not necessarily mean a restoration of full testosterone functionality for the older man,' added Montano.

Daily News & Analysis

2011-06-20T23:52:00.000-07:00

New Math in HIV Fight
By Mark Schoofs

Scientists using a powerful mathematical tool previously applied to the stock market have identified an Achilles heel in HIV that could be a prime target for AIDS vaccines or drugs.

The research adds weight to a provocative hypothesis—that an HIV vaccine should avoid a broadside attack and instead home in on a few targets. Indeed, there is a rare group of patients who naturally control HIV without medication, and these “elite controllers” most often assail the virus at precisely this vulnerable area.

“This is a wonderful piece of science, and it helps us understand why the elite controllers keep HIV under control,” said Nobel laureate David Baltimore. Bette Korber, an expert on HIV mutation at the Los Alamos National Laboratory, said the study added “an elegant analytical strategy” to HIV vaccine research.

“What would be very cool is if they could apply it to hepatitis C or other viruses that are huge pathogens—Ebola virus, Marburg virus,” said Mark Yeager, chair of the physiology department at the University of Virginia School of Medicine. “The hope would be there would be predictive power in this approach.” Drs. Baltimore, Korber and Yeager weren’t involved in the new research.

One of the most vexing problems in HIV research is the virus’s extreme mutability. But the researchers found that there are some HIV sectors, or groups of amino acids, that rarely make multiple mutations. Scientists generally believe that the virus needs to keep such regions intact. Targeting such sectors could trap HIV: If it mutated, it would disrupt its own internal machinery and sputter out. If it didn’t mutate, it would lie defenseless against a drug or vaccine attack.

The study was conducted at the Ragon Institute, a joint enterprise of Massachusetts General Hospital, the Massachusetts Institute of Technology and Harvard University. The institute was founded in 2009 to convene diverse groups of scientists to work on HIV/AIDS and other diseases.

Two of the study’s lead authors aren’t biologists. Arup Chakraborty is a professor of chemistry and chemical engineering at MIT, though he has worked on immunology, and Vincent Dahirel is an assistant professor of chemistry at the Université Pierre et Marie Curie in Paris. They collaborated with Bruce Walker, a longtime HIV researcher who directs the Ragon Institute. Their work was published Monday in the Proceedings of the National Academy of Sciences.

To find the vulnerable sectors in HIV, Drs. Chakraborty and Dahirel reached back to a statistical method called random matrix theory, which has also been used to analyze the behavior of stocks. While stock market sectors are already well defined, the Ragon researchers didn’t necessarily know what viral sectors they were looking for. Moreover, they wanted to take a fresh look at the virus.

So they defined the sectors purely mathematically, using random matrix theory to sift through most of HIV’s genetic code for correlated mutations, without reference to previously known functions or structures of HIV. The segment that could tolerate the fewest multiple mutations was dubbed sector 3 on an HIV protein known as Gag.

In an interview with WSJ’s Mark Schoofs, NIAID director Dr. Anthony Fauci reflects on his thirty years spent fighting AIDS, and how he believes science is at a turning point where it has the potential to dramatically shrink the size of the AIDS epidemic across the globe.

Previous research by Dr. Yeager and others had shown that the capsid, or internal shell, of the virus has a honeycomb structure. Part of sector 3, it turns out, helps form the edges of the honeycomb. If the honeycomb suffered too many mutations, it wouldn’t interlock, and the capsid would collapse.

For years, Dr. Walker had studied rare patients, about one in 300, who control HIV without taking drugs. He went back to see what part of the virus these “elite controllers” were attacking with their main immune-system assault. The most common target was sector 3.

Dr. Walker’s team found that even immune systems that fail to control HIV often attack sector 3, but they tend to devote only a fraction of their resources against it, while wasting their main assault on parts of the virus that easily mutate to evade the attack. That suggested what the study’s authors consider the paper’s most important hypothesis: A vaccine shouldn’t elicit a scattershot attack, but surgical strikes against sector 3 and similarly low-mutating regions of HIV.

“The hypothesis remains to be tested,” said Dan Barouch, a Harvard professor of medicine and a colleague at the Ragon institute. He is planning to do just that, with monkeys. Others, such as Oxford professor Sir Andrew McMichael, are also testing it.

The Ragon team’s research focused on one arm of the immune system—the so-called killer T-cells that attack other cells HIV has already infected. Many scientists believe a successful HIV vaccine will also require antibodies that attack a free-floating virus. Dr. Chakraborty is teaming up with Dennis Burton, an HIV antibody expert at the Scripps Research Institute in La Jolla, Calif., to apply random matrix theory to central problems in antibody-based vaccines.

Copyright © 2011 Wall Street Journal

2011-06-17T00:53:00.000-07:00

HIV and Aging — A Report on NYC

The U.S. Centers for Disease Control and Prevention (CDC) estimates that more than a million adults and adolescents are living with HIV in the United States. New York City, the epicenter of HIV, has the largest amount of diagnosed persons in the United States. The HIV/AIDS time line began in July 1981, when The New York Times reported an outbreak of a rare form of cancer among gay men in New York City. This ‘cancer’ was identified as Kaposi’s sarcoma, a disease that later became known as HIV/AIDS. Emergency rooms in NYC began to see more and more seemingly healthy young men with flu-like symptoms and a rare form of pneumonia. This began what today is one of the biggest health concerns in modern history.

According to a study made by AIDS Community Research Initiative of America (ACRIA), almost 27 percent of all people living with AIDS in the United States are over 50 years old. In New York City this number goes up to 35 percent. Thanks to research and the introduction of highly effective antiretroviral therapy (HAART), mortality rates and increased life expectancy for people living with HIV and AIDS is higher than ever. Soon we will see a large number of senior citizens with HIV and AIDS. There are three groups of older adults with HIV, the newly infected, the newly diagnosed and the aging individual/longtime survivor. These groups have different but overlapping medical and psycho-social needs.

Research has demonstrated that older adults and seniors with HIV or AIDS face multiple forms of discrimination. Not only do they face the everyday discrimination everyone with HIV and AIDS confronts, but they also have to deal with discrimination related to their age and their health care. For example, a lot of physicians do not perceive older adults to be at risk for HIV infection; and therefore they are less likely to be tested for the virus. In fact, a study of people between the age of 60 and 79 years old who had died in a long-term healthcare facility found that five percent were HIV antibody positive although none had been diagnosed with HIV.

Seniors in the context of HIV and AIDS have somewhat become invisible. They are rarely targeted in HIV prevention campaigns and therefore, they may not realize that their behaviors can put them at risk for HIV infection.

Some two out of three HIV infected older adults in NYC suffers from depression. Depression for older people can be particularly destructive. Caregivers often fail to recognize the symptoms of depression in the elderly; it is often seen as a characteristic of aging rather than an illness. Loneliness and HIV related stigma are two major reasons for the high numbers of depression among HIV positive older adults.

Even though nations and individuals have made progress in treating this condition, HIV and Aids is still highly stigmatized. A lot of older adults feel ashamed and guilty about their condition and don’t feel comfortable telling their family and friends. We can speculate that HIV and AIDS are often related to sex and drugs which may make some people uncomfortable and they would prefer not being associated with it. The study made by ACRIA showed that fewer than half told all their family members and only one-third told their friends that they were HIV positive. Older adults and seniors grew up during a time when discussions about sexuality were considered improper or vulgar; one simply did not talk about sex in the same way that we do today. Some individuals who chose to tell friends and family felt that the ignorance about how HIV is spread still is a problem. After they revealed their illness some felt that people around them would for instance stop touching them and reject them. For example, one person said that after revealing his illness to his family, they would give him plastic plates, knives and forks. Some of these problems even occur within health clinics.

What can be Done?
It is essential that researchers start conducting more research targeting the older population. Many people with HIV infection are now living long enough to experience HIV as a chronic illness. More research is needed on HIV/AIDS and aging, so that we can understand the interaction and overlapping with age-related symptoms and HIV. We need to change the knowledge level and attitudes towards HIV and aging. To prevent new infected cases, we need to start campaigns that specifically targets older adults. Physicians must challenge the myths and start asking older patients about their sexual activity. Doctors must not overlook the possibility that older people are at risk for HIV. If we can do this, I think we come a long way.

S.Klemetti@globalaging.org

Copyright © 2011 Global Aging

2011-06-17T00:48:00.000-07:00

Differential effect of CLK SR Kinases on HIV-1 gene expression: potential novel targets for therapy
Raymond WongAhalya BalachandranAnnie MaoWendy DobsonScott Gray-OwenAlan Cochrane

RNA processing plays a critical role in the replication of HIV-1, regulated in part through the action of host SR proteins. To explore the impact of modulating SR protein activity on virus replication, the effect of increasing or inhibiting the activity of the Cdc2-like kinase (CLK) family of SR kinases on HIV-1 expression and RNA processing was examined.

Results: Despite their high homology, increasing individual CLK expression had distinct effects on HIV-1, CLK1 enhancing Gag production while CLK2 inhibited the virus.

Parallel studies on the anti-HIV-1 activity of CLK inhibitors revealed a similar discrepant effect on HIV-1 expression. TG003, an inhibitor of CLK1, 2 and 4, had no effect on viral Gag synthesis while chlorhexidine, a CLK2, 3 and 4 inhibitor, blocked virus production.

Chlorhexidine treatment altered viral RNA processing, decreasing levels of unspliced and single spliced viral RNAs, and reduced Rev accumulation. Subsequent experiments in the context of HIV-1 replication in PBMCs confirmed the capacity of chlorhexidine to suppress virus replication.

Conclusions: Together, these findings establish that HIV-1 RNA processing can be targeted to suppress virus replication and identified chlorhexidine as a lead compound in the development of novel anti-viral therapies.

Copyright © 2011 7thspace.com

2011-06-17T00:30:00.000-07:00

Blocking pemature reverse transcription fails to rescue the HIV-1 nucleocapsid-militant replication defect
James ThomasTeresa ShatzerRobert Gorelick

The nucleocapsid (NC) protein of HIV-1 is critical for viral replication. Mutational analyses have demonstrated its involvement in viral assembly, genome packaging, budding, maturation, reverse transcription, and integration.

We previously reported that two conservative NC mutations, His23Cys and His44Cys, cause premature reverse transcription such that mutant virions contain approximately 1,000-fold more DNA than wild-type virus, and are replication defective. In addition, both mutants show a specific defect in integration after infection.

Results: In the present study we investigated whether blocking premature reverse transcription would relieve the infectivity defects, which we successfully performed by transfecting proviral plasmids into cells cultured in the presence of high levels of reverse transcriptase inhibitors.

After subsequent removal of the inhibitors, the resulting viruses showed no significant difference in single-round infective titercompared to viruses where premature reverse transcription did occur; there was no rescue of the infectivity defects in the NC mutants upon reverse transcriptase inhibitor treatment. Surprisingly, time-course endogenous reverse transcription assays demonstrated that the kinetics for both the NC mutants were essentially identical to wild-type when premature reverse transcription was blocked.

In contrast, after infection of CD4+ HeLa cells, it was observed that while the prevention of premature reverse transcription in the NC mutants resulted in lower quantities of initial reverse transcripts, the kinetics of reverse transcription were not restored to that of untreated wild-type HIV-1.

Conclusions: Premature reverse transcription is not the cause of the replication defect but is an independent side-effect of the NC mutations.

Copyright © 2011 7thspace.com

2011-06-17T00:16:00.000-07:00

Body Satisfaction Increased With Fat Gains in Prezista Study

Although treatment experienced HIV-positive men and women had slightly greater gains in trunk fat after switching to a new regimen containing Prezista (darunavir), they also reported increased satisfaction with their bodies. These data were published in the July issue of AIDS Patient Care and STDs.

Of all of the side effects to HIV medication, body shape changes—both the loss of body fat in the face and limbs and gains of body fat in the trunk and other areas—are among the most distressing to people living with HIV. In fact, body shape changes have been identified as an independent cause of adherence problems in people taking antiretroviral (ARV) therapy.

Though body shape changes are less of a risk with the drugs that are more commonly used today, they do still occur in some people. This is particularly true in people who are heavily treatment experienced, who must sometimes combine the newer ARV drugs with older medication.

To determine the impact of Prezista on body shape changes and people’s perception of their bodies, Judith Currier, MD, from the University of California in Los Angeles, and her colleagues examined data from a large study of Norvir (ritonavir)–boosted Prezista in a diverse group of treatment-experienced people. The study, called GRACE, was the first that was specifically designed to compare the safety and effectiveness of an ARV medication between men and women and between white and black study participants.

In this particular analysis, Currier and her colleagues measured changes in trunk over time and also surveyed the GRACE study participants about their perceptions of their bodies and their satisfaction with their appearance. In all, 287 HIV-positive women and 142 HIV-positive men were examined for this analysis, all of whom received at least one dose of Prezista. In general, women in the study had less severe HIV disease progression at the study’s start.

Currier’s team found that although the participants gained weight and their waist size increased during the course of the study—by 2.5 centimeters (cm) in women and 1.3 cm in men—the participants nevertheless reported greater body satisfaction by the end of the study. In women, those who reported being either “satisfied” or “very satisfied” with their body appearance increased from 42 percent to 58 percent over the course of the study. In men, those “satisfied” or “very satisfied” increased from 56 percent to 63 percent.

Given the discrepancy between people’s actual body shape changes and their reported satisfaction with their bodies, the authors are calling for further study. First, the authors suggest that additional exploration is needed to better understand the reasons behind the body shape changes. Second, they urge that we need a better and more thorough understanding about how people perceive their bodies and how this may affect adherence.

Copyright © 2011 AidsMeds

2011-06-17T00:06:00.000-07:00

Better Assessment Of Drug Resistance May Improve Treatment Of People With HIV
By April Clayton and Courtney McQueen

Results from a recent small Spanish study indicate that a more sensitive technique for detecting drug resistance, called deep sequencing, more accurately identified drug resistance in HIV-positive individuals who had previously been treated with antiretrovirals and were suffering from drug failure.

“Our study suggests that more sensitive genotypic HIV drug resistance assays, such as deep HIV sequencing, may help clinicians design antiretroviral treatment combinations better suited for [patients] infected with multidrug-resistant viruses,” said Dr. Roger Paredes, a key investigator of the study, in correspondence with The AIDS Beacon.

“Deep sequencing may help [clinicians] choose more effective drugs as well as avoid antiretrovirals to which, in fact, the virus is resistant,” he added.

Drug resistance is one of the main causes of antiretroviral drug failure. HIV-positive individuals are considered resistant to an anti-HIV drug if their viral load (amount of HIV in the blood) does not remain low after drug therapy or testing confirms the presence of an HIV strain that is resistant to one or more classes of antiretrovirals.

Resistance testing examines the genes of the HIV in a person’s blood to detect whether the virus has mutations that make it resistant to particular drugs. Previous studies have indicated that even low levels of drug-resistant HIV increase the chances of treatment failure, although those studies have primarily involved previously untreated people with HIV (see related AIDS Beacon news)

The authors of this study investigated whether an enhanced form of resistance testing, known as deep sequencing, could provide better assessments of drug resistance in heavily pre-treated HIV patients when compared to the more traditional form of resistance testing, called population sequencing.

Deep sequencing detects the same mutations as population sequencing but is more sensitive, so it can detect mutations present in 1 percent or more of the HIV circulating in a person’s blood. Population sequencing can usually only detect mutations present in 15 percent or more of the HIV.

Seven HIV-positive individuals participated in the study. Participants had taken a median of 15 antiretroviral drugs for a median of 13 years. The average age of the participants was 44, and five of the seven were male.

All participants had shown resistance to the three main classes of antiretrovirals: nucleoside-reverse transcriptase inhibitors (NRTIs), protease inhibitors, and non-nucleoside reverse transcriptase inhibitors. In addition, all participants had failed salvage therapy with at least one of the following: Prezista (darunavir), Aptivus (tipranavir), Intelence (etravirine), or Isentress (raltegravir).

