Stop the presses: New HIV prevention medication

Though this is not in my normal vein of blogging, I thought it was super important to update you all on the results of a small-ish study testing the efficacy of a female-controlled HIV prevention medication that was published in late July.

Human Immunodeficiency Virus (HIV) is a heartless virus infecting ~33.4 million people worldwide (WHO statistics). It infects and impairs immune function, commonly leading to death via infection by secondary infections like pneumonia and tuberculosis. While education, treatments, and therapies are allowing those carrying the HIV virus live longer, healthier lives, HIV is still a terrifying virus due to its ability to rapidly mutate and develop resistance to pharmaceuticals.

HIV is commonly transmitted via exchange of body fluids via sexual encounters and contaminated needles, which lends it a negative image. However, HIV is also transmitted via untested, contaminated blood and plasma samples, and can be transmitted from mother-to-child. Once thought to be a disease of homosexual males and drug users, the new face of HIV/AIDS is increasingly female.

Education and free screening has played a large part in lowering transmission of HIV from person to person in many nations, however many social and economic barriers remain in undeveloped nations. Specifically, Africa retains dangerously high transmission rates and many of the previous abstinence and barrier (i.e. condom) based education programs are showing limited results in African nations. This is why it was so exciting when a South African study revealed the efficacy of a female-controlled HIV prophylactic (i.e. prevention method) in a study called CAPRISA 004 (published here).

CAPRISA 004 used ~900 women (450 in a control group, 450 in an experimental group) to test the efficacy of an anti-retroviral drug used as a vaginal gel before and after sex. Think of it like a spermicidal gel, but for HIV. To understand how this gel works, it's important to understand how HIV works, so here's a brief overview:

(source)

HIV is a virus, and it doesn't have all the machinery it needs to take over your body and make more of itself, which is it's main job. It needs a HOST - you. Once inside your cell, it replicates itself, but to avoid detection, it does its replication a little bit differently than you and I.

For you and I, DNA is the code for life, and from DNA, we make RNA. For HIV, RNA is the code for life, and from the RNA, it makes DNA. Yes, it's opposite.

To do this, HIV has a protein called reverse transcriptase. This enzyme makes DNA from RNA. The DNA can then integrate into our DNA and hijack our bodies for propagation and transmission of the disease. It's really cool and really scary at the same time. 

The drugs that combat HIV best are reverse transcriptase inhibitors, also called anti-retrovirals. But HIV has the ability to quickly adapt to treatments, so often a 'cocktail' of drugs has to be administered to be effective. Even then, it's usually just contained and dormant

These drug cocktails are not only expensive, but they are hard on your body. You see, we have a form of a reverse transcriptase as well. It's called telomerase. Telomerase puts little caps on our chromosomes (our stored DNA) to prevent them from unravelling and degrading or getting mutated. Telomerase is SUPER important and has been linked to aging and certain cancers. So, if you already have HIV, taking the drugs makes sense. However, you don't want to prevent getting HIV with a drug that will slowly kill you, so they aren't a great choice for prevention...unless they are site-specific (like at the vaginal entry) and wear off quickly.

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So, the CAPRISA 004 study used a reverse transcriptase inhibitor called tenofovir (pictured below as the administered salt), which is already used in HIV treatment cocktails, as a prophylactic vaginal gel.

 The study was designed like this:

Both urban and rural women in a high-risk area of South Africa were screened. Only those who were HIV-negative and available for the duration of the study (up to 30 months) were allowed to participate. Women also had to pass tests that showed they understood the design of the study and that this gel was not proven to prevent HIV. Almost 900 women were selected, and they were equally seperated into a control group and an experimental group. The women were not informed which group they were participating in (termed a 'blind' study), and the health care professionals who monitored the women's health were also in the dark about which group the women were in (termed 'double blind' study).

The women were given applicators full of gel (either control or containing the drug) and instructed to insert the gel up to 12 hours before sex and as soon as possible within 24 hours after sex. The women were then asked to bring all applicators back, whether used or new, each month when the received their testing. For every two used applicators that were returned, a sexual act was assumed. The women were also asked how many sexual acts they participated in during the month, and this was also accounted for. The women received two rapid-result HIV tests monthly (commercially available test kits). If these were positive or disagreed, the women were then tested via genotyping (i.e. PCR). Once a positive result was acquired, the women were discontinued from the program and given free counseling and medical attention. The women also received quarterly pelvic exams.

At the end of the study, the results were analyzed statistically. In the experimental group, which had the drug-laced gel, HIV incidence was 39% lower than the placebo group. Of these women, 40% of the women reported using the gel less than 50% of the time. Of the remaining women (termed 'high adherers' because they adhered to the program better), the tenofovir gel lead to 54% lower incidence of HIV than the placebo.

The authors are quick to point out that a larger study is now happening, but these results are very important and indicative of a reliable prevention method that can be used both in Africa and abroad.

(source)

The remaining question is whether this will actually make a difference in Africa if the other abstinence and barrier-focused programs failed. I think it might. This is why:
 

(DISCLAIMER: The following statements are my opinions, not scientific facts. While I try to form these opinions as intelligently as possible, I may be wrong. I can deal with that. Read at your own risk.)

1) I don't think abstinence is a long-term option for HIV prevention. Why? We're mammals. We are hard-wired to procreate. Ask any woman whose baby bomb has gone off. Some people can control these urges better than others, but it's unrealistic to expect all people to abstain from sex at all times.

2) The previous barrier-based programs focused on condom usage. They required male cooperation in this endeavor. While I'm no feminist, experience and history has taught me that women are very interested in their health and well being, and will take measures to protect themselves more often than men. Think microfinance, think birth control pills, think mortality rates of men and women.

3) Even if you don't believe women will be more responsible with prevention methods than men, you have to admit that two methods are better than one. As many religious-based groups like to point out, condoms don't work 100% of the time in the transmission of viruses, so a condom + a gel might be more safe and effective. In this study, women were encouraged to use both when possible.

I hope this was informative! If you have questions, just leave them as a comment and I'll do my best to address them. Back later this week with a food post!