"When a treatment regimen includes only one direct-antiviral agent, as in VRTX’s PROVE-3 study, the role of interferon and ribavirin in mopping up mutations to the single antiviral is obvious and unquestioned"
actually preclinical data show that you only need interferon to prevent resistance to protease inhibitor, hence the rationale for proceeding into trials without ribavirin (incidentally adding a polymerase also inhibited resistant mutants to proteases preclinically - do you really thing that will turn out better in the clinic if one dares to try the combo - with or without a third direct antiviral - without SOC down the road)
incidentally has vrtx published on resistance to telaprevir in relapsed pts? it wouldn't surprise me if many did NOT have telaprevir resistant mutants - meaning the relapses were related to lack of immune control
my money is that ribavirin and interferon aren't going anywhere anytime soon - every trial without the former has failed, no one has tried a trial without interferon yet (don't tell me inform-1 is one such trial since all arms have interferon/ribavirin "consolidation" after protease/polymerase). perhaps one will reduce the duration of interferon-ribavirin, but i doubt one willl ever get as good a result with jsut using direct antivirals as one could have gotten with a few weeks of SOC following any course of direct antiviral therapy. to use the HIV analogy is a stretch since you are talking about years of therapy to prevent resistance versus months with HCV with goal of a cure in the latter. if one was looking to suppress HIV for months 2 agents would suffice
i'm not saying there is no chance for interferon-less cocktails down the road, but i think ribavirin will probably have to be in the mix somewhere, and we have no idea yet if ribavirin has efficacy in the absence of interferon. I see the biggest threat to interferon/ribavirin being oral immunomodulating agents
jmo
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