Biotech Values

[DewDiligence]

The viral relapses seen in genotypes 1 are interesting wrt virus biology. My take is that there is a pool of genotype 1 virus not reached by the drugs and not measured by current testing protocols; once the drug is removed that pool reinfects the liver cells and the disease rebounds.

It seems clear that this accounts for at least some of the observed relapses. From genisi’s post in #msg-72295557: “We know the RVR achieved with GS-7977 means the level of virus were below the limit of detection but it is possible that there were very low viral titers, below the limit of detection of current assays, which haven't necessarily mutated (nukes do have high barrier for mutation), but simply survived and rebounded.”

…can you address that pool by lengthening time of treatment or do you need a different drug?

This is the question the various HCV drugmakers are trying to answer in their current mid-stage trials, but it’s not an either-or situation, IMO.

…are the viriads in that unreached pool actively replicating or is it a quiescent reservoir that dies out as the virus' natural lifecycle ends?

Not sure I understand the question insofar as the answer seems clear for patients who relapse. For patients who don’t relapse, there could be an unreached pool of virions that eventually die a natural death, but what practical consequence does this have if a treatment regimen is able to produce an SVR?