Results showed that deep sequencing detected all of the drug resistant mutations found by population sequencing, plus additional resistance mutations in six of the seven participants.

In particular, deep sequencing improved the assessment of resistance to Intelence, showing higher risk of resistance in two patients with signs of failing Intelence-based therapy. The technique also slightly modified assessments of HIV resistance against Sustiva (efavirenz), Crixivan (indinavir), and NRTIs in various participants to indicate higher risks of resistance, compared to the population sequencing.

The two methods identified the same participants as having drug resistance to Aptivus and Isentress, and the deep sequencing confirmed that four of five participants who had failed Isentress-based antiretroviral therapy did not show resistance to the drug and could potentially take it again.

Dr. Paredes stated that the researchers are currently conducting a larger study to investigate whether the use of deep sequencing can lead to improved treatment outcomes for treatment-experienced patients starting salvage therapy with Norvir (ritonavir)-boosted protease inhibitors, Intelence, or Isentress.

For more information, please see the study in PLoS One.

Copyright © 2011 Aids Beacon

2011-06-16T00:18:00.000-07:00

New molecule promises to fight TB, HIV
By Hasmukh Dattani

A molecule extracted from a marine micro-organism, found off the coast of Rameshwaram, could potentially be the next biggest development in treating TB and HIV, claimed researchers here on Wednesday.

Offering new hope to those living with HIV as well as TB patients, a group of scientists from the Tuberculosis Research Centre (TRC), IIT-Madras and Periyar University claim to have extracted the molecule, Transitmycin, from the marine micro-organism, ‘Streptomyces sp’, that was isolated from a soil sample collected from the coral reef off the coast of Rameshwaram. The brominated and pigmented antibiotic has been found to be active against both TB and HIV, said researchers.

“Transitmycin inhibited drug sensitive, multidrug resistant (MDR) and XDR Mycobacterium tuberculosis strains as well as bacterial pathogens,” said Dr Vanaja Kumar, principal investigator and head of the department of bacteriology at the TRC. It was also found to be active against latent bacilli, said the researchers. Enthusing them further, the compound was found to inhibit two most widely prevalent clades of HIV-1, the subtypes B & C.

Experts said the latter subtype was most prevalent in India and parts of the African continent, reportedly responsible for the worst epidemics and around half of all infections.

Importantly, this compound is found to be effective against both Mycobacterium and HIV, a unique feature that enables the treatment of patients who have been infected with both these pathogens unlike the existing medicines that cannot be administered simultaneously as they counteract, said the scientists.

Preclinical research, including animal studies, are to be taken up prior to testing this compound in human clinical trials, they said, adding that it would be ready in 10 years if the plan fell in place.

Copyright © 2011 Indian Express

2011-06-14T23:44:00.000-07:00

Researchers Find High Rates Of Heart Disease And High Cholesterol In People With HIV
By April Clayton

Results from a recent Brazilian study indicate that a high proportion of HIV-positive individuals on antiretroviral therapy have abnormal cholesterol and triglyceride levels. Additionally, almost 40 percent of HIV-positive individuals in the study were at an increased risk for heart disease.

Based on their results, the authors of the study suggested that intervention programs be implemented to reduce the risk of heart disease in people with HIV taking antiretrovirals.

Although antiretroviral therapy slows the progression of HIV and has helped prevent HIV-related deaths, it can lead to side effects such as weight gain, high cholesterol and triglyceride levels, and insulin resistance or pre-diabetes.

Results of several previous studies have indicated that the use of protease inhibitors in particular is associated with high levels of cholesterol in people with HIV (see related AIDS Beacon news).

These side effects can lead to serious health problems, such as heart disease and diabetes.

In this study, researchers investigated the rates of high cholesterol and triglyceride levels and risk for cardiovascular disease in 113 people with HIV who were on antiretroviral therapy. The average age of study participants was 39 years old and 68 percent were male.

Results showed that two-thirds of study participants (67 percent) had problems with their cholesterol or triglyceride levels. Almost 54 percent of participants had low levels of “good” cholesterol and 36 percent had high levels of triglycerides; 27 percent had borderline-high or high cholesterol.

Results also showed that participants taking a protease inhibitor-based regimen had a more than five-fold higher risk for abnormal cholesterol or triglyceride levels than patients on antiretroviral therapy without protease inhibitors.

In addition, almost 40 percent of individuals with HIV had changes in body fat distribution, particularly body fat accumulation.

The researchers also assessed the risk for heart disease in 97 participants. Results showed that 37 percent of the HIV-positive men and 40 percent of the HIV-positive women had a high risk for heart disease.

The researchers found no link between age, length of HIV infection, gender, viral load (amount of HIV in the blood), or CD4 (white blood cell) count and risk of abnormal cholesterol or triglyceride levels.

For more information, please see the study in the Brazilian Journal of Infectious Diseases (abstract).

Copyright © 2011 The AIDS Beacon

2011-06-14T00:08:00.000-07:00

The Swiss Statement and Its Repercussions

There is evidence of some groups of gay men knowing, from the late 1990s onwards, that people with an undetectable HIV viral load were much less infectious, and were using this knowledge in sexual decision-making. Public discussion of this became much more high profile after a paper was issued by the Swiss Federal Commission for HIV/AIDS in January 2008.

The authors of the Swiss Statement have since said that they were surprised at the amount of attention their paper got and the global discussion it set off. It was intended purely as an incountry guideline directed at doctors and, significantly, at legal professionals. Much of the motivation for the statement lay in the fact that Switzerland had prosecuted and convicted a number of HIV+ people for exposing partners to HIV, and the doctors wanted there to be a statement saying that HIV+ people posed no risk to their partners if they were undetectable on stable antiretroviral therapy. They stated that unprotected sex between a positive person on antiretroviral treatment, and without an STI, and an HIV-negative person did not comply with the criteria for an “attempt at propagation of a dangerous disease” in the Swiss penal code nor for “an attempt to engender grievous bodily harm”.

Although the statement purely concerns the position of individuals and was not connected with the mathematical-modelling studies that were starting to be issued which looked at the possibility of using viral control as a prevention measure, it was significant because it transformed the discussion around viral undetectability and infectiousness from one in which using viral load status to inform sexual-risk decisions was seen as dangerous, and a rationalisation for having unprotected sex, to one in which it became possible to talk about its legitimate use as a prevention measure.

Nonetheless, the statement caused widespread concern amongst some prevention and public health advocates who felt it was based on weak evidence in some areas and risked undermining people’s efforts to maintain and promote condom-based safer sex.

The statement said that people with HIV are not sexually infectious (“ne transmettent pas le VIH par voie sexuelle”), as long as the following conditions are met:

The HIV+ individual takes antiretroviral therapy consistently and as prescribed and is regularly followed by his/her doctor.
Viral load is ‘undetectable’ and has been so for at least six months.
The HIV+ individual does not have any STIs.

The original statement made no distinction between vaginal and anal sex, though all the evidence the writers cited in support of the statement concerned heterosexual transmission, such as the Rakai study, and they have since said that the statement only covered heterosexual transmission.

The statement had five co-authors, four of them Switzerland’s foremost HIV experts: Professor Pietro Vernazza, of the Cantonal Hospital in St Gallen, and President of the Swiss Federal Commission for HIV/AIDS; Professor Bernard Hirschel from Geneva University Hospital; Dr Enos Bernasconi of the Lugano Regional Hospital; and Dr Markus Flepp, President of the Swiss Federal Office of Public Health’s Sub-committee on the clinical and therapeutic aspects of HIV/ AIDS. Significantly, its fifth author was a community activist, François Wasserfallen of the European AIDS Treatment Group, thus ensuring that community ‘buy-in’ for the statement was present from the start.

The headline statement says that “after review of the medical literature and extensive discussion” the Swiss Federal Commission for HIV/AIDS resolves that, “An HIV-infected person on antiretroviral therapy with completely suppressed viraemia (‘effective ART’) is not sexually infectious, that is, cannot transmit HIV through sexual contact.”

The Commission states that an HIV+ person in a stable relationship with an HIV-negative partner, who follows their antiretroviral treatment consistently and as prescribed and who does not have an STI, is “not putting their partner at risk of transmission by sexual contact”.

However, they emphasise that, “Couples must understand that adherence will become omnipresent in their relationship when they decide not to use protection, and due to the importance of STIs, rules must be defined for sexual contacts outside of relationship.”

They add that heterosexual women will have to consider eventual interactions between contraceptives and antiretrovirals before considering stopping using condoms. They also say that insemination[ix] via sperm washing is no longer indicated when “antiretroviral treatment is efficient.”

The Commission goes on to say that it “is not for the time being, considering recommendations that HIV+ individuals start treatment purely for preventative measures.” Aside from the cost involved, they argue, it cannot be certain that HIV+ people would be sufficiently motivated to follow, and apply to the letter, antiretroviral treatment on a long-term basis without medical indications. They note that poor adherence is likely to facilitate the development of resistance, and that, therefore, antiretroviral therapy as prevention is indicated only in “exceptional circumstances for extremely motivated patients”.

The Commission also says that their statement should not change prevention strategies currently taking place in Switzerland. With the exception of stable HIV+ couples where HIV-positivity and the efficacy of antiretroviral therapy can be established, measures to protect oneself must be followed at all times. “People who are not in a stable relationship must protect themselves,” they note, “as they would not be able to verify whether their partner is positive or on efficient antiretroviral therapy.”

At a meeting in Mexico City in August 2008, Pietro Vernazza clarified some aspects of the statement. “We never thought of it as a statement that was to be delivered worldwide,” he said, but rather “it was meant only to be delivered to Swiss physicians to help them discuss sexual risk-taking with their patients and their steady partners.” He regretted the “ne transmettent pas” in the statement’s title and said that this absolute phrasing was ‘misleading’ in that it appeared to rule out the possibility of any residual risk.

“We also made it clear that the only person who can assess perfect adherence and regular check-ups would be a steady partner, and that it should only be the informed [HIV-negative] partner who could assess the risks for themselves.” The statement, he said, was “good news for a small number of people, but [for everyone else] prevention messages remain unchanged”.

Nonetheless, he defended the applicability of the statement at least to heterosexual couples in the light of subsequent research, including the Wilson paper in The Lancet, which said that gay male couples where the HIV+ partner was on treatment could reduce their transmission risk to virtually zero if they also used condoms, and said the estimated residual risk to heterosexual couples where the HIV+ partner was on treatment was of the same order as other possible, but unlikely, hazards such as the risk of dying in an air crash or avalanche.

Copyright © 2011 The Body

2011-06-13T23:54:00.001-07:00

With Koronis, Is A Cure For HIV On The Horizon?
Kerry A. Dolan

Here’s a compelling thought: All the HIV drugs currently on the market work by suppressing some form of the virus and its ability to replicate itself. What if you created a drug that did the opposite–one that uses the replication process to get the virus to mutate more often, something that makes the HIV virus eventually weaken and collapse?

Scientists at Koronis Pharmaceuticals, a small private biotech company in Seattle, have a drug candidate that does just that. It’s been tested in 80 people who have HIV and for whom existing drugs were no longer effective. Results from the Phase 2-A trial, released in January, showed that Koronis’ experimental drug does increase the frequency of mutations in the HIV genome.

More trials have to be done to determine if the Koronis drug can essentially take down the HIV virus, but at least one analyst believes it could be a game changer. Katherine Xu, a biotech analyst for William Blair, said in a report earlier this year that the Koronis drug has “huge potential for disruption.” One scenario she paints: that the Koronis drug be given in combination with an existing drug like Atripla and “after a year or so, the viruses could be mutated out of existence and the patients could achieve a cure,” Xu wrote in a report for Wedbush Securities, where she worked until recently. “If it were to be successful, it would be great news for the field,” Xu told me last week in a phone interview.

Scientists at Koronis have been able to eradicate HIV in a petri dish. Doing so in humans is likely to be much more difficult, but worth a try. Traditional HIV drugs attempt to block viral replication. Koronis CEO Donald Elmer explains that the Koronis drug uses the viral replication process to induce additional mutations in the HIV genome by mismatch base pairing. “These additional mutations progressively debilitate the virus, which ultimately results in collapse of the viral population,” he says.

This month marks 30 years since the virus now called HIV made its first horrific emergence among gay men. Incredible progress has been made in the decades since, but almost all of that is evidenced in the U.S. and Europe. Of the 33 million people living with HIV, 25 million are not currently being treated; 90% of the $14 billion a year spent on treating HIV is focused in North America and Europe.

“Outside the U.S., HIV is still a pandemic,” says Koronis CEO Elmer, who says that treating HIV is complicated and requires regular monitoring –something that just isn’t happening in poor countries. Thus the urgent need for a new kind of treatment. A lurking concern –and another reason to pursue new kinds of drugs — is the rise of drug-resistant HIV.

The next step for Koronis is to come up with $15 million to $20 million to perform a clinical trial that would combine its drug candidate with an approved drug that is currently used for HIV treatment. The company has raised $43 million since it was founded in 2002 but is in need of outside cash. It’s in discussions with the six big companies that operate in the HIV sector – Gilead (GILD), Bristol-Myers Squibb (BMY), Abbott Laboratories (ABT), Viiv (which is a joint venture between Pfizer and GlaxoSmithKline), Johnson & Johnson and Merck – but is pursuing other avenues as well –including a possible partnership with a non-U.S. company. It’s open to investment from deep-pocketed individuals who want to help further HIV drug development.

Finding a cure for HIV has been a holy grail for scientists in the field. It’s way too early to say for sure that the Koronis drug is the route to that cure. But until it undergoes further tests, it’s too early to rule it out as well.

Copyright © 2011 Forbes Magazine

2011-06-12T01:54:00.000-07:00

Premature aging seen as issue for AIDS survivors
By LISA LEFF, Associated Press

SAN FRANCISCO (AP) — Having survived the first and worst years of the AIDS epidemic, when he was losing three friends to the disease in a day and undergoing every primitive, toxic treatment that then existed, Peter Greene is grateful to be alive.

But a quarter-century after his own diagnosis, the former Mr. Gay Colorado, now 56, wrestles with vision impairment, bone density loss and other debilitating health problems he once assumed he wouldn’t grow old enough to see.

“I survived all the big things, but now there is a new host of things. Liver problems. Kidney disease. It’s like you are a 50-year-old in an 80-year-old body,” Greene, a San Francisco travel agent, said. “I’m just afraid that this is not, regardless of what my non-HIV positive friends say, the typical aging process.”

Even when AIDS still was almost always fatal, researchers predicted that people infected with HIV would be more prone to the cancers, neurological disorders and heart conditions that typically afflict the elderly. Thirty years after the first diagnoses, doctors are seeing these and other unanticipated signs of premature or “accelerated” aging in some long-term survivors.

Government-funded scientists are working to tease apart whether the memory loss, arthritis, renal failure and high blood pressure showing up in patients in their 40s and 50s are consequences of HIV, the drugs used to treat it or a cruel combination of both. With people over 50 expected to make up a majority of U.S. residents infected with the virus by 2015, there’s some urgency to unraveling the “complex treatment challenges” HIV poses to older Americans, according to the National Institutes of Health.

“In those with long-term HIV infection, the persistent activation of immune cells by the virus likely increases the susceptibility of these individuals to inflammation-induced diseases and diminishes their capacity to fight certain diseases,” the federal health agency’s chiefs of infectious diseases, aging and AIDS research wrote, summing up the current state of knowledge on last September’s National HIV/AIDS and Aging Awareness Day. “Coupled with the aging process, the extended exposure of these adults to both HIV and antiretroviral drugs appears to increase their risk of illness and death from cardiovascular, bone, kidney, liver and lung disease, as well as many cancers not associated directly with HIV infection.”

