Drugging Our Way Out of the HIV Epidemic


When antiretroviral drug cocktails hit the scene in 1996, they were so effective they became known as ‘the Lazarus drug.’ Many AIDS patients recovered seemingly overnight. Over the past 15 years, these drugs have saved the lives of millions of people infected with HIV. Several new studies suggest antiretrovirals could save millions more if we start using them for prevention as well as treatment.

Last July, researchers reported that a vaginal gel laced with an antiretroviral called tenofovir reduced HIV acquisition among South African women by 39% overall and by 54% in women who used the gel faithfully. Then, in November, a separate team of researchers reported that an oral antiretroviral pill taken daily reduced the risk of HIV infection among men who have sex with men by 44%. This year, on May 11, researchers announced the results of another study. They found that HIV-infected individuals — both men and women — who took antiretroviral drugs were a whopping 96% less likely to pass the virus on to their partners than individuals who didn’t take the drugs. The results are preliminary, but Myron Cohen, the HIV researcher who led the study and spoke on Monday at the New York Academy of Sciences, said he is confident that the large effect will hold.

These fantastic results beg the question: Can we drug our way out of the HIV epidemic?

Researchers have long suspected that people who take antiretrovirals are less likely to pass HIV on to their sexual partners. The idea makes a lot of biological sense. Antiretroviral drugs stop HIV from replicating, which means fewer copies of the virus floating around in HIV patients’ blood and, presumably, their genital secretions. But the hypothesis had never been proven in a randomized clinical trial. So in 2005, Cohen began a study to test the hypothesis.

He and his colleagues recruited 1,763 discordant couples—meaning one person was infected with HIV and the other wasn’t—in Botswana, Brazil, India, Kenya, Malawi, South Africa, Thailand, the US, and Zimbabwe. They randomly assigned each couple to one of two groups. In the first group, HIV-infected individuals received antiretrovirals right away. In the second group, the researchers more or less followed the standard treatment guidelines, delaying treatment until the disease progressed.

On April 28, the independent committee charged with overseeing the trial met at the National Institutes of Health for their tenth meeting. At each meeting, the committee members would review the data and decide whether the trial should continue. After this most recent meeting, they told Cohen they had a recommendation, but they couldn’t yet tell him what it was. Cohen, who has never been allowed to see the results, assumed the worst—that the early treatment hadn’t worked. Then he received a phone call. The committee told him they had seen such a dramatic benefit that they wanted to release the results.

On May 11, Cohen held a press conference to announce the results. During the study, 28 individuals had become infected with their partner’s strain of virus. But only one of those infections occurred in the early treatment group. The other 27 infections occurred in couples not taking antiretrovirals.

Ever since the press conference, Cohen has been inundated with media requests. The success is well deserved. HIV prevention researchers have been working long and hard for decades with little to show for it (One notable exception: The 2007/2008 circumcision trials, which found that male circumcision can cut a man’s risk of contracting HIV by 50%).

On Monday, Cohen compared the trial to “pushing a boulder up a hill.” But I think the most daunting challenge lies ahead. How do you take all these positive results – not just from Cohen’s study, but from the others as well – and develop an effective public health strategy?

Cohen found that early treatment can prevent new infections. So putting everyone who has HIV on treatment immediately should dramatically curb the spread of HIV. But antiretrovirals are expensive. Advocate for earlier treatment, and you dramatically increase the number of people who need pills. According to the World Health Organization, roughly 33 million people are infected with HIV. Of those, five million are receiving treatment. Another 10 million aren’t taking antiretrovirals but should be. So to prevent new infections, we need provide treatment to between 10 million and 28 million people. Who will pay for their medicine? Many of the people infected with HIV barely earn enough to feed themselves, let alone purchase expensive drugs.

And what about all the individuals who are infected with HIV but don’t know it? People seem to be most infectious right after they become infected themselves. Studies suggest that anywhere between 8% and 40% of new infections are caused by people who are in this “acute” stage. But people with acute infections often test negative for the virus because they haven’t yet developed antibodies. So how do you find these people?

Here’s another issue. Millions of people infected with HIV depend on antiretrovirals for their survival. So if we want to use antiretrovirals for prevention, we need to find a way to do it without creating more drug resistance. How?

Although answering these questions may prove challenging, I’m not suggesting we should throw in the towel. Science is giving us the data, now it’s up to us to decide how to use it. Antiretrovirals aren’t the long-awaited magic bullet that will end the HIV epidemic — we can’t drug our way out of this — but they can save lives and prevent new infections. It’s a start.

Image credit: e-MagineArt.com

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5 thoughts on “Drugging Our Way Out of the HIV Epidemic

  1. The only thing this piece got right was the headline, “Drugging Our Way Out of the HIV Epidemic.” The writer completely ignores the highly toxic nature of the ARV’s. If you need graphic evidence, see the excellent New York Magazine piece linked at my 2009 “Special HIV-AIDS Report,” including the video of the wasted faces: http://www.terrymichael.net/Htm_InteriorPages/HIV_AIDS_Special_Report.html
    How many will have to die of liver and kidney dysfuction and heart disease from the “life saving treatments” before we reassess the single pathogen theory of what was a multi-factorial immune deficiency syndrome?

  2. Terry, you bring up a really good point. ARVs are not benign, and we still have much to learn about their cumulative effects. What happens when people take these pills for decades? So that’s just one more thing public health officials will have to take into account when they consider how (and whether) to use ARVs for prevention.

    But I think you’ll agree that, however imperfect they may be, ARVs have saved lives. And they have the potential to save even more lives both as a treatment and a form of prevention.

  3. cassandra —

    nice job of summerizing the latest clinical results on HIV prevention. i have two comments/questions:

    1) one of the potential drawbacks that you cite to drug prevention is that “often” early infections are not detected. yet just last week you made a big point of the very high rate of detection of early infection, with a window of 2-3 weeks. so much so that you objected to gay men being deferred from donating blood.

    2) i find drug resistance to be the most worrisome issue. right at the beginning of the epidemic, with the first effective antiretroviral — AZT, it was found that monotherapy has a very high risk of resistance. giving combo therapy for prevention multiplies the other problems that you describe. did dr. cohen give any numbers for the rats of resistance in the groups that he studied?

  4. Skeptico,
    Excellent points! Let me address your first question. When you go to the doctor and get tested for HIV, you typically get the ELISA test, which identifies antibodies to the virus. Since it takes a while for your body to produce antibodies — maybe 30 days to three months — the test can’t detect HIV right away.

    The blood supply is screened using a more sensitive test (a nucleic acid-based test or NAT) that looks for viral genes. So even if you’ve only been infected for a couple of weeks, the test will be positive.

    Why don’t we use the NAT tests to screen people? Maybe because they’re expensive and complicated to run. When blood banks use these tests, they pool blood from many donors so they can use fewer tests.

    Using NAT tests in hospitals, clinics, and testing sites, would likely catch more acute HIV cases. But there are a couple larger issues. 1.How do we convince people to get tested in the first place? And even if they do get tested regularly, say once a year, we’re not likely to catch them when they’re in the acute phase. And 2. physicians don’t typically start treatment for HIV right away. They wait until the disease has progressed. So even if we catch someone who is acutely infected, all we can do is say — “Listen, you have HIV. Don’t have sex. Or have safe sex.” And then it’s up to them to comply.

    Regarding your second question, Dr. Cohen didn’t give any numbers. He’ll announce the full results at the International Aids Society meeting in Rome in July.

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