Hi, I'll look up more stuff later on real websites. Right now, I'm just going off of this article AND I've been drinking with kerble, but sorry, this doesn't at first glance look like it's going to suffice.
What studies to date show is a compound that attacks HIV at its molecular membrane level, disrupting the virus from interacting with their primary targets, the "T-helper" class white blood cells that comprise and direct the human immune system. Further, CSAs appear to be deadly to all known strains of HIV.
The problem with HIV is not
just in disrupting it from interacting with its primary targets, the problems are high rates of mutation and that HIV, in an unknown time frame (maybe right away, maybe 72+ hours later - it could happen either way), hits and is internalized
within memory T-cells which lay dormant in the lymph system for...well, for damn near forever. (Once the virus is inside the cell, its viral membrane is gone.) This is why an HIV+ person can have undetectable viral loads (from drug therapy) and yet still, if going off drugs, have another wave of HIV bust out like a mamajamma. Of course, your mama doesn't even bother to put on the PJs. It would just disrupt the constant flow of sailors.
HIV, like other retroviruses, has only a few genes. The gene for the membrane is env, for "envelope". Now, env makes membrane lipids (hydrophobic, standard membrane lipid structure) and two proteins: gp120 and gp41. HIV makes some other proteins, too, but we're just talking about the membrane here.
The deal is that 1) HIV can enter a memory T-cell in an unknown time frame and lay dormant for decades and 2) once HIV starts replicating, that damn reverse transcriptase starts fucking everything up by making 3 to 6 errors for EVERY RNA to DNA transcription (this can alter, and
often does, the HIV membrane structure).
The other HIV genes (gag and pol especially) don't stand as much mutation as env.
HIV can also have cell-to-cell direct spread (never entering the intercellular space). So, that's another way the membrane attack isn't going to work out.
We do multi-drug therapy for HIV precisely because of the high rate of mutations. A virus will mutate and slip past Drug A, so we add Drug B to catch it on the other end.
If they could catch every HIV virus before it entered T-cells (especially the dormant helper T-cells), they could eradicate it. This is the idea behind HIV drug prophylaxis for those exposed to HIV, but it isn't 100% successful and it has to be administered right away.
Most people don't have unprotected sex and then immediately run for a harsh course of drugs that will give them diarrhea for a month.
*hiccup*