In San Francisco, where already more than half of the 9,734 AIDS cases are in people 50 and over, University of California, San Francisco AIDS specialists are collaborating with geriatricians, pharmacists and nutritionists to develop treatment guidelines designed to help veterans of the disease cope with getting frail a decade or two ahead of schedule and to remain independent for as long as possible.

“Wouldn’t it be helpful to be able to say, are you at high risk, low risk or moderate risk for progressing to dependency in the next five, the next 10 years, being less mobile, less able to be functional in the workplace. Are you going to be safe in your home, are you going to remember to take all those medications? How are they going to interact?” explained Dr. Malcolm John, who directs UCSF’s HIV clinic. “All those questions need to be brought into the HIV field at a younger age.”

Research so far suggests that HIV is not directly causing conditions that mimic old age, but hastens patients toward ailments to which they may have been genetically or environmentally predisposed. Plus, their immune systems are being weakened over time even when they are being successfully treated for AIDS, John said.

“That’s probably true for a lot of these things. We aren’t saying HIV’s starting the problem, but it’s added fuel on top,” he said.

Stokes, a patient of John’s who goes by only his last name, is a prime example. At 53, HIV-positive since 1985 and in substance abuse recovery for the last 11 years, he says he is happier than he ever has been. Yet the number of ailments for which he is being treated would be more commonly found in someone 30 years his senior: a condition called Ramsay Hunt syndrome that causes facial paralysis, a rare cartilage disorder for which he has undergone four ear surgeries, bone death in the hip and shoulder, deterioration of his heart muscle, osteoporosis and memory loss.

A specialist recently diagnosed a Kaposi’s sarcoma spot on Stokes’ ankle. Although the cancer is not life-threatening, the sight of young men disfigured by KS lesions was a harbinger of the early AIDS crisis, and its presence on his own body is unsettling.

At his therapy group for men with HIV, aging “comes up frequently,” he said. “I say, ‘Just think what we have come through to have a life today.’“ At the same time, he acknowledges sometimes feeling self-conscious about his physical appearance and worries if “people are not attracted to me and unwilling to go the length of what it means to be with me, no matter how brilliant my mind or my zest for life.”

Loneliness, financial worries and concerns about who will care for them and where can weigh on long-term AIDS survivors in the same way as all adults living in a society that values youth, Charles Emlet, a social work professor at the University of Washington, Tacoma, said.

As they get older and sicker, many feel “doubly stigmatized,” he said. Some people who have lived with the virus for a long time have been getting by on private disability benefits that will run out when they turn 65, forcing them to move to less expensive locations or to consider turning to estranged family members. Like soldiers from a distant war, many lost partners and their closest friends to AIDS.

Such emotional side effects, combined with the physical toll of managing chronic health problems, put older AIDS patients at risk for depression. At the same time, Emlet has uncovered evidence that a majority of long-term survivors also share another trait that typically comes with advanced age: that is, the ability to draw strength from their difficult experiences.

“The older adults I’ve interviewed, many of them talk about how much it means to them to give back, to do something positive with the years they never expected to have,” he said.

Peter Greene can relate to that. At times, like the days he is so exhausted he can’t get out of bed or the pain from his multiple maladies is too intense, he asks himself “the Carrie Bradshaw question—are we really lucky to still be alive?”

As frightening and uncertain as this phase of AIDS is, he thinks he knows the answer.

“I’ve tried to make the time I have count, and really, now that I have the body of an 80-year-old, I probably have the wisdom of an 80-year-old as well, which counts for a lot,” Greene said. “Everything becomes clear at the end of your life and in some ways, thinking you’ve been dying all these years, you get moments of clarity that I don’t think everyone gets.”

Copyright © 2011 The Associated Press. All rights reserved.

2011-06-10T23:46:00.000-07:00

HIV damages B-cells as well as T-cells: new treatment targets identified
Gus Cairns

The signature effect of HIV infection, and the cause of AIDS, is disruption of the T-lymphocyte branch of the immune system and in particular the destruction of CD4+ T-helper cells.

A team of researchers at the US National Institute of Allergies and Infectious Diseases (NIAID) has now found that HIV also causes a very specific form of damage to the other half of the adaptive immune system, the B-cells, and in particular the memory B-cells, which recognise previously-experienced infections and generate antibodies against them.

By using probes to delete specific genes within B-cells, they discovered that HIV infection creates an unusual population of exhausted, non-responsive cells called tissue-like B-memory cells. In previous experiments with cells taken from HIV-negative people, they found that that these cells are characterised the activation of genes which cause the cell to produce proteins that inhibit the cell’s function and that two of these inhibitory proteins had an especially strong effect on B-cell function.

Now, in cells taken from people with HIV, they have found that, by deleting the genes that manufactured these inhibitory proteins, they could restore the anti-HIV activity of these B-cells, at least in the test tube, that this rejuvenated activity was long-lasting, and that the cells exhibited a number of other markers of increased immune activity.

Although the gene-therapy techniques used in these experiments were sophisticated and can cause unpredictable immune reactions in themselves, the inhibitory proteins thus identified could become new therapeutic targets.

Background
One of the puzzles of HIV infection has always been that, while the immune system does mount an antibody response to HIV – indeed it is these antibodies that are detected in the standard HIV test – this response only partially controls viral replication, and eventually fails to entirely.

B-lymphocytes are the bone-marrow cells and their job is to secrete antibodies. Antibodies are soluble protein molecules that either directly destroy foreign invaders, render them harmless, or tag them for destruction by other parts of the immune system.

A strong antibody response to a pathogen can either prevent an infection happening altogether or can clear it from the system. Once an infection is experienced, the body creates a population of ‘memory’ B-cells that swiftly mount an antibody response if the invading pathogen is encountered again.

Vaccines generally work by imitating an infection and thus setting up a memory B-cell response in advance of an actual infection. T-cells, the thymus cells, work in a similar way but destroy infected cells rather than manufacture antibodies.

In HIV infection, the body mounts a very strong antibody response in the first few weeks that partially works, bringing the viral load down from millions to, on average, about 50,000 copies/ml. However it does not contain viral replication any further or eliminate HIV infection, and eventually weakens so that the viral load increases again.

Research findings
Dr Lela Kardava and her team from NIAID discovered that people with HIV had an unusual subset of B-memory cells called tissue-like cells that were characterised by the presence, on their surface, of a variety of inhibitory receptor molecules. The cells behaved much the same as exhausted T-cells do in HIV infection: they were sluggish and failed to react to foreign substances and to HIV itself.

In a series of experiments, Kardava’s team knocked out specific genes coding for these inhibitory proteins and found that by doing so they were able to restore some of the B-cells’ antibody responses. They did so by incubating cells with pieces of small interfering RNA (siRNA), molecules that target and interfere with specific genes. Previous experiments in cells taken from HIV-negative people had shown that ‘downregulating’ the inhibitory proteins with siRNA led to an 80-90% increase in the ability of the B-cells to proliferate.

They deleted nine inhibitory molecules in turn in cells taken from a group of people with chronic HIV infection. These individuals were either not taking ARV therapy or had only recently started and had an average viral load of 2096 copies/ml, with an average CD4 count of 427 cells/mm3.

They found that the deletion of two inhibitory receptors called FCRL4 and SIGLEC6 had particularly strong rejuvenating effects. The siRNA targeting the genes coding for these proteins led to a 30-66% reduction in the expression of these proteins in the cell. This in turn led to a doubling of the number of cells which, in response to standard immune stimuli, secreted anti-HIV antibodies.

These responses were long-lasting; the anti-HIV antibody responses of the cells that had had FCRL4 and SIGLEC6 ‘downregulated’ (reduced) demonstrated a similar increase in responsiveness to HIV several weeks later. Cells with the downregulated inhibitory proteins also secreted five times as much of the powerful pro-inflammatory chemical (cytokine) interleukin-6 and 50% more of the chemokine MIP-1a, indicating that modulating B-cell exhaustion may have a number of other immune-modulating effects.

Implications
The NIAID team are working on the hypothesis that the exhaustion seen in the B-cells of people with HIV is very similar to that seen in T-cells: the cells essentially stop working as a defensive manoeuvre against a virus whose constant stimulation would otherwise cause more damage by exciting the body into a constantly inflammatory state.

If, however, therapies could be devised than enabled B-cells to mount better antibody responses to HIV without undesirable side-effects, they could in theory form part of a ‘functional cure’ that rendered HIV infection less harmful – or might even be part of a way to eliminate HIV from the body.

The NIAID team say: “Our findings suggest that the development of strategies aimed at reversing the deleterious effects of these inhibitory receptors may improve immune responses against...persisting viruses.”

Reference
Kardava L et al. Attenuation of HIV-associated human B cell exhaustion by siRNA downregulation of inhibitory receptors. Journal of Clinical Investigation, early online edition doi: 10.1172/JCI45685. 2011.

Copyright © 2011 AidsMap.Com

2011-06-10T23:38:00.000-07:00

Group looks to spur development of new HIV vaccine

Positive HIV tests may soon become a thing of the past if a new foundation made up of leading infectious disease experts has its say.

Fourteen scientists and HIV awareness advocates from around the world recently joined forces to form the Foundation for Vaccine Research. The main purpose of the group is to raise awareness of the dire need for the development of an effective vaccine against the sexually transmitted disease.

Toward this end, the members will lobby lawmakers for research funding and encourage more scientists to explore the possibilities for developing an effective vaccine. While the foundation says that prevention is more important than cures, only 2 percent of money spent developing drugs to fight infectious diseases is put toward vaccines. The rest goes to medicines to address existing infections.

“I hope that the creation of the Foundation will galvanize efforts to create innovative financing mechanisms and other incentives that will expedite vaccine research and development, particularly for HIV,” said Mauro Schechter, the group’s board director.

He added that in many parts of the world, there are no financial incentives for developing vaccines. His group hopes to change this.

Copyright © 2011 Private MD Labs

2011-06-09T15:01:00.001-07:00

Simultaneous HIV and AIDS diagnosis occurs frequently in the United States
By Todd A. Heywood

Americans infected with HIV are often finding out that not only are they infected with the virus, but it has done significant enough damage to their immune system that they fit the clinical diagnosis of AIDS.

USA Today reports that many of the nation’s hardest hit communities also have higher late stage diagnosis scenarios.

Experts at the Centers for Disease and Control and Prevention (CDC) have long estimated that 20% of people infected with HIV don’t know it. One-third are diagnosed so late in the course of their infection that they develop AIDS within one year. The new analysis found that the states with the biggest epidemics and the greatest number of late diagnoses are Florida, New York, Texas, Georgia and New Jersey.

The Centers for Disease Control and Prevention estimates that between 20 and 25 percent of the people infected with HIV do not know. This is particularly important in light of a recent National Institutes of Health study that found successful anti-retroviral treatment dropped infections between partners where one is positive and the other is not. The medications have a 96 percent efficacy rate in preventing infection in those relationships.

Not only does knowing one is infected make it easier to control the virus and live a healthy life, two studies have found that 66 to 70 percent of all new infections in the U.S. can be traced to a person who was unaware of their HIV infection. That also ties into a study released in September which found 1 in 5 gay or bi men in 21 urban areas — including Detroit — were HIV infected. Of those who were infected, the study found 44 percent were unaware of their status. Another study released last week found that of those who identified as having reported being tested on the previous 12 months, seven percent were actually infected. The study authors recommended that men who have sex with men ought to consider more frequent testing.

Copyright © 2011 The Michigan Messenger

2011-06-08T15:10:00.000-07:00

Byronik's note: Viral tropism is the specificity of a virus for a particular host tissue, determined in part by the interaction of viral surface structures with receptors present on the surface of the host cell.

And that explanation was about as clear as mud to me until I read this: “A tropism test is a blood test that reveals how your HIV enters T-cells. HIV can enter T-cells via an R5 or X4 co-receptor. A tropism test reveals which of these receptors your HIV uses.”

2011-06-08T03:09:00.000-07:00

Tropism impacts on virological success of first-line HIV therapy
Michael Carter

HIV tropism has a significant impact on the virological success of first-line antiretroviral therapy, a Spanish study published in the July 1st edition of the Journal of Infectious Diseases suggests.

Individuals whose HIV used the CXCR4 co-receptor were significantly less likely to achieve an undetectable viral load than patients whose virus used the CCR5 co-receptor. The association between the CXCR4 co-receptor and poorer outcomes was especially strong in patients infected with HIV subtype B.

In this study patients were receiving treatment with tenofovir/FTC (Truvada) and either nevirapine or atazanavir/ritonavir. No patients received a drug from the CCR5 inhibitor class.

“It may be worthwhile to perform baseline viral tropism testing before beginning any antiretroviral regimen,” comment the investigators.

HIV uses a co-receptor to latch onto CD4 cells.

In the earlier stages of infection, virus using the CCR5 co-receptor predominate, whereas virus utilising CXCR4 tends to be associated with the later stages of HIV infection.The preference for a receptor type is called tropism, and can be determined by tropism testing.

In patients who are not taking antiretroviral treatment, the presence of CXCR4 virus has been associated with faster disease progression. Tropism testing is recommended before starting treatment with the CCR5 inhibitor maraviroc (Celsentri), the only licensed drug in this class of antiretroviral.

However, the impact of co-receptor tropism on the outcomes of first-line HIV treatment that does not contain a CCR5 inhibitor is largely unknown.

Investigators from the Hospital Carlos III in Madrid therefore performed a retrospective study involving treatment-naïve patients who were enrolled into a randomised study. This was designed to compare the efficacy of therapy based on atazanavir (Reyataz) boosted by ritonavir (Norvir) with treatment including nevirapine (Viramune). The patients also took Truvada (FTC/tenofovir), and results showed that the combinations were equally effective.

Blood samples obtained at the start of therapy were tested to determine which co-receptor was used by patients’ virus.

Changes in viral load and CD4 cell count after six and twelve months of treatment were compared according to co-receptor.

A total of 569 patients were randomised and 428 completed 48 weeks of treatment.

Virus using the CXCR4 co-receptor was found in 14%, and 22% of individuals were infected with a non-subtype B strain of HIV.

At baseline, patients with CXCR4 virus had significantly higher viral load (5.4 vs. 5.2 log10 copies/ml; p =0.044) and lower CD4 cell counts (145 vs. 188 cells/mm3; p < 0.001) than individuals with virus using the CCR5 co-receptor. After a year of therapy, patients with CXCR4 virus were significantly less likely than individuals with CCR5 virus to have an undetectable viral load (77% vs. 92%; p = 0.009).

This association between the CXCR4 co-receptor and poorer virological control at week 24 (p = 0.012) was confirmed in multivariate analysis. There was also a trend towards poorer treatment response at week 48. It is harder to isolate HIV tropism in patients with non-B subtypes. Therefore the investigators performed further analysis, which was this time restricted to individuals with HIV subtype B. This showed a strong association between the CXCR4 co-receptor and poorer virological control at both week 24 (p = 0.001) and week 48 (p < 0.001).

“When we limited our analyses to participants infected with clade B viruses, the strength of the impact of viral tropism on virological response was more robust than in the whole study population,” observe the authors.

Unlike some other research, there was no evidence that the CXCR4 co-receptor had a negative impact on CD4 cell recovery. “In antiretroviral-naïve patients beginning antiretroviral therapy, baseline HIV-1 tropism seems to be an independent predictor of virologic response,” conclude the investigators, adding “this observation may have important clinical implications for the monitoring of antiretroviral therapy and interpretation of comparative trials.”

Reference
Seclen E et al. Impact of baseline HIV-1 tropism on viral response and CD4 cell count gains in HIV-infected patients receiving first-line antiretroviral therapy. J Infect Dis 204: 139-44, 2011 (click here for the free abstract).

All material that appears at www.aidsmap.com and subsections thereof is copyright © NAM Publications, 2011. All rights reserved.

