Acyclovir and Transmission of HIV-1 from Persons Infected with HIV-1 and HSV-2.
--Daily acyclovir therapy did not reduce the risk of transmission of HIV-1, despite a reduction in plasma HIV-1 RNA of 0.25 log10 copies per milliliter and a 73% reduction in the occurrence of genital ulcers due to HSV-2.
Well crap.
Im sure you all can figure out from that one sentence in that abstract why this is disappointing, but let me give you the back story.
Way back in the 1990s, scientists noticed that HIV-1 and HSV-2 were able to form this awful, unholy alliance. Proteins made by HSV-2 could increase transcription of HIV-1 (you make more HIV-1 viruses). Even if you arent showing any HSV symptoms (you have HSV but dont get outbreaks), if you are also infected with HIV-1, you have more HIV-1 viruses in your blood and genitals.
More viruses, better your odds for transmitting to someone else.
If you do have outbreaks, open sores... well, that pops up your risks for transmitting HIV-1 even higher.
Happily, a drug we use to treat herpes has been around for a million years, acyclovir. It works great, its super cheap, AND, in people who are infected with HIV-1 too? They have lower HIV-1 viral loads than dual infected people who arent on acyclovir!
Lower viral loads, fewer outbreaks, lower your chances of transmitting HIV-1 to your partner, right?
Eh. Wrong, at least according to this paper.
Even though patients taking acyclovir only (no antiretrovirals) had lower HIV-1 titers and fewer HSV-2 outbreaks, they still transmitted to their partners at the same rate as patients who got placebo instead of acyclovir.
So I repeat: Well crap.
This could have been a pretty easy/cheap way to stop a few new HIV-1 infections.
*sigh*
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While disappointing, the effects of acyclovere were pretty small, a drop in plasma HIV numbers by 0.25 log10. Effective HIV therapies usually drop viral loads down several log10's, not a fraction of 1.
Their retention rate was pretty awesome though; 92% over 2 years. Heck, back in the day I was involved in a small, off-label GM-CSF trial with HIV patients, and only half stuck around for 6mo.
Any idea why this didn't work? Is probability of transmission just not that strictly correlated to viral load? This result is confusing.
"Any idea why this didn't work? Is probability of transmission just not that strictly correlated to viral load? This result is confusing."
I'm sure this was directed at Addie, but here's my take.
Viral load does play a role in transmission; transmission goes down when viral loads are low. However, the actual drop in viral loads in this study were rather small in comparison to what you would see with HAART therapy. Since the change was quite small, no real differences in transmission were seen.
Is there any reason to have this study with placebos and not use HAART? That seems a little odd to me.
Joshua-- For an HIV-1 virus to be affected directly, it needed to be dual infected with HSV-1. Thats probably kinda rareish, and is probably why viral load didnt drop a ton.
Indirectly, stopping the HSV lesions, thus stopping an open sore to directly transmit virus... man I really thought that would help a lot.
But it didnt. *sigh*
But yes, viral load is associated with transmission-- more virus, better odds of transmission.
MS2-- Africa. Hard to get antiretrovirals there, much less HAART. Can get cheapo acyclovir... which is why we were hoping this would work, at least a little bit.
*sigh*