By Judith Lavelle
Some argue that the stigma behind preexposure prophylaxis is fading. But how does it work?
Let’s talk about a little pill that makes many people’s sex life a bit less nerve-racking. It’s most effective in its protection when taken everyday, but in certain doses, it can do the trick up to 72 hours after unprotected sex. Insurance companies are begrudgingly changing their policies to cover it is as a preventative therapy, and while some ethicists and cultural critics worry it will only encourage promiscuity, others hail it as incredibly empowering.
And, no, I’m not talking about birth control.
Preexposure prophylaxis–or PrEP, as it’s being called–is just hitting its stride and becoming more widely embraced as a method to prevent the spread of HIV. Some suggest that the drug may help couples bridge the “viral divide” (allowing HIV-positive and HIV-negative lovers maintain a sexual relationship with less anxiety about contracting the virus), the promise dissipates fear left and right, users are starting to get vocal, and and this month, The Advocate is spreading the word about the therapy through its “31 Days of PrEP” campaign. But how does PrEP add to the (ideally) already-utilized, low-tech methods of condoms, communication and routine status testing?
For the the most common formulation, under the trade name Truvada, the secret lies in two active ingredients, emtricitabine and tenofovir disoproxil fumarate.
Even though the buzz surrounding Truvada is still hot, emtricitabine and tenofovir disporoxil fumarate aren’t new players in the fight against AIDS. Both have been used in combination therapies–the “AIDS cocktail” for HIV-positive patients–since the mid-nineties. What’s new is the practice of regularly taking the medications before being exposed to HIV.
And despite their different structures, the two chemicals do essentially the same thing: throw a wrench in an important piece of the human immunodeficiency virus’s machinery–reverse transcriptase.
In an unhindered attack, HIV uses this enzyme to convert the genetic material it injects into a human cell, the viral RNA, into DNA. That DNA then highjacks the cell’s resources to do the virus’s bidding–turning cells into virus-production factories and allowing the disease to spread throughout the body.
But given the complex and so-far irreversible nature of AIDS, even emtricitabine and tenofovir disporoxil fumarate–which very effectively halt the conversion of viral RNA to DNA by thwarting the efforts of reverse transcriptase–can only slow the spread of the virus instead of rid it from a person who has already been infected. So Truvada and its counterparts are not a miracle cure for AIDS, the disease that ensues when HIV takes hold of a person’s entire system.
Even with that limitation, the drugs are particularly useful for getting in and doing their job as early as possible–which is why they’re showing such promising effectiveness (some say up to 90% of the time) stepping in when the virus is new to the body. But since this isn’t perfect, that comparison to hormonal birth control applies here too. Reducing the risk comes down to being safe in as many ways as possible–so barrier methods, regular testing and education are still powerful tools in protecting against HIV.