2011-06-07T23:53:00.000-07:00

Older HIV+ People May Benefit from Earlier ART
By Liz Highleyman

SUMMARY
Starting antiretroviral treatment at higher CD4 T-cell counts predicted better long-term immune recovery in a large U.S. cohort, while age over 50 years and hepatitis B or C coinfection were linked to smaller CD4 cell gains.

Combination highly active antiretroviral therapy (HAART) typically leads to viral suppression and recovery of CD4 T-cells, but outcomes can vary from person to person.

As described in the May 20, 2011, advance online edition of the Journal of Acquired Immune Deficiency Syndromes, Li Xiuhong from Johns Hopkins Bloomberg School of Public Health and colleagues looked at predictors of CD4 cell counts and HIV viral load among people on long-term HAART.

The analysis included 614 men in the long-running Multicenter AIDS Cohort Study (MACS), an observational trial that has followed gay and bisexual men with HIV/AIDS in 4 U.S. cities since 1984. The group included in this analysis had been taking combination therapy for 5 to 12 years.

Nearly half (47%) were younger than 40 years when they started HAART and 12% were older than 50. About half (53%) used protease inhibitor regimens (70% of them boosted with ritonavir), while 42% used non-nucleoside reverse transcriptase inhibitors (NNRTIs) and 5% used triple nucleoside/nucleoside reverse transcriptase inhibitor (NRTI) combinations.

Results

At 5-12 years after starting HAART, the overall median CD4 T-cell count was 586 cells/mm3. A majority of participants had more than 500 cells/mm3, the current threshold for HAART initiation. 78% of HIV RNA measurements showed undetectable viral load. Predictors of higher CD4 counts after 5-12 years on HAART included:

Higher CD4 T-cell count before starting HAART;

Higher total lymphocyte count (CD4 T-cells plus other immune cells) before HAART (> 1200 cells/mm3).

Larger CD4 T-cell gains during the first 5 years on HAART;

Good HIV viral load suppression during first 5 years on HAART;

Remaining on a stable first or second HAART regimen;

Good adherence;

Not having hepatitis B or C coinfection;

Age 50 years or older at HAART initiation.

CD4 cell gains tended to plateau after 5 years in people who started HAART with lower CD4 counts.

Older men experienced good CD4 cell recovery on average, with a mean adjusted CD4 count of 643 cells/mm3 after 10-12 years on HAART. However, among men who started therapy with 201-350 cells/mm3, the average was 578 cells/mm3 for those older than 50 compared with 670 cells/mm3 for those younger than 40 at HAART initiation.

Stated another way, the mean CD4 count of older men who started HAART with 351-500 cells/mm3 was similar to that of younger men who started with 201-350 cells/mm3 (643 vs 670 cells/mm3, respectively).

HIV RNA suppression during the first 5 years on HAART predicted subsequent viral suppression.
Based on these findings, the study authors concluded, “Immunological and virological responses in the first 5 years post-HAART predicted subsequent CD4 T-cell counts and HIV-1 RNA levels.”

“The association between age and subsequent CD4 T-cell count supports incorporating age in guidelines for use of HAART,” they added, suggesting that older people may benefit from starting treatment sooner, while their CD4 counts are still high.

Investigator affiliations: Departments of Epidemiology and Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD; David Geffen School of Medicine at UCLA, Los Angeles, CA; Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA; Division of Infectious Diseases, Feinberg School of Medicine, Northwestern University, Chicago, IL.

Reference
L Xiuhong, JB Margolick, BD Jamieson, et al. CD4+ T-Cell Counts and Plasma HIV-1 RNA Levels Beyond 5 Years of Highly Active Antiretroviral Therapy (HAART). Journal of Acquired Immune Deficiency Syndromes (abstract). May 20, 2011 (Epub ahead of print).

Copyright © 2011 HIVandHepatitis.com

2011-06-07T14:17:00.000-07:00

HIV Superinfection Not Seen in Amsterdam Gay Men
By Liz Highleyman

Over the course of the AIDS epidemic public officials have cautioned that HIV positive people should avoid unprotected sex with each other in order to prevent “superinfection,” or infection with additional viral strains that could potentially be more aggressive or drug-resistant. Some advocates, however, promote “serosorting” as a responsible risk-reduction strategy for HIV positive gay men.

Several prior studies have failed to find evidence of superinfection, or indicate that it happens only rarely — around 50 cases total — typically during the early years after infection with the initial virus.

As described in the June 2011 Journal of Infectious Diseases, Andrea Rachinger from the University of Amsterdam and colleagues looked for evidence of superinfection over time among participants in the Amsterdam Cohort Studies on HIV Infection and AIDS.

The researchers analyzed HIV-1 C2-C4 envelope (env) and gag sequences generated from longitudinal blood samples from 15 gay/bisexual men who had not yet started antiretroviral therapy. Serum samples had been collected around the time of self-reported risk for HIV sexual transmission, including unprotected anal sex or having other sexually transmitted infections.

The study authors used maximum likelihood phylogenetic analysis to detect evidence of new HIV strains in a total of 124 serum samples. They looked at a median of 8 samples per participant with a median follow-up period of 5.8 person-years, or about 88 total person-years.

Phylogenetic analysis of a total of 907 C2-C4 env sequences and 672 gag sequences revealed no case of HIV superinfection, yielding a superinfection incidence rate of 0 per 100 person-years.

Based on these findings, the authors wrote, “We conclude that HIV-1 superinfection incidence is low in this subgroup of homosexual men who reported unsafe sexual behavior.”

However, they suggested, “Additional studies are required to estimate the impact of also other factors, which may determine the risk to acquire HIV-1 superinfection.”

Investigator affiliations: Department of Experimental Immunology, Sanquin Research, Landsteiner Laboratory, and Center for Infection and Immunity Amsterdam (CINIMA) at the Academic Medical Center of the University of Amsterdam; Cluster of Infectious Diseases, Department of Research, Health Service of Amsterdam; Department of Internal Medicine, CINIMA, Academic Medical Center of the University of Amsterdam, Amsterdam, Netherlands.

Reference
A Rachinger, P Manyenga, JA Burger, et al. Low Incidence of HIV-1 Superinfection Even After Episodes of Unsafe Sexual Behavior of Homosexual Men in the Amsterdam Cohort Studies on HIV Infection and AIDS. Journal of Infectious Diseases 203(11):1621-1628 (abstract). June 2011

Copyright © 2011 HIVandHepatitis.com

2011-06-06T16:23:00.000-07:00

Older AIDS Survivors Face New Challenges
From U.S. Centers for Disease Control and Prevention

The first sizeable group of AIDS patients to navigate the aging process is now faced with medical, psychological and financial obstacles that early patients could not imagine living to see.

CDC data note that upwards of 25 percent of US HIV patients are at least 50 years old. And, according to the latest Central Nervous System HIV Antiretroviral Therapy Effects Research study, 52 percent of Americans with HIV have a cognitive impairment, compared to 10 percent of the general population. The American Academy of HIV Medicine adds that HIV-positive people 55 and over are three times more prone to chronic illnesses — such as hypertension, diabetes, osteoporosis, and cancer — than uninfected 70 year olds.

“The problems people with HIV face are really changing,” said Dr. C. Bradley Hare, medical director at San Francisco General Hospital. Hare recalls the days when his patients were primarily in their 20s and dying en masse. Now, his clinic’s 3,000 HIV patients have an average age of 47.

Specialists are only beginning to have enough older HIV-patients to study to determine whether their ailments are due to the virus, drug treatments or the aging process. “You’ve been dealing with HIV for 30 years and you finally have that under control, and now you’re facing a new raft of medical problems. It seems unfair,” said Hare.

In addition, a 2006 AIDS Community Research Initiative of America study observed that long-term HIV survivors are nearly 13 times more likely to experience depression. Britain’s Terrence Higgins Trust notes that aged AIDS patients are more apt to be unemployed or less financially solvent.

Adapted from: Agence France Presse 05.30.2011

2011-06-06T03:14:00.000-07:00

Treatment is Key to Prevention of HIV/AIDS, Doctors Say
By Dan Fost

Doctors fighting HIV/AIDS have a new strategy working for them: Use the treatment of the disease as a way to prevent it — a strategy borne of the growing effectiveness of that treatment in the three decades since the disease first emerged.

“Treatment revolutionized AIDS,” says Diane Havlir, MD, professor of Medicine at UCSF and chief of the AIDS program at San Francisco General Hospital and Trauma Center. “Treatment changed AIDS from a uniformly fatal disease to a chronic disease.”

And now, Havlir says, “today’s treatment is also prevention.” Timely treatment can stop the spread of HIV/AIDS in many ways. In patients, it stops the virus from progressing into AIDS, and it prevents damage to organs such as the heart, liver and kidneys, which occurs in untreated AIDS. Treatment also greatly reduces the risk of HIV transmission.

Diane Havlir, MD

Havlir cites the most encouraging news to date, the National Institute of Allergy and Infectious Diseases’ HPTN 052 study, released in May 2011, which reported a 97 percent reduction in HIV transmission among discordant couples — couples in which one partner is HIV-infected and the other is HIV-negative — when the HIV-infected partner is treated with antiretroviral therapy relatively early in the course of HIV infection.

The so-called 052 study – conducted by the HIV Prevention Trials Network (HPTN) — released its results four years early because the prevention effectiveness of the antiretroviral drugs now commonly used to treat HIV infections was so clear-cut.

That news put one more arrow in the quiver of scientists and doctors looking not only to attack HIV, but to stop it.

“Certainly we’re hoping that the next 30 years of HIV can be the last 30 years, especially in San Francisco, where we have the community resources and knowledge to put an end to the epidemic,” says Grant Colfax, MD, director of the HIV Prevention and Research Section in the San Francisco Department of Public Health AIDS Office. Colfax, who trained at UCSF, is adjunct faculty at the university today.

“We have very good data now that show that when you know your HIV status, and you get treatment if you’re HIV positive, combined with psychosocial supports that decrease stigma, there’s a dramatic decrease in HIV as a result of testing and treatment,” Colfax says.

Employing New Tools, Tactics
Preventing transmission is key to the epidemic in the U.S., where 50,000 new infections per year are still reported. Some of the exciting new tools and tactics employed in the war on HIV and AIDS include:

Pre-exposure prophylaxis (PrEP). The National Institutes of Health announced in November 2010 that high-risk gay men who take retroviral medication (tenofovir) before they’re infected can prevent HIV infection. While such a strategy is costly, and could be difficult to sustain depending on whether people consistently take the medicine, Colfax hails the study results as “momentous” and says San Francisco is moving forward to test the practicality of this approach.

CAPRISA microbicides. CAPRISA (the Centre for the AIDS Program of Research in South Africa) announced in July 2010 that when women used an antiretroviral microbicide (tenofovir gel) before intercourse, they significantly reduced their chances of getting HIV. The study was particularly significant because 60 percent of new HIV infections in Africa occur in women and girls. “Microbicide has particular potential among women who may not necessarily be empowered to negotiate condom use with a partner,” Colfax says.

052. In the 1990s, when Highly Active Antiretroviral Therapy, or HAART, came into use, the side effects of the drugs was so severe that they weren’t given to people unless they were very ill or had a low level of immunosuppression, as measured by low CD4 count or viral load. The drugs have improved so that now they can be given to people much earlier in the course of the virus. The new HPTN 052 study showed the drugs can also be effective when given to infected people while their immune systems are still relatively healthy. The study was the first randomized study to find that giving antiretrovirals to someone can reduce the risk of sexual transmission of HIV to an uninfected partner.

Male circumcision. In Africa, as governments begin to promote male circumcision, infection rates are starting to drop, according to Craig R. Cohen, MD, MPH, a UCSF professor and director of Family AIDS Care and Education Services (FACES), an HIV/AIDS care and treatment program in Kenya. Several trials of male circumcision “demonstrated a 60 percent reduction in the number of new infections in men,” Cohen says. World Health Organization guidelines promote voluntary male medical circumcision, and Kenya encourages it as well.

Condoms Cornerstone of Protection
Despite the new tools, some of the best forms of prevention remain the tried and true: Use a condom, and don’t share needles. “Condoms remain a cornerstone of HIV prevention,” Colfax says. “The goal is to provide people with as many prevention options as possible.”

“The most effective way to stop the spread of the disease is to get tested, and if you test positive, get treated.” Diane Havlir, MD

Even people participating in PrEP and other prevention trials receive condoms and risk reduction messages, he says.

Additional prevention strategies include frequent HIV testing, and if found to be positive, getting treatment early.

As the stigma associated with AIDS lifts in many regions, more people are willing to take those steps. But in some places, from rural America to Africa, the stigma persists. Many HIV-positive patients show up at the doctor’s office or clinic with late-stage disease, which severely limits the efficacy of treatment.

In San Francisco, “we started a universal HIV treatment program,” says Havlir, whose many hats include director of the AIDS Services, Prevention, Intervention, Research and Education (ASPIRE) Program at UCSF. “We were the first in the world to do this. As soon as an individual is identified with HIV, we are offering treatment for the individual’s benefit.”

Models by UCSF investigators Edwin Charlebois, Moupali Das, Travis Porco and Havlir show that more than just the individual will potentially benefit.

“If we treated all persons with HIV currently in care in San Francisco, we’d have a 50 percent reduction in new infections in five years.” The strategy can have impact well beyond San Francisco.

“African countries struggling with high rates of untreated AIDS stand to benefit enormously from universal treatment,” she says. “Untreated AIDS has massive social and economic collateral damage. People drop out of the workforce, and kids drop out of school to work and support the family. We see all these damages of AIDS and HIV, which our group is postulating can be reversed with universal use of antiretroviral therapies.”

“Everyone says, ‘Oh, antiretroviral therapy is so expensive,’” Havlir says. “Our hypothesis is that it may be the least expensive option, because you get all these benefits. We are working on that with the World Bank, the World Health Organization and others.”

Cohen sees the same thing. “There was a large trial in Uganda, Kenya and Tanzania testing people for HIV – the whole community,” he says. “Once someone tested positive, they immediately started treatment, and did not wait for their CD4 (white blood cell) count to go down. If you bring down a community’s viral load, you can decrease the rate down to almost zero.”

Tests that like show such a strategy may be feasible as well as cost-effective, he says. “You can prevent not just HIV, but potentially other diseases like TB and malaria. And it could improve economic performance in a community where, if someone is infected with HIV, the economic performance goes down.”

The rapid pace of new strategies emerging inspires the researchers to believe that progress will continue, perhaps even picking up speed. “Treatment is prevention,” Havlir says. “We’ve seen it work and it’s a critical part of the strategy to end the AIDS epidemic.”

The HIV treatment pendulum.(Editorial): An article from: Internal Medicine News

The University of California, San Francisco, CA 94143, (415) 476-9000
© 2011 The Regents of the University of California. All rights reserved.

2011-06-05T20:09:00.000-07:00

HIV patient Timothy Brown is the boy who lived
By Melissa Healy, Los Angeles Times

Almost 20 years after he was diagnosed, the 45-year-old is, essentially, cured. A bone-marrow transplant to treat his leukemia transferred a genetic variation that made his system resistant to HIV.

His case gives some experts hope that a broader cure might be possible. (Eric Risberg, AP)

To many of the nation’s million people living with a diagnosis of HIV/AIDS, Timothy Brown is the Harry Potter of the disease: Like the young wizard who survived Lord Voldemort’s wrath, he is the boy who lived.

Today, almost 20 years after he became infected, Brown is, essentially, cured.

Brown, now 45, is known in medical-journal circles as “The Berlin Patient,” a moniker assigned him by a February 2009 case study published in the New England Journal of Medicine.

In a “Brief Report,” oncologist Gero Huetter and his colleagues at Berlin’s University Hospital described the unique stem-cell transplant of an HIV-infected patient — Brown — who had acute myeloid leukemia, and the remarkable result: Twenty months after the procedure, the virus had not reappeared in Brown’s body, even though he was no longer taking antiretroviral drugs.

