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I decided to drop my Emtriva and Viread and try out Reyataz monotherapy for a month, as used in the pilot study recently published. This should have brought the half-life of my drugs down to 17 hours. I suggested to my physician that if I had developed a viral load through this we could obtain a Phenosense drug resistance test, and if not after a two day drug holiday.
I suspect that he would have recommended against his if he were dealing with a different patient, but ultimately my physician is as interested in obtaining a Phenosense for me as I am. For better or worse, after a month of Reyataz monotherapy, my viral load remained undetectable, so I dropped the Reyataz for two days (actually 51 hours) prior to the Phenosense. A 17 hour half-life should reduce drug level by 87.5% after 51 hours. We don't actually have the Phenosense results back yet, but the ultra-sensitive viral load test is - and once again it was undetectable, so it doesn't look promising.
This is annoying as I was able to rise from an undetectable viral load to 43,200 after six days off Crixivan combined with Sustiva in February 1999. Obviously a two day drug holiday was not long enough to produce virus. At a minimum this suggests that Reyataz monotherapy for me is quite robust.
In retrospect, I wish we had ordered a Reyataz blood level to see how the level compared with the 80 ng/ml considered to be the minimum therapeutic dose. I didn't think to document the Reyataz level at the time because I was confident of drug failure, but things don't always turn out the way you expect.
We did a blood chemistry to monitor the effect of an increased dose of Tricor on my lipids, so by accident we know my bilirubin levels fell exactly by half. In a steady-state therapy Bilirubin is a good surrogate marker of Reyataz level, but there is no good published evidence how bilirubin declines relative to Reyataz level during a drug holiday. I suspect Bilirubin follows Reyataz blood level down, but with some delay required for metabolism of the bilirubin. I have no idea how long that might be.
The old rule of thumb for the was that HIV can infect a cell and produce new virus within 18 to 23 hours.
Some studies have shown a slower turn-around, such as this example:
HIV entry into CD4 cells completed -- 2 to 6 hours;
Reverse transcription of the viral genetic material is finished by 10 to 14 hours;
Expression of early HIV genes occurs mostly between 14 to 48 hours.
But in practice, where you have many cells which are already currently infected with HIV, but supressed, you should be able to express a significant amount of virus in far less time than is required for a complete viral life-cycle.
In any event its good news, although not what I had hoped to accomplish.
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> I stopped my drugs for two days, to get a viral load over 500, for a
> viral drug sensitivity test (Phenosense).
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> Unfortunately after two days without antivirals my viral load remained
> undetectable (under 50)."
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> Did your physician suggest this? Interesting.
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> I don't know what the data are, but it would be very surprising to me
> if a viral rebound were detectable so soon after stopping
> medications. It takes a while for medications to reach
> subtherapeutic concentrations, and even if they do begin to replicate
> like mad, it takes a long time to explode back to levels that are
> detectable in the blood.
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> John Barrow
> pozbod@...
>
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