I have to smile every time Yoda or anyone writes about DAAs dominating the HCV market and removing IFN from the equation. We have now seen 3 or 4 different DAA combinations fail in trials. Think about the biology behind the disease, including the number of viral particles, the nature of the virus's replication machinery, the amount of drug needed for a complete response, the potential of off-target events with small molecules and the need to drive an immune response in order to maintain a sustained response. Is it surprising that researchers are having a hard time finding a DAA combination that will provide a sustained response with an acceptable side effect profile?
IFN could still very well be removed from the equation down the road. I wouldn't assume that a few DAA failures means that DAA combos as a whole will fail. I believe the BMY PI/NS5A combo has shown good early results. Despite the initial failure, IDIX still has potential for its own HCV DAA combo down the road with 184 and the NS5A inhibitor. ACHN also is in the running here for its own HCV DAA combo, albeit a bit further behind BMY. As Dew has mentioned, it's probably going to take 3 HCV DAAs to do the trick (PI+NS5A+nuke most likely).