The bone marrow Brown received in a time-tested treatment for leukemia had given him an extraordinary gift. It had also transferred to Brown’s immune system an uncommon genetic variation — present in an estimated 10% of northern Europeans — that rendered it resistant to HIV.

It’s been a winding road to medical fame, Brown said in an interview last week. Raised in Seattle, he came out as gay at 18 and soon began a restless journey across Europe. He settled briefly in Barcelona, where he believes he became infected, and finally in Berlin, where he lived for almost 20 years.

When he learned he was HIV-positive in 1995, a friend told him gravely that he probably had two years to live.

“I didn’t know who to be angry at,” Brown said.

Ten years later, he was alive and taking antiretroviral medications. Then, in 2006, a bout of exhaustion sent him to the doctor, who diagnosed leukemia and proposed the customary treatment: Wipe out Brown’s immune system with radiation and rebuild it with the bone marrow of a healthy donor.

Here was the crucial trick: From the 230 possible matches found for Brown, Huetter deliberately picked a donor who carried genetic resistance to HIV, hoping they might lick both diseases in a single shot.

Now living in San Francisco, Brown has found himself a bit of a celebrity at AIDS functions around the city. Two weeks ago, he spoke at an event titled “Cure — Still a Four-Letter Word?” organized by the American Foundation for AIDS Research. Afterward, he says, “everybody wanted to get their picture taken with me.”

It was as if, he said, he had become the living, breathing embodiment of hope for an end to AIDS.

Los Angeles Times

2011-06-03T23:47:00.000-07:00

Scientists reactivate immune cells exhausted by chronic HIV

Scientists at the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, have demonstrated why certain immune cells chronically exposed to HIV shut down, and how they can be reactivated.

Healthy B cells have a balanced mix of surface proteins that the immune system can use, like the gas pedal and brake of a car, either to activate the cell or to damp down its activity. However, in people with long-term HIV infection who have not begun antiretroviral therapy, their B cells—responsible for producing anti-HIV antibodies—display a surplus of inhibitory receptors, the surface proteins used to apply the brakes on a B cell. Scientists from the NIAID Laboratory of Immunoregulation led by Lela Kardava, Ph.D., Susan Moir, Ph.D., and Anthony S. Fauci, M.D., NIAID Director and Chief of the laboratory, wanted to know if this phenomenon can help explain why B cells become "exhausted" and essentially shut down in people who are HIV-infected but treatment-naive.

To test their hypothesis, the scientists used molecules called small interfering RNAs (siRNAs), which acted at the genetic level to prevent exhausted B cells from replenishing inhibitory receptors. After treatment with siRNAs, the exhausted cells responded more normally to conditions that typically would spur a B cell into action, such as the presence of a virus, demonstrating that the excess of inhibitory receptors may explain why exhausted B cells are so unresponsive.

Because B cells generally are difficult to manipulate, the new siRNA-based approach may hold promise for scientists seeking to develop therapies to improve the human antibody response against HIV and other pathogens by altering the expression of specific B-cell genes.

Provided by NIH/National Institute of Allergy and Infectious Diseases

2011-06-01T00:01:00.000-07:00

Long-term CD4 cell gains on treatment weaker in over-50s
By Michael Carter

People with HIV aged 50 and over have weaker immune restoration after starting antiretroviral treatment - earlier treatment should be a priority in this group.

US investigators have found people with HIV aged 50 and over have weaker immune restoration after starting antiretroviral treatment, and recommend that earlier treatment should be a priority in this group.

The study, published in the online edition of the Journal of Acquired Immune Deficiency Syndromes, also showed that the majority of patients had a CD4 cell count above 500 cells/mm3 after five or more years of therapy and that 75% of individuals had an undetectable viral load.

Combination antiretroviral therapy became available in 1996 and rapidly transformed the prognosis of patients with HIV.

However, published data examining the long-term effectiveness of such treatment is currently limited.

Therefore investigators from the Multicenter AIDS Cohort Study (MACS) monitored the CD4 cell counts and viral load of 614 HIV-positive gay men who had been taking potent antiretroviral therapy for between five and twelve years.

The investigators were especially eager to see if any factors were associated with longer-term outcomes, and hypothesised that age, and HIV disease stage before the initiation of therapy, as well as CD4 cell count and viral load during the first five years of treatment, would affect immunological and virological responses in the longer-term.

At the time HIV therapy was started, 47% of men were aged under 40 and 12% were aged over 50.

A total of 4431 CD4 cell counts and viral load measurements were obtained from patients between years five and twelve of treatment.

Just over half (53%) the patients were taking therapy based on a protease inhibitor, and 70% of these individuals were treated with a ritonavir-boosted drug. Non-nucleoside reverse transcriptase inhibitor (NNRTI)-based treatment was taken by 42% of individuals, with efavirenz (Sustiva) the most widely used drug (70%). A small proportion of patients (5%) were treated with a triple nucleoside reverse transcriptase inhibitor(NRTI) combination, a regimen which is now considered suboptimal.

Median CD4 cell count five to twelve years after starting therapy was 585 cells/mm3.

In the first five years of therapy, significant increases in CD4 cell count were observed regardless of baseline CD4 cell count. However, CD4 cell counts stabilised after five years for patients who initiated therapy when their CD4 cell count was in the region of 350 cells/mm3. There continued to be modest increases for people who started treatment with weaker immune systems.

Factors associated with poorer CD4 cell count gains after five years were a lower baseline CD4 cell count (p < 0.01), and co-infection with hepatitis B virus (p = 0.01).

Patients who had an undetectable viral load for at least 50% of the first five years of therapy had higher CD4 cell counts in the longer term (p < 0.01), as did individuals who remained on their first or second combination of drugs (p = 0.03).

Age at the initiation of HIV therapy also predicted longer-term outcomes. The mean CD4 cell count after five years of therapy was significantly lower for men who started treatment when they were aged 50 or over, compared to people who started treatment when they were aged under 40.

Younger men who started therapy when their CD4 cell count was in the region of 201 to 350 cells/mm3 had a mean CD4 cell count of 670 cells/mm3 after ten or more years of treatment.

In contrast, the mean CD4 cell count at this time point for the over 50s who initiated therapy with a similar count was 578 cells/mm3, a significant difference (p < 0.01).

To achieve a similar long-term CD4 cell count as the under 40s, older patients would have needed to start therapy when their CD4 cell count was above 350 cells/mm3.

“Our data support using age in the guidelines for initiating HAART [highly active antiretroviral therapy], such that persons who are older than 50 years should start treatment at higher CD4 counts,” write the authors.

Investigators also found that long-term outcomes were associated with total lymphocyte count.

A count above 1200 cells/mm3 at the time HIV therapy was started was associated with a significantly higher CD4 cell count after five years of treatment (p < 0.01).

“This finding supports the inclusion of TLC [total lymphocyte count] in HIV treatment guidelines,” comment the investigators.

Overall, 78% of viral load measurements obtained after five years of therapy were undetectable.

Viral load in the first five years predicted subsequent outcomes, and virological control was significantly better in the long term for patients who were undetectable in this period (p < 0.01).

Switching treatment on two or more occasions was associated with poorer control of viral load in the longer term (p = 0.06).

Unsurprisingly, individuals who reported 100% adherence had good control of virus after year five.

“In this study, several factors were found to be associated with lower CD4 cell counts in men who received HAART for 5-12 years. Important modifiable factors were older age and lower CD4 cell count at the time of HAART initiation,” comment the researchers.

Nevertheless, they are encouraged by their overall findings, writing “this study shows that the effectiveness of HAART persists for up to 12 years”.

Reference
Xiuhong LM et al. CD4+ T-Cell Counts and Plasma HIV-1 RNA Levels Beyond 5 Years of Highly Active Antiretroviral Therapy (HAART). J Acquir Immune Defic Syndr, online edition: doi: 10.1097/QAI.0b013e31821e9f21, 2011 (click here for the free abstract).

European Aids Treatment Group

2011-05-31T22:42:00.000-07:00

Can Cannabis Reduce HIV Disease Progression?
By Liz Highleyman

Cannabis has been shown in studies to improve appetite, relieve chronic pain, and reduce nausea due to chemotherapy. Many people with HIV/AIDS use medical marijuana to combat wasting and other symptoms, which raises questions about what effects it might have on HIV and its progression.

Many immune cells express cannabinoid receptors, indicating that cannabis may influence immune function. Some prior research suggested that marijuana use is associated with HIV disease progression, but such studies were prone to confounding by socioeconomic and other factors related to illegal drug use.

As described in the June 2011, issue of AIDS Research and Human Retroviruses, Patricia Molina and colleagues from Louisiana State University Health Sciences Center examined the impact of ongoing administration of delta-9-tetrahydrocannabinol (THC) in macaque monkeys exposed to simian immunodeficiency virus (SIV).

Eight rhesus macaques received twice-daily intramuscular injections of either THC or a placebo. After 28 days, they were intravenously inoculated with a highly infectious dose of SIV. The researchers looked and immune and metabolic indicators of disease progression during the initial 6-month asymptomatic phase after infection.

Results
THC administration did not significantly increase viral load or exacerbate immune dysfunction.

After exposure to SIV, the monkeys showed measurable viral loads, decreased CD4/CD8 T-cell ratios, and increased CD8 cell proliferation.

Administration of cannabis prior to infection produced little or no effects on these parameters.

THC-treated monkeys lost CD4 cells more slowly than the placebo group.

Monkeys given THC had a significantly lower early mortality rate compared with placebo-treated animals.

THC-treated monkeys had lower plasma and cerebrospinal fluid SIV viral load than those in the placebo group.

Monkeys in the THC group also experienced less wasting, though the difference did not reach statistical significance.

In a laboratory study, THC decreased SIV replication in MT4-R5?cells in vitro.
“These results indicate that chronic [THC] does not increase viral load or aggravate morbidity and may actually ameliorate SIV disease progression,” the study authors concluded.

“Two of the [placebo-treated] animals succumbed to SIV infection shortly after 5 months, and a third reached end stage at 7 months,” they elaborated in their discussion. “Among the [THC-treated] animals, the first animal did not reach end stage until 11 months post-SIV inoculation. “

“We speculate that reduced levels of SIV, retention of body mass, and attenuation of inflammation are likely mechanisms for [THC]-mediated modulation of disease progression that warrant further study,” they wrote.

Investigator affiliations: Departments of Physiology, Pharmacology, Medicine, Microbiology, and Pathology, Louisiana State University Health Sciences Center, New Orleans, LA; and School of Public Health, Alcohol Research Center, and Alcohol and Drug Abuse Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, LA.

Reference
PE Molina, P Winsauer, P Zhang, et al. Cannabinoid Administration Attenuates the Progression of Simian Immunodeficiency Virus. AIDS Research and Human Retroviruses 27(6): 585-592 (free full text). June 2011

HIVandHepatitis.com.

2011-05-28T01:20:00.000-07:00

HIV viral load detectable after just 2 days without meds
By Fran Lowry

There is a dose–response relation between days of missed HIV medications and the subsequent viral load.

The total amount of nonadherent time with HIV antiretroviral therapy over the course of a month affects the risk of having a detectable viral load starting at 14 days, but an interruption of just 2 days will cause the viral load to rise, according to research presented here at the 6th International Conference on HIV Treatment and Prevention Adherence, sponsored by the International Association of Physicians in AIDS Care (IAPAC).

The findings, from an analysis of the MACH-14 study, were presented by Becky L. Genberg, PhD, MPH, from Brown University, Providence, Rhode Island.

There is a dose–response relation between days of missed HIV medications and the subsequent viral load. Moreover, it appears that consecutive days of missed medications of approximately 2 weeks are the most damaging to patient health, compared with shorter interruptions or overall medication-free days, Dr. Genberg said.

“When patients stop taking their medication, their viral load starts to go up almost immediately,” she told Medscape Medical News.

The MACH-14 study combines data from 16 studies at 14 sites in the United States. In this analysis, Dr. Genberg and her team focused on 768 individuals with 2399 viral load measures, and looked at patterns of nonadherence in the 28 days prior to measuring the viral load.

The study sample was 73% male, 42% African American, 34% white, and 17% Hispanic/Latino. The median age was 40 years (interquartile range [IQR], 35 to 46), and 31% were treatment-naïve at baseline. The median viral load was 400 copies/mL (IQR, 400 to 1454).

After adjustment for sociodemographics, total nonadherent days, and time since longest interruption, a dose–response relation between the length of the longest treatment interruption and increased viral load was observed.

The study found that viral load began to increase in as little as 48 hours after discontinuing HIV medication.

After 2 to 6 days, the viral load increased 25%. Between 14 and 20 days, viral load continued to increase significantly (P < .001), and participants whose treatment interruption lasted 3 weeks or longer saw their viral load increase 3-fold, Dr. Genberg said.

“The patterns of adherence seem to matter. We would like a more careful consideration, looking at nonadherence and the different patterns of nonadherence,” she said in an interview. “We would also like to focus on understanding ways to prevent and to intervene to prevent these consecutive treatment interruptions to maximize the effectiveness of treatment.”

“The capacity to pool large datasets is vital to answer questions regarding the impact of different patterns of nonadherence on HIV treatment outcomes,” said conference cochair Christopher M. Gordon, PhD, chief of the Secondary HIV Prevention and Translational Research Branch and associate director for prevention at the National Institute of Mental Health in Bethesda, Maryland.

“These findings have important implications for adherence interventions in both domestic and international settings,” he told Medscape Medical News. “Providers could make more concerted efforts to reduce longer episodes of nonadherence, and in settings where drug stock-outs or other socioeconomic barriers make treatment interruptions more likely, systemic or structural interventions may be needed to prevent these gaps in treatment.”

Jose M. Zuniga, PhD, president of IAPAC and conference cochair, noted that the results of the study “speak directly to a growing call from clinicians, as well as patients, for more sophisticated discussions about the importance of maintaining optimal adherence to antiretroviral therapy.”

He told Medscape Medical News: “ ‘Because I said so’, and ‘because you should’ are no longer strong enough reasons for patients to observe proper medication-taking behaviors.”

Dr. Zuniga added that tools are needed to help clinicians deal with a variety of adherence-related challenges. These include polypharmacy challenges “posed by an aging population of patients on antiretroviral therapy who are taking myriad other drugs, including for comorbid conditions such as cardiovascular disease and/or viral hepatitis.”

This study was supported by the National Institute of Mental Health and the Agency for Healthcare Research and Quality. Dr. Genberg, Dr. Gordon, and Dr. Zuniga have disclosed no relevant financial relationships.

Presented May 23, 2011. 6th International Conference on HIV Treatment and Prevention Adherence: Abstract 70087.

European Aids Treatment Group

2011-02-08T02:26:00.000-08:00

The trouble with Wikileaks

In fact, Kim Philby, who spied for the Soviets during the hottest period of the Cold War, observed in his 1968 book, My Silent War, that secret documents, though glamorous, are frequently a snare and a delusion.

Quote, “Is it a first draft, a second draft or the finished memorandum? Was it written by an official of standing, or some dogsbody with a bright idea? Even if it is unmistakably a direct instruction to the United States Ambassador from the Secretary of State dated last Tuesday, is it still valid today? In short, documentary intelligence, to be really valuable, must come as a steady stream, embellished with an awful lot of explanatory annotation.”

Philby concluded, “An hour’s serious discussion with a trustworthy informant is often more valuable than any number of original documents.”

— Spoken by Brooke Gladstone of WNYC’s “On The Media” on National Public Radio, Dec. 3, 2010.

2011-02-06T14:28:00.000-08:00

George W. Bush has a heart attack and dies. Obviously he goes to Hell, where the Devil is waiting for him.

