I think I'm going to put up something a little more scientific this time, so if you haven't read Abbie's posts on gag, pol, and env, you should do so, even thought it won't make any difference for this post, it's just good reading on retroviruses in general. You should also check out the BBC's article on DARC and HIV-1. Once you've done that, I'm going to get to the science of why DARC plays a role in HIV-1 infection and progression.
So far, we know:
HIV-1 can bind to DARC on red blood cells (RBCs)
RBCs can act as a reservoir for HIV-1 if they express DARC
What this means is that HIV-1, in individuals lacking DARC, is capable of binding far fewer targets than in individuals with DARC expressed on RBCs.
This means that HIV-1 binds to CD4+ T cells far easier when DARC is not present, allowing infection to begin far faster.
This also means that it is much easier to acquire HIV-1
Now, if DARC is present, HIV-1 will bind to RBCs instead of CD4+ T cells slowing infection rate and possibly preventing it in low level innoculations due to the limited viability of HIV-1. If the virus is successfully prevented for a period of time, I would suspect viability would decrease further from room temperature when at body temperature making extremely low titers of virus far less likely to lead to infection.
My next virus-related topic will be something like "why are retroviruses so damn hard to get rid of"
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