Below are links to a few papers on measurement and modeling of the decay characteristics of HIV with treatment. It is worth noting that there is a first-phase rapid decay and a much slower second-phase decay. Though the exact mechanism for the later is still unknown, it is likely related to the infection of long-lived cells. Second-phase decay in AIDS patients treated with HAART takes years.
Raltegravir alters decay kinetics of HIV
Decay dynamics of HIV-1
Dendritic cells and decay of HIV
Personally, I feel best about AZT right now of the three drugs available. It prevents replication at the most basic point in the virus’ life cycle. It is the broadest spectrum if you will. It has been around the longest. There is vast experience with it over many years of treatment. It may be that raltegravir requires reduction of viral load before adding. Or it may be that we are like the genetically susceptible infected mice for whom it isn’t the right drug (Raltegravir autoimmunity). We desperately need viral load measures and organized clinical trials. But until then, I’ll keep reporting…
I have heard from people considering AZT alone, sometimes at below HIV doses. I would still prefer more than one drug. We can’t know anything about how readily this virus will become resistant to drugs. We don’t know anything about XMRV’s RT error rate. We don’t know anything about viral load in target tissues.
I stayed off both drugs, on AZT alone, for 5 days. I continued to get sicker until I was well below baseline. Last night it seemed clear to me that I had been better off on the AZT/raltegravir protocol, so I decided to go back on raltegravir. Amazingly, I feel much better today. The horribleness seems to be fading into the background again. I am reporting now because I don’t know how it is going to turn out. But it is an almost A-B-A experiment. However the experiment turns out, what has happened already greatly surprises me.
It would have been a fairy tale if the drugs had just worked. So much for logic! I actually didn’t expect it to be that easy. The good news is that if the drugs can move the illness, it is supportive of the hypothesis that XMRV is causative in the pathogenesis of the disease. It seems to me, that if altering the viral load, or altering the build-up of viral particles in the cytoplasm can shift the clinical picture in either direction in days or weeks, viral replication must not be so slow. It is a pretty stunning observation if you think about it. Must be a really good (successful) pathogen to be replicating so freely in relative equilibrium with the host over so many years. Doesn’t kill for a very long time. Clinical observation is that trying to alter things often doesn’t work out so well with CFS patients. Hence the observation that the patients are “sensitive”. Actually I think we are very tough.