“I’m not sure what to do,” says the Devil. “You’re on my list, but I have no room for you. As you definitely have to stay here, I’m going to have to let someone else go. I’ve got three folks here who weren’t quite as bad as you. I’ll let one of them go, but you have to take their place. I’ll even let you decide who leaves.”

George W. thinks that sounds pretty good, so he agrees. The Devil opens the first room. In it is Richard M. Nixon and a large pool of hot water. He keeps diving in and climbing out, over and over. Such is his fate in Hell.

“No!” says George W. “I don’t think so, I’m not a good swimmer and don’t think I could stay in hot water all day.”

The Devil leads him to the next room. In it is Tony Blair with a sledgehammer and a room full of rocks. All he does is swing the hammer, time after time.

“No! I’ve got this problem with my shoulder. I would be in constant agony if all I had to do was break rocks all day.” George W. says.

The Devil opens the third door. In it, George sees Bill Clinton lying on the floor with his arms staked out over his head and his legs staked in a spreadeagle pose. Bent over him is Monica Lewinsky doing what she's famous for. Bush looks at this in disbelief for a while and finally says, “Yeah. I can handle this.”

The Devil smiles and says, “OK, Monica. You’re free to go!”

2011-01-17T12:29:00.000-08:00

David Kitson obituary

Anti-apartheid activist who was eventually shunned by the ANC high command

Denis Herbstein

David Kitson looked as though he wouldn’t hurt a fly, but in his day he had been a bomb-instructor for the African National Congress’ military wing and spent 20 years in prison. His interrogators did not know he was a member of the liberation army’s high command. “They thought I was one of those middle-class fuddies who get involved in things,” Kitson, who has died aged 91, once said.

There was little thought of revolution when he studied mechanical engineering at Howard College, Durban (now KwaZulu-Natal university), but it was a useful preparation. Graduating in 1942, he served “up north” as a sapper with the South African army. Thus his future adversaries taught him how to prepare explosives. After the war he moved to London – where his Jewish father had been born – working for de Havilland Aircraft as a draughtsman. He was active in the engineering union Tass, while doubling as secretary of the Communist party branch in Hornsey, north London. Tass sponsored him for two years at Ruskin College, Oxford. Afterwards, when at British Oxygen, he was offered promotion on condition he end his union activities. He refused and was sacked. After that, jobs were difficult to find.

He married Norma Cranko, a South African Jewish woman who was also active in the Communist party, and with her he returned to South Africa in 1959, ostensibly to introduce their son, Steven, to his grandparents. Within months, the police fired on unarmed protesters at Sharpeville, killing 69. There was now no thought of returning to Britain. Kitson’s first allegiance was to the Communist party, which, like the ANC, had been driven underground. When the ANC’s armed wing, Umkhonto we Sizwe (MK, or Spear of the Nation), launched its sabotage campaign in December 1961, Kitson was teaching the bombers their trade. He was a dependable behind-the-scenes cadre, not a coal-face primer of bombs.

But when virtually the entire leadership of MK was arrested at Rivonia, on the outskirts of Johannesburg, and several leading communists had fled the country, the lower ranks were catapulted in to replace them. Kitson was now one of four members of a high command directing the revolutionary struggle. Arrest was inevitable. He held out for 131 days.

Kitson was not subjected to intense physical torture but did suffer interrogation. “With modern methods they are going to get something out of you sooner or later,” he once told me, “so you proceed with a series of lies.” He gave away nothing of importance, managing to withhold his membership of the high command. Norma was held for three weeks. His lawyers thought hanging was a distinct possibility, so the 20-year sentence (for sabotage and membership of the Communist party) came almost as a relief, even if there was no prospect of remission for good behaviour. Pretoria local prison housed the white “politicals”, and their treatment was nothing like that meted out to black prisoners on Robben Island. But there were bullying warders and a vindictive minister of justice stopped their studies for three years.

Kitson acquired arts and science degrees (in mathematics), and was even allowed to study Russian, before the authorities cottoned on. He remained a hardliner, not overly keen on the “liberal nonsense” spouted by his student neighbours likewise jailed for sabotage. He was philosophical about his plight, regarding himself as “a casualty of the conflict”, and he made no objection when Norma divorced him, moved to Britain, and married fellow South African Sidney Cherfas. However, when Steven visited from London and was arrested, allegedly for sketching the prison, Kitson’s equanimity was tested.

Norma later divorced Sidney, amicably, and remarried David when he was released from prison. Arriving in London, Kitson found himself in a political cauldron. Norma had founded the City of London anti-apartheid group, whose non-stop protests on the pavement outside South Africa’s Trafalgar Square embassy had become a tourist attraction. The confrontational style incurred the wrath of the sedate Anti-Apartheid Movement’s national leadership.

In return, Norma treated her critics with disdain. The ANC and the influential London cell of the South African Communist party told Kitson to denounce his wife. He refused. The couple were suspended from the ANC, a speaking tour of Britain was cancelled, and his old union, Tass, had the offer of a lectureship in mathematical statistics at Ruskin College withdrawn from him. David and Norma moved to Zimbabwe.

In time, at the behest of Walter Sisulu and Nelson Mandela, the couple were reinstated by the ANC and honoured as “veterans of the struggle”. It was half-hearted. There was no invitation to Mandela’s historic inauguration. After Norma died in 2002, Kitson returned to Johannesburg. The hero of the struggle died a non-person in the new South Africa. He is survived by his daughter Amandla. Steven died in 1997.

• Ian David Kitson, activist, born 25 August 1919; died 9 November 2010

© The Guardian

2011-01-06T23:55:00.000-08:00

Study Linking Vaccine to Autism was ‘Fraud’

2010-12-18T15:31:00.000-08:00

The great South African communist and fighter against apartheid David Kitson has died in Johannesburg aged 91.
FRFI 218 December 2010/January 2011

A senior member of the South African Communist Party (SACP) in the 1960s, he became a commissar of the national high command of Umkhonto we Sizwe (MK), the armed wing of the ANC, after the arrest of the ‘Rivonia Eight’ ANC leaders, including Nelson Mandela, Govan Mbeki and Walter Sisulu, in 1963.

David Kitson was arrested in 1964 and, with four others, was charged with sabotage and being a member of the high command of MK, and jailed for 20 years. His wife Norma was detained a month later.

Norma Kitson subsequently was forced into exile in London and with the Revolutionary Communist Group formed City of London Anti-Apartheid Group, which in 1982 held a non-stop picket outside the South African Embassy over deteriorating conditions faced by David and his fellow prisoners, who were being held on Death Row in Pretoria Central Prison. After 86 days, the prisoners were moved to better conditions, and this victory was the impetus later for the four-year Non-Stop Picket against apartheid and for the release of all South African political prisoners maintained by City AA outside the South African Embassy from 1986 until Mandela’s release in 1990.

City AA, committed to opposing the racism of the British state as well as the apartheid system in South Africa, and to support for all organisations fighting for national liberation in South Africa, found itself bitterly opposed by the ANC/SACP exile establishment in London which wanted to channel all protest through the Anti-Apartheid Movement (AAM), which it controlled.

When David was released in 1984 and joined Norma and their children Steven and Amandla in London, he found himself caught up in the vicious efforts of the ANC/SACP to politically isolate Norma, City AA and the RCG.

Despite the fact that David was the most senior MK leader and longest-serving political prisoner at the time to be released from South Africa, at the AAM AGM in 1984, a few months after his release, a significant proportion of the movement’s leadership refused to join in a standing ovation when he stood to speak, or even applaud him, and he was denied a seat on the AAM National Committee. Having fought against the apartheid state, David now found himself having to struggle against the opportunism of the movement in Britain. When he refused, as he put it, to ‘jump through hoops’, he and Norma were suspended from the ANC. With the collusion of erstwhile communist Ken Gill, leader of David’s union TASS, David was told he would be reinstated as an ANC member and get funding to take up a promised emeritus post at Ruskin College, Oxford, only if he publicly denounced his wife and City AA. Always one to take a principled stand, David rejected this poisonous blackmail and, as a result, found himself without a job or source of income.

In an obituary in the South African Sunday Times, Chris Barron writes of the attempts to isolate David politically:

‘One view is that his return to London after his imprisonment constituted an embarrassment and a reproach to members of the SACP, including Joe Slovo, who had fled SA in 1963 in defiance of a central committee directive that they should stay. Kitson obeyed the directive and paid heavily for it. He and Slovo had ideological differences, and it has been argued that Slovo had much to lose if Kitson was restored to his old seniority in the movement.’

As David said at his trial: ‘There came a point where I could choose to run or I could choose to stand. And so I stood.’

Significantly, the head of the ANC in London, who informed David, by post, of his suspension and who was a key player in the political attacks on City AA, was Solly Smith, later unmasked as a South African police spy along with other prominent London members.

While in London, David maintained comradely relations with the RCG and spoke at a number of our public meetings. After returning to live in Harare in the 1990s, he wrote regularly for FRFI on the situation in Zimbabwe. He moved back to South Africa after Norma’s death in 2002. Steven Kitson died in 1997.

FRFI salutes David’s unwavering courage and communist principles and we extend our sympathy to his comrades and family.

© Fight Racism! Fight Imperialism! 2010

2010-11-23T09:25:00.000-08:00

Civil partnership refused to heterosexual couple

Kristin and Ian at Bristol register office © Chris Houston.

Bristol, UK - Nov. 23, 2010. A heterosexual Quaker couple, Ian Goggin and Kristin Skarsholt, were refused a civil partnership at Bristol Register Office this morning, Tuesday, Nov. 23. The registrar cited the legal ban on opposite-sex civil partnerships as the reason for the refusal.

“We want a civil partnership for two reasons. It better reflects our relationship, and we can’t condone the baseless discrimination between civil marriages and civil partnerships,” Goggin (21) said.

Skarsholt (22) said, “We are disappointed that we were not able to have our relationship legally recognised. Ian and I genuinely wish to secure legal recognition as civil partners. We are determined to fight through the courts to end the legal segregation that continues to keep straight and gay couples in separate institutions.

“Just as our gay friends are excluded from civil marriage, we are being excluded from having a civil partnership. This is discriminatory segregation on the basis of sexual orientation. It is wrong,” she said.

Goggin said, “Although the register staff were extremely helpful, they were unable to offer us a civil partnership. They felt obliged to act in accordance with the law as it currently stands. We thank them for their politeness. We regret this rejection but our resolve to carry on the campaign for equality remains strong.

“We are hopeful that our forthcoming legal case, led by Professor Robert Wintemute and Peter Tatchell, will eventually end discrimination against heterosexual couples in civil partnership law. Next time we come here to apply for a civil partnership we are confident there will be a happier outcome,” he said.

Skarsholt and Goggin are both Bristol-based students at the University of West England. Skarsholt is studying Arabic and Ian is studying music technology. She was born in Norway and he in Ireland. They’ve been in a relationship together for two years. They met at a Quaker retreat.

Skarsholt and Goggin’s application today is part of the new Equal Love campaign, which seeks the repeal of the twin prohibitions on gay civil marriages and heterosexual civil partnerships.

Skarsholt and Goggin are the fourth of eight couples who will file applications at register offices across the country, in an effort to overturn the “sexual segregation” in civil marriage and civil partnership law.

The Equal Love campaign is organised by the gay rights group OutRage! and coordinated by the human rights campaigner Peter Tatchell.

The couple is being advised by the Equal Love campaign’s legal expert, Robert Wintemute, Professor of Human Rights Law at Kings College London.

"By excluding same-sex couples from civil marriage, and different-sex couples from civil partnership, the UK Government is discriminating on the grounds of sexual orientation, contrary to the Human Rights Act,” Wintemute said.

“The twin bans violate Article 14 (protection against discrimination), Article 12 (the right to marry) and Article 8 (the right to respect for family life).

“The rights attached to civil marriage and civil partnership are identical, especially with regard to adoption of children, donor insemination, and surrogacy. There is no longer any justification for excluding same-sex couples from civil marriage and different-sex couples from civil partnership. It's like having separate drinking fountains or beaches for different racial groups, even though the water is the same. The only function of the twin bans is to mark lesbian and gay people as inferior to heterosexual people," he said.

Equal Love’s campaign coordinator, Peter Tatchell, was in Bristol for the civil partnership application attempt and to support Skarsholt and Goggin. He said, “We seek heterosexual equality. In a democratic society, everyone should be equal before the law. There should be no discrimination based on sexual orientation.

“Denying heterosexual couples the right to have a civil partnership is discriminatory and offensive. We want to see it ended, so that straight couples like Tom and Katherine can have the option of a civil partnership.

“The bans on same-sex civil marriages and on opposite-sex civil partnerships are a form of sexual apartheid. There is one law for straight couples and another law for gay partners. Two wrongs don’t make a right.

“We see the Equal Love campaign as a historic quest for justice; morally equivalent to the campaigns to overturn the bans on inter-racial marriage in apartheid South Africa and the Deep South of the USA.

“From Nov. 2 onwards, eight couples will file applications at register offices in London, Northampton, Bristol and Havant. Four same-sex couples will apply for civil marriages and four heterosexual couples will apply for civil partnerships. One couple will make an application every week until Dec. 14. Once all the applications have been refused, the eight couples will consult our lawyer and agree a joint legal action.

“Our aim is to secure equality in civil marriage and civil partnership law. We want both systems open to all couples, gay and straight, so that everyone has a free and equal choice.

“Just as gay couples should be able to marry, civil partnerships should be available to straight couples.

“Same-sex marriage is the growing trend all over the world. It exists in Canada, Argentina and South Africa, as well as seven of our European neighbours: Portugal, Spain, Belgium, the Netherlands, Sweden, Norway and Iceland. We want marriage equality in Britain too.

“Political support for ending the ban on gay marriage is growing. London Mayor, Boris Johnson, and former Conservative Party Vice-Chair, Margot James MP, have both come out in favour of allowing lesbian and gay couples to marry in a registry office, on the same terms as heterosexual partners.

“This view is also endorsed by the leader of the Labour Party, Ed Miliband, and by the deputy prime minister Nick Clegg of the Liberal Democrats.

“Both the Liberal Democrat and the Green party conferences have voted overwhelmingly in favour of ending the bans on gay civil marriages and heterosexual civil partnerships.”

Public attitudes have shifted strongly in favour of allowing gay couples to marry. A Populus opinion poll in June 2009 found that 61 per cent of the public believe that: “Gay couples should have an equal right to get married, not just to have civil partnerships.” Only 33 per cent disagreed.

RELATED LINKS:

Equal Love on the Web
Equal Love on Twitter
Equal Love on Facebook

2010-11-20T16:45:00.000-08:00

Smash the racist English Defence League (EDL) & The British National Party

Demonstrations by far-right activists such as the English Defence League are fuelling Islamic extremism, West Midlands police said today.

Groups such as the EDL lay the groundwork for the recruitment of Muslims to radicalism, according to counter-terrorism officers.

Since the EDL emerged last summer, it has held demonstrations in towns and cities against Islamic extremism, with another planned for Preston city centre on Saturday, Nov. 27.

But the West Midlands counter-terrorism unit said there is evidence that violence or damage towards Muslim property associated with EDL demos encourages extremist retaliation afterwards.

Detective Superintendent John Larkin told BBC Radio 5 Live: “They look for the hook to pull people through and when the EDL have been and done what they’ve done, perversely they leave that behind.”

Hope Not Hate campaign chairman Nick Lowles said: “This demonstrates how hate breeds hate.

“The EDL breeds Islamic extremism and Islamic extremism breeds the EDL.

“It’s time to break the chain.

“…make a stand against extremism on both sides of the divide.”

2010-11-20T16:30:00.000-08:00

Please change your Facebook profile pic to “Some people are gay. Get over it!” this week for National Anti-Bullying Week, and show support to anyone experiencing homophobic bullying in schools and Stonewall’s campaign to tackle this. Please encourage all your Facebook Friends to do the same to show the anti-gay bullies they won’t win!

