Re: Effect of ribavirin on the “front end” of HCV treatment
I think there’s some confusion in this thread because people are talking about two different things: i) the anti-replication effect of ribavirin per se; and ii) the incremental value of ribavirin in achieving RVR when it is combined with interferon.
I posted in #msg-36533555 that ribavirin as monotherapy has been found to produce a mean reduction in viral load of ~0.8 logs, which is not much. (This figure is based on comments from the CC’s of various HCV companies during the past few years.)
However, ribavirin’s low efficacy as a monotherapy does not imply that it has little incremental value in achieving RVR in combination with interferon; to the contrary, no less an authority than Josh Boger thinks that this is ribavirin’s main contribution in HCV therapy!
How can the two paragraphs above be reconciled — i.e. how can a drug with such weak anti-replication efficacy produce a substantial increase in RVR when added to interferon? This is the question to which no one knows the answer (yet).
“The efficient-market hypothesis may be the foremost piece of B.S. ever promulgated in any area of human knowledge!”