This sounds like a sort of plausible mechanism, but do you have any actual evidence that this occurs in real life? I admit that I’ve wondered whether the PrEP studies with lenacapavir actually measure what they thing they measure given that the same lenacapavir may prevent HIV from replicating enough to be detectable.
That being said, Wikipedia doesn’t really agree with your mechanism. See:
I think, though, that the underlying assumption is that the old virus hangs out, forever waiting for the moment to strike.
Cells senesce and die and get replaced, and the immune system is always active in the background. If the virus particles are released, the immune system is going after it and cleaning up. As essentially no new virus is being created, this is the body's opportunity to clear the virus at a slower, manageable pace where it doesn't have to contend with a rapid, expanding infection.
It feels like one of those ideas that's technically true in all the right ways, but misses one crucial piece that would make the whole thing accurate.
> Cells senesce and die and get replaced, and the immune system is always active in the background. If the virus particles are released, the immune system is going after it and cleaning up. As essentially no new virus is being created, this is the body's opportunity to clear the virus at a slower, manageable pace where it doesn't have to contend with a rapid, expanding infection.
If this really applied to HIV, then people with HIV who take effective antivirals for long enough would be cured. But they generally aren't.
This is great information and obviously new to me. I had thought it only interfered with cap formation but it appears to also interfere with capsid penetration of the nucleus and therefore integration of the virus with the host cell genome.
That being said, Wikipedia doesn’t really agree with your mechanism. See:
https://en.m.wikipedia.org/wiki/HIV_capsid_inhibition
It seems that the drug may inhibit disassembly of the capsid.