2010-11-15T16:18:00.000-08:00

David Kitson and me

If you’ve never heard of David Kitson and you’re not a Marxist nerd, I’ll attempt to express my loss in the language of contemporary popular culture: Yoda just died.

But I won’t make myself out to be a communist Jedi. I was never more than an activist in a solidarity organization called the City of London Anti-Apartheid Group. City AA, as we called it, was like a fan club and the ANC’s armed wing, Umkhonto we Sizwe (MK for short), was the band. And, to strain a lame analogy even further, if MK was The Beatles, David Kitson was John Lennon. Let me gather my painful recollections and I’ll try to explain what David Kitson means to me.

I was recruited to City AA by David’s son Steven, in the fall of 1986, shortly after dawn, on the wide sidewalk in front of the South African Embassy on Trafalgar Square. I’d been up all night (the first of many) with City AA’s non-stop picket for the release of Nelson Mandela but Steven wanted me to stay on through the day as a “legal steward” for the scheduled mass demonstration.

That was when Steven first told me his father had served 19 years and five months in a South African prison for his leading role in MK. I didn’t know Steven and his mother Norma had both been detained and tortured by the Apartheid regime and, somehow, I’d missed the UK television coverage of David’s release and arrival in England. So I picked up the details on the street, the same day I learned the words of my first South African freedom song, which was all about a train leaving for Zimbabwe.

David could quite easily have avoided arrest if he had simply fled to London, as so many of his comrades had chosen to do. On trial for treason, he had stood in the dock and explained, “I could have run or I could have stood. So I stood.”

As a white South African with a solid career in engineering, David could have enjoyed a very privileged lifestyle on the backs of the disenfranchised majority, but he was an old-school Leninist and a member of the illegal South African Communist Party.

Even the SACP was too racist for David. But, within the constraints of Party discipline, he opposed the doctrine known as Colonization of a Special Type (CST) as the SACP drafted the program, published in 1962, as The Road to South African Freedom. The Party sidelined his theoretical intervention by simply not inviting him to a key meeting. They cited tactical considerations: it was too dangerous for him to attend. He was a key figure in the armed resistance and there was too much risk his presence would be betrayed to the South African authorities.

How convenient! Such are the machinations of that ambiguous world of bureaucrats and informers, where the dialectic of legal and illegal action meet the dialectic of theory and practice. This was in the early 1960s and while communists were shadowy marginalized figures in South Africa they were a significant force in the UK where David’s powerful labor union TASS was led by his esteemed comrade Ken Gill.

When David began his prison sentence, he received word from Gill that, when he was eventually released, the union would give him a “job for life” on the faculty of Ruskin College in Oxford, England. To this end, David developed his academic qualifications while in prison and took three more degrees.

He did this in the appalling conditions of Pretoria Local prison’s death row, where the extreme cold made him seriously ill. By then, Norma and the kids had relocated to London where they mounted a day-and-night picket in front of the South African Embassy, for 86 days, demanding that David be moved to a warmer cell. When they eventually moved him, the prison guards intimated to David that his wife, in London, was responsible for this. I always think of that anecdote when somebody tries to tell me political demonstrations never achieve anything.

Norma’s 86-day picket had enjoyed massive support from Britain’s left-wing establishment including cabinet members, labor leaders and the British Anti-Apartheid Movement, whose bureaucratic leadership suggested Norma’s picketers should form their own AAM branch, which became City of London Anti-Apartheid Group (City AA).

But there was a big problem when the AAM leadership attempted to impose its sectarian policies. City AA contended that solidarity organizations outside South Africa have no right to tell the African people who their leaders ought to be, and continued to extend their support to the PAC, SWANU and any other organization that was fighting Apartheid.

So, when David was finally released from prison, the dead hand of Stalinism visited him again and the ANC's London representatives demanded he denounce City AA and his wife or be suspended from the ANC. He refused. After all, City AA had saved his life. In reprisal, the Stalinist bureaucrats took away all the promised benefits: David doesn’t get his job at Ruskin College, his daughter Amandla doesn’t go to university in East Germany and there’s no place in the ANC choir for Steven. This was all communicated to David and Norma in a letter from the ANC's Solly Smith who, it turned out, much later, was a spy for the South African government all along.

So, by 1986, when first I ever saw David, I was helping to organize the picket for the release of Nelson Mandela. David, the revered sage, would appear on special occasions to make a speech.

For a long time, I wasn’t even allowed to know where City AA’s office was. Some committee members were wary of my alleged military background and they suspected me of being a government spy. Eventually, I joined the committee as picket organizer and then, when the office organizer was expelled for misappropriating correspondence, I was co-opted as City AA’s office organizer. On my first day at the secret office, David knocked on the door and, with disarming humility, said, “Tell me what I can do to help out.”

I was lost for words. I stammered something about feeling I should be the one helping him. I didn’t even know how to address him. If I were a communist, I should call him comrade. But my instinct was to call him sir, which seemed somehow inappropriate.

I had a lot more contact with Steven and Norma. Steven was City AA’s treasurer and Norma was deputy convener. I was embarrassingly deficient in terms of Marxist theory but did what I could to make up for this with hard work and my own defiant brand of pragmatism.

I worked closely with the Revolutionary Communist Group, which had played a leadership role in City AA since its inception. Its leader once told those of us who did not belong to a political organization we should go ahead and join one and then draw its support to the Mandela picket as part of a non-sectarian alliance. I attended a small meeting of the Humanist Party which, as it turned out, organized through a decentralized cellular structure across national boundaries. When City AA planned a march for Mandela to Trafalgar Square from north London, the only way I could mobilize Humanist Party support was to give a bundle of leaflets to a Humanist delegate who was attending a party conference in Paris.

It worked. I happened to be standing on a sidewalk with Norma and David as hundreds of Humanist Party members marched past, some with enormous homemade Mandela banners. David turned to me and asked, “Are these your people?” I can hardly remember a prouder moment.

If that was the high, then my low came in 1989 when I resigned from the committee over a disagreement with a high ranking RCG member. I wrote my resignation in the form of a spoof newsletter which somebody chose to circulate publicly on the picket. At the next City AA meeting, I was expelled from City AA and banned from the Non-Stop Picket.

Shunned by my former comrades, I began reading a monthly newspaper called The Leninist, chiefly because I’d heard David Kitson subscribed to it. Sometimes, they printed his letters. I think I was trying to catch up on the Marxist education I had so sadly lacked while in the anti-apartheid struggle.

Membership of the Leninist group was banned within the Communist Party of Great Britain and, when the CPGB finally disbanded, the Leninists took the CPGB name and attempt to reforge the party along more principled lines. This appealed to me and I was drawn into the newly relaunched Daily Worker. Imagine my surprise when, in two short years, I found myself marginalized in an ideological debate with the Provisional Central Committee and then, at the same time, facing a possible prison sentence on a charge of conspiracy.

As Marx himself put it, “History repeats itself, first as tragedy then as farce.” If David was the tragic hero, I seemed to be in danger of being the comic relief. My editor and I had pretty much decided to leave The Daily Worker, but we had qualms. No matter what your ideological differences with a Communist organization might be, to actually leave is to open yourself up to accusations of desertion, betrayal and collusion with the forces of oppression.

This should have been water off a duck’s back to me, by now. But my comrade had been a communist since his working-class boyhood in the Welsh valleys. The only way we could go through with this was if we talked it over with David Kitson, and the opportunity presented itself at a Justice for Kitson meeting in one of those big fancy houses in north London. It might have been Camden or Kentish Town. I remember a bust of Lenin on a grand piano.

I must have been the only person there under 65 and I didn’t know any of these people other than David himself. At the first opportunity, I just blurted out that I needed to talk to him in private. We stepped into a small room and he asked me what was up. I told him our sad story. He stopped me in mid stream and warned me, “You know I’m fairly close with your National Organizer. What if I repeat this conversation to him?”

“It doesn’t matter,” I said. He listened patiently until I’d explained how the leadership had suckered me into open debate and then stitched me up with disciplinary procedures, the protocols, the dialectics…“

“How many people in the organization?” he asked.

“About 15,” I said.

“Go ahead and leave,” he said.

And I never saw him again.

2010-11-14T08:24:00.000-08:00

Obituary: David Kitson: SACP member, MK commissar
By Chris Barron, South Africa Sunday Times

David Kitson, who has died in Johannesburg at the age of 91, was a senior member of the SA Communist Party and a commissar of the national high command of MK, the armed wing of the ANC.

He was appointed after the arrest of ANC leaders at Lilliesleaf farm in Rivonia in 1963.

He and his wife, Norma, helped key members of the underground escape SA before they themselves were captured in 1964.

Together with Mac Maharaj and three others, he was charged with sabotage and being a member of the high command of MK, and jailed for 20 years.

Norma, who died in Harare in 2002 at the age of 68, went into exile in England in 1967. There she initiated a round-the-clock picket of South Africa House in Trafalgar Square, which, until the release of Nelson Mandela in 1990, was the most effective engine of publicity for the struggle against apartheid and particularly the plight of political prisoners in SA.

She also became the driving force of the City of London Anti-Apartheid Group, which was bitterly opposed by the ANC/SA Communist Party establishment in London, which thought the Anti-Apartheid Movement, firmly under their control, should be the only show in town.

When Kitson was released in 1984, he joined his wife and two children in London. He was the most senior resistance fighter and longest-serving political prisoner to be released from SA and was feted by the British media. But the ANC promptly suspended both him and Norma.

He was told he would be reinstated and allowed to take up his union-funded position at Ruskin College, Oxford, where he had spent two years as a research fellow before joining the struggle — but only if he publicly denounced his wife and the City of London Anti-Apartheid Group. He regarded the ANC/SACP proposal as political blackmail and rejected it.

As a result, the SACP leaned on his union to withhold its funding and he found himself without a job or source of income. He remarked later that the withdrawal of income was “a standard technique within the liberation movement for bringing people to heel”.

When Mandela and Walter Sisulu were released in 1990, they insisted that he and Norma be reinstated, but that never happened. They were not invited to Mandela’s inauguration.

Complaining that the ANC/SACP had frozen them out of any role in the new SA, Kitson and his wife went to live in Harare. He returned to SA after her death.

No reasons for their suspension were ever given, and it has remained a subject of fierce speculation. One view is that his return to London after his imprisonment constituted an embarrassment and a reproach to members of the SACP, including Joe Slovo, who had fled SA in 1963 in defiance of a central committee directive that they should stay. Kitson obeyed the directive and paid heavily for it. He and Slovo had ideological differences, and it has been argued that Slovo had much to lose if Kitson was restored to his old seniority in the movement.

Ironically, the head of the ANC in London who informed Kitson, by post, of his suspension was Solly Smith, later unmasked as an SA police spy.

Kitson is survived by his daughter, Amandla. His son, Steven, died in the 1990s.

© Sunday Times of South Africa

2010-11-11T15:21:00.000-08:00

Extracts from actual letters sent to Leicester Council and housing associations

1. I want some repairs done to my cooker as it has backfired and burnt my knob off.

2. I wish to complain that my father hurt his ankle very badly when he put his foot in the hole in his back passage.

3. And their 18-year-old son is continually banging his balls against my fence.

4. I wish to report that the tiles are missing from the outside toilet roof. I think it was that bad wind the other night that blew them off.

5. I am writing on behalf of my sink, which is coming away from the wall.

6. Will you please send someone to mend the garden path, my wife tripped and fell on it yesterday and now she is pregnant.

7. I request permission to remove my drawers in the kitchen. Fifty per cent of the walls are damp, 50 per cent have crumbling plaster and the rest are plain filthy.

8. The toilet is blocked and we cannot bath the children until it is cleared.

9. Will you please send a man to look at my water? It is a funny color and not fit to drink.

10. Our lavatory seat is broken in half and is now in three pieces.

11. I want to complain about the farmer across the road, every morning at 6:00 am his cock wakes me up and it’s now getting too much for me.

12. The man next door has a large erection in the garden, which is unsightly and dangerous.

13. Our kitchen floor is damp. We have two small children and would like a third so please send someone round to do something about it.

14. I am a single woman living in a downstairs flat and would you please do something about the noise made by the man I have on top of me every night.

15. Please send a man with the right tool to finish the job and satisfy my wife

What to do when rental property stinks: how bad does it have to get?: An article from: Utah Business

2010-11-11T14:21:00.000-08:00

Go figure!

This woman is 51. She is a TV 'health guru' advocating a holistic approach to nutrition and ill health, promoting exercise, a pescetarian diet high in organic fruits and vegetables. She recommends detox diets colonic irrigation and supplements, also making statements that yeast is harmful, that the colour of food is nutritionally significant, and about the utility of lingual and faecal examination.

This woman is 50. She is a TV cook, who eats nothing but meat, butter and desserts.

2010-11-11T03:56:00.000-08:00

How you can help the Equal Love campaign:

Please Facebook and tweet the Equal Love campaign events and media coverage to all your friends: www.equallove.org.uk and #equalloveuk on Twitter

We need to pressure MPs and the government to end the twin bans on gay marriages and heterosexual civil partnerships. Please email your MP and MEPs. Ask them to write to the Prime Minister on your behalf, requesting that the government legalise same-sex marriage and opposite-sex civil partnerships. You can email your MP and MEPs direct via this website: http://www.writetothem.com/

Write letters to national and local newspapers urging that civil marriages and civil partnerships be opened up to all couples, regardless of sexual orientation.

Help fund the Equal Love campaign. This campaign is partly funded by the Peter Tatchell Human Rights Fund. To make a donation via PayPal — or to download a donation form or a standing order mandate — go to: www.petertatchell.net/donate.htm
Cheques should be made payable to: “Peter Tatchell Human Rights Fund” and sent to: Peter Tatchell Human Rights Fund, PO Box 35253, London, E1 4YF, England, UK.

You can also join the Equal Love facebook group
http://www.facebook.com/pages/Equal-Love/163531170333628

Or the Equal Love on Twitter. Don’t forget to always use #equalloveuk. http://twitter.com/#!/EqualLoveUK

2010-11-07T20:57:00.000-08:00

All Out Tues. Nov. 9

MUMIA’S LIFE IS IN DANGER!
Please post and distribute widely —

All Out Tues. Nov. 9! MUMIA’S LIFE IS IN DANGER!

MUMIA ABU-JAMAL faces his likely last court hearing on November 9, 2010, in Philadelphia. Mumia is innocent, but this hearing is about sentencing only; and…

Mumia’s death sentence is likely to be reinstated. Why is this happening? See below for details.

Come out Nov. 9, 2010 to say:
MUMIA IS INNOCENT! FREE MUMIA!
END THE RACIST DEATH PENALTY!

PHILADELPHIA: Demonstrate to Free Mumia Now! Come to the Third Circuit Court, Sixth and Market, Philadelphia, at noon on Tuesday, November 9. The hearing starts at 2 p.m.

NEW YORK CITY: Get on the NY Mumia Coalition’s bus to Philadelphia! SEATS ARE CLOSE TO SELLING OUT! Call in now to the Mumia hotline at: (212) 330-8029. Leave a message to request a seat on the bus to Philadelphia. If you can’t get a seat on the Coalition’s bus, reserve on commercial bus or rail.

OAKLAND: Noon on Tuesday, November 9: Come to 14th and Broadway in downtown Oakland. Called by the Labor Action Committee To Free Mumia Abu-Jamal. INFO: (510) 763-2347.

OAKLAND LAC RALLY ENDORSED BY: Campaign To End The Death Penalty; Mobilization To Free Mumia; Revolution Books of Berkeley; Noelle Hanrahan & Prison Radio; Peoples Radio; ANSWER Coalition of SF; Black Student Union, Laney College; Black Student Union, SFSU; Marsha Feinland; Peace and Freedom Party of California; Minister of Information JR; Prisoners of Conscience Committee; International Bolshevik Tendency; International Socialist Organization; Clarence Thomas, co-chair of Million Worker March West & member, ILWU Local 10. Organizations listed for purposes of identification only.

SAN FRANCISCO: 7 PM on Tuesday November 9: Come to Centro del Pueblo, 474 Valencia St. The new film, “JUSTICE ON TRIAL, the Case of Mumia Abu-Jamal,” will be screened. JUSTICE ON TRIAL tells the truth about Mumia Abu-Jamal’s innocence. Hans Bennett of Abu-Jamal News, and other speakers. Donation. Called by the Mobilization To Free Mumia Abu-Jamal. Info: (510) 268-9429.

OTHER ACTIVITIES:

SAN FRANCISCO, 2 P.M. MONDAY NOV 8:

The important new film on Mumia, “JUSTICE ON TRIAL, the Case of Mumia Abu-Jamal,” will be shown at San Francisco State University.

Unlike the other recently produced film, “Barrel of a Gun” (see the next item, below), JUSTICE ON TRIAL tells the truth about Mumia Abu-Jamal’s innocence.

Come to the Richard Oaks Multi-cultural Center, Room T-145 in the Student Center, at SFSU, at 19th and Holloway, San Francisco. Sponsored by the Black Student Union of SFSU, and the Labor Action Committee To Free Mumia Abu-Jamal. Info: (925) 784-9206

PHILADELPHIA: 6:30 PM, MONDAY, NOV. 8:

DEBATE! — Come to the National Constitution Center, 6th & Arch Streets. A debate between DA Seth Williams, and attorney/activist Michael Coard, will follow a showing of a film which seeks to condemn Mumia to death for a crime he didn’t commit. The film, “Barrel of a Gun,” by Tigre Hill, denies Mumia’s innocence, but you can be there for the debate that follows the film to support Mumia.

Also debating will be Prof. Johanna Fernandez of Educators for Mumia and Mumia 101, the writer/director of the new film, JUSTICE ON TRIAL, which tells the truth about Mumia’s case. She will be challenging Tigre Hill, the producer of “Barrel of a Gun.”

The Concerned Family and Friends of Mumia Abu-Jamal (ICFFMAJ) have purchased blocks of tickets for this event, at $13 each, to make sure friends of Mumia are in the audience, and not just the FOP. To purchase a ticket, call (215) 476-8812. In New York City, call (212) 330-8029.

SAN FRANCISCO, 7 PM, SATURDAY DECEMBER 4:

Showing of the important new film, “JUSTICE ON TRIAL, The Case of Mumia Abu-Jamal”

Come to the Twin Space, 2111 Mission St, San Francisco. Sponsor: Minister of Information JR. Info: (415) 504-5289

WORLDWIDE:

FRANCE — ON NOVEMBER 9, 2010:
PROTESTS SCHEDULED IN FRANCE AT US CONSULATES:
Paris, 6 P.M., Place de la Concorde
Bordeaux,
Lyon
Marseille
Nice
Rennes
Strasbourg
Toulouse

HAMBURG — 5:30 PM, Tuesday Nov 9: RALLY! Come to: Hamburg-america-center Entwicklungsgesellschaft mbH & Co. KG, Am Sandtorkai 48, 20457 Hamburg. The rally is endorsed by the International Bolshevik Tendency and the Antikrisen-Bündnis Hamburg.

LONDON — 5 to 7 P.M., Tuesday Nov 9: DEMONSTRATE: US Embassy, 24 Grosvenor Sq, London W1. FOR FREEDOM FOR MUMIA! Mumia’s case returns to court on November 9, 2010. At stake is whether he will be murdered by the state or granted a new jury trial [on the sentencing issue]. Mumia is innocent! He is a political prisoner! Mumia should be released unconditionally immediately! FREE MUMIA FREE MUMIA FREE MUMIA

FREE ALL POLITICAL PRISONERS NOW. BRING FLASHLIGHTS
Contact:ThePanAfrikanVoice@gmail.com 07597078221/07949738851

TORONTO — 6 PM, Tuesday Nov 9. Come to the U.S. Consulate, 360 University Avenue (between Dundas and Queen) to demand:

Free Mumia! Abolish the Racist Death Penalty!

At a meeting on Wednesday, October 27, representatives of a number of organizations met and formed a committee to organize a united front demonstration for Mumia Abu-Jamal on 9 November. The following organizations have endorsed the demonstration to date: Angola 3 Support Committee, Black Action Defense Committee, Fightback, Ginger Project, International Bolshevik Tendency, OPIRG (UofT), Socialist Action, Socialist Alternative, Toronto Young New Democrats. Other endorsements are expected, and all defenders of Mumia are welcome.

Why is this happening?

Targeted by the FBI’s infamous COINTELPRO counter-intelligence and disruption program since the age of 15, and now by the Fraternal Order of Police (FOP), Mumia Abu-Jamal is seen as an enemy of the state. His innocence is considered irrelevant, and in US courts, following recent rulings, innocence is no defense.

The US Supreme Court has already thrown out, without comment, Mumia’s last appeal against his frame-up conviction before a racist judge in a blatantly unfair trial in 1982. This rejection meant the Supreme Court had to ignore mountains of evidence of Mumia’s innocence, as well as precedents such as its own ruling in Batson v Kentucky, which was supposed to prevent racism in jury selection.

Now, on November 9 2010, the Third Circuit is to decide between removing the stay on Mumia’s death sentence, or ordering a new hearing to decide between a new death sentence, or life in prison without the possibility of parole. These are the only two possible outcomes in the courts at this time. The US Supreme Court has pre-arranged the Nov 9th hearing to make an immediate reinstatement of Mumia’s death sentence the likely outcome.

We can have no confidence in the corrupt, racist US legal system to resolve this, because the cops, courts and key politicians are all involved up to their ears in Mumia’s frame-up! This includes the current governor of Pennsylvania, Ed Rendell, as well as the Obama administration and its attorney general, Eric Holder.

We need mass actions, and labor actions, to say: Mumia Is Innocent! Free Mumia Now! End the Racist Death Penalty!

This message compiled from various reports by: The Labor Action Committee To Free Mumia Abu-Jamal, PO Box 16222 • www.laboractionmumia.org

2010-11-06T17:53:00.000-07:00

The Battle of Hastings

by Marriott Edgar (1880 — 1951)

I’ll tell of the Battle of Hastings,
As happened in days long gone by,
When Duke William became King of England,
And ‘Arold got shot in the eye.

It were this way — one day in October
The Duke, who were always a toff
Having no battles on at the moment,
Had given his lads a day off.

They’d all taken boats to go fishing,
When some chap in t’ Conqueror’s ear
Said "Let’s go and put breeze up the Saxons;"
Said Bill — "By gum, that’s an idea."

Then turning around to his soldiers,
He lifted his big Norman voice,
Shouting — "Hands up who’s coming to England."
That was swank ‘cos they hadn’t no choice.

They started away about tea-time
The sea was so calm and so still,
And at quarter to ten the next morning
They arrived at a place called Bexhill.

King ‘Arold came up as they landed -
His face full of venom and ‘ate
He said ‘lf you’ve come for Regatta
You’ve got here just six weeks too late.’

At this William rose, cool but ‘aughty,
And said ‘Give us none of your cheek;
You’d best have your throne re-upholstered,
I’ll be wanting to use it next week.’

When ‘Arold heard this ‘ere defiance,
With rage he turned purple and blue,
And shouted some rude words in Saxon,
To which William answered — "And you."

‘Twere a beautiful day for a battle;
The Normans set off with a will,
And when both sides was duly assembled,
They tossed for the top of the hill.

King ‘Arold he won the advantage,
On the hilltop, he took up his stand,
With his knaves and his cads all around him,
On his ‘orse with his ‘awk in his ‘and.

The Normans had nowt in their favour,
Their chance of a victory seemed small,
For the slope of the field were against them,
And the wind in their faces an’ all.

The kick-off were sharp at two-thirty,
And soon as the whistle 'ad went
Both sides started banging each other
‘Til the swineherds could hear them in Kent.

The Saxons had best line of forwards,
Well armed both with buckler and sword
But the Normans had best combination,
And when half time came neither had scored.

So the Duke called his cohorts together
And said — ‘Let’s pretend that we’re beat,
Once we get Saxons down on the level
We’ll cut off their means of retreat.’

So they ran — and the Saxons ran after,
Just exactly as William had planned,
Leaving ‘Arold alone on the hill-top
On his ‘orse with his ‘awk in his ‘and.

When the Conqueror saw what had happened,
A bow and an arrow he drew;
He went right up to ‘Arold and shot him.
He were off-side, but what could they do?

The Normans turned round in a fury,
And gave back both parry and thrust,
Till the fight were all over bar shouting,
And you couldn’t see Saxons for dust.

And after the battle were over
They found ‘Arold so stately and grand,
Sitting there with an eye-full of arrow
On his ‘orse with his ‘awk in his ‘and.

2010-11-05T18:42:00.000-07:00

The brothers Wilson (Craig Wilson and Warren Obligacion Wilson) are broadcasting live on http://75.84.63.217:8000/listen.m3u, supporting local artists, music, film and art. If you want to know more about them, listen to their live podcasts.

2010-07-28T16:18:00.000-07:00

Who needs a new library in downtown San Diego?

Today, the city of San Diego has broken ground on a $185-million public library: what an astonishing waste of money!

If you’re one of those whose immediate response is, “I use the library all the time, as do many others,” let me explain my apparent blasphemy. Although I’m appalled by the prospect of a new central library in downtown San Diego, I’m not against libraries as such. I’ve been a card carrying member of several libraries since I was about 5.

But that was back in the UK and, in the consensus politics of the early 1960s, British libraries functioned as an idealist bureaucracy for the provision of books, all books, any books. Did we need public libraries? We needed them absolutely. Free access to books was high up in the post-war British working people’s unwritten bill of rights.

You could step up to the counter and ask for “The Ship Aground” by C. Fox Smith and, if they didn’t have it, they’d have it rushed in from the nearest branch that did have it. And, if no branch had it, they’d buy a new copy just so you could borrow it.

Of course all this changed in the cold reality of the 1980s, when local governments, the whole world over, had to cut spending. The librarians were at the mercy of the accountants. And what do they know of keeping books, whom only bookkeeping know?

It seemed to make good business sense to break up all the valuable collections and sell them off for cash. After all, a book that isn’t requested from one year’s end to the next clearly doesn’t justify its shelf space. And, with the proceeds, every branch could purchase the complete works of Tom Clancy in hardback.

And that’s the problem with the business model. By offering the books most requested by most customers, the library actually stops being a worthwhile library. And by worthwhile library, I mean an organization that will provide any book you need, no matter where your research may take you.

And why should the elitist demands of obscure academics be furnished from the public purse? Don’t the universities have academic libraries? Well, some do. And that’s very helpful for those who qualify for a reader’s card or can afford the subscription. For the rest of us, there’s the public library, now ghettoized into artificial categories such as “Lesbian & Gay Literature,” “African American Studies” because some bureaucrat once thought this would make James Baldwin more accessible to minorities.

I don’t read as many books now as I did in my youth. I remember a summer vacation when I read fully 12 books in a week, requiring my mother to drive me back to the library twice, because my ticket only allowed me to borrow four at a time.

I used to stroll around the library and browse, coming out with fascinating works that happened to call out to me from the shelf, or the stack. I don’t have that sort of time on my hands now. And there’s no long line at the returns counter nowadays, so I don’t think I’m unusual in that respect. Are we staying away from the existing libraries because we need a bigger one?

There are still times when I need a specific book immediately. So what do I do? I access the catalogs of the county library and the city library by means of the Internet, I reserve the book online, and then drive over to La Mesa, La Jolla or wherever to pick it up. But I have to telephone in advance in case the branch is closed. The financial straits of the new millennium have forced closures and sabbaticals to save on wages. San Diego can’t even afford to run the libraries we already have.

Very occasionally, I have had to venture downtown through the very beautiful art deco portals of San Diego’s central library to pick up my book. But I used to spend a lot of time there, about ten years ago when I first moved to San Diego. I was particularly fond of the “Humor” section, where I found the forgotten works of S. J. Perelman, James Thurber, Stephen Leacock and Art Buchwald, apparently unopened and undusted since the 1950s.

If I don’t need a specific book immediately, I go online and check Amazon.com for used copies. Somebody will be offering a fair copy of what I need for around five bucks and it will arrive within about three days: much better value than a Netflix account.

The world has changed. Public libraries have changed. Now they’re designed to facilitate easy Internet use rather than printed matter. The knee-jerk assumption that the low-paid masses deserve subsidized access to literature should be re-examined. Even the unemployed have some kind of access to computers in Southern California and we can expect the cost to come down more rapidly than the new downtown library goes up.

They say it will be fully built by 2013, by which time every child in San Diego will probably possess his or her own Kindle. Is the $185-million price tag justified? Hell, no. They even had to throw in a charter high school. Who asked for another school when budget constraints mean we can’t afford to pay teachers in the schools we already have?

Having said all that, Los Angeles has a really great downtown public library. I had occasion to kill a few hours there a while back and I was impressed by the comprehensive collection of books. And, when I needed a wi-fi connection for my computer, there were about 25 to choose from. But I couldn’t help noticing it was named the Richard Riordan Central Library. After which great civic benefactor will San Diego’s magnificent monument to literacy be named?

Is that it? San Diego has been developing its plans for a new downtown library for 30 years, during which time, every mayor since Pete Wilson has, in vain, imagined his name over the transom. And, despite the potholed streets, the undermanned police department and the dilapidated sewers, we’re going to spend the $185 million for whatever amenities our politicians need to stuff under the “iconic” dome.

THE SHIP AGROUND

2010-05-28T10:46:00.001-07:00

Shorts 'N Spirits Showcase (S3LA)

In the spirit of Celebrate the Web, Mental Eclectic CEO Craig Wilson is proud to present June’s Shorts ‘N Spirits Showcase Los Angeles (S3LA), a night of independent webseries Tues. June 8, 2010 from 7 p.m. to 10 p.m. @ Capitol City, 1615 North Cahuenga Blvd., Hollywood, CA 90028. Tickets $5 from EventBrite or $10 at the door.

More than LonelyGirl 15 and The Guild, the world of independently produced webseries is a tight-knit community thriving from the community they’ve created, Celebrate the Web showed this with great precision. SAG, WGA and the Producers’ Guild have acknowledged the wealth of opportunity and talent being cultivated in the webseries world in the last year by writing up contracts and categories specifically for the media that has been created.

YouTube, once the only and most visible option, has been joined by other distribution outlets like BlipTV, StrikeTV, and now with the launch of Somebody’s Basement breaking new ground in the new media world actors have more power as self-producers, giving them more freedom, ownership rights, and visibility than ever before.

“What if everyone came together in Somebody’s Basement to see what’s going down? Yep. Just like groups of musicians gather ‘round and jam, we’re gonna do that. And we’re inviting you, awesome self-producing actors, to be a part of Somebody’s Basement.” Bonnie Gillespie & Kieth Johnson come together with some rockstar producing partners to offer self-producing actors a venue for their offerings. “We created a place where original characters; actor journals; interviews with industry professionals; and reviews of products, services, and classes for actors—heck, even restaurant reviews, for cryin’ out loud—all co-exist.”

S3LA is proud to have Somebody’s Basement as a sponsor providing a SB Premier Pick for our June webseries event.

S3LA with its San Diego counterpart, S3SD, provides a home for indie filmmakers to showcase their work and also the opportunity to be voted “audience favorite” for limited distribution in Los Angeles, San Diego, Seattle, and Kansas City.

June’s webseries line up features:

The Ballad of Mary and Ernie
Bumps in the Night
Gold the Series
Newsworthy
Perry’s Previews
Squatters
Universal Dead
Somebody’s Basement Premier Pick: TBA