…preclinical data show that you only need interferon to prevent resistance to protease inhibitor…
I would respectfully submit that you’re misinterpreting the body of published research.
Protease inhibitors are not unique in this regard; rather, their differences from polymerase inhibitors in antiviral efficacy and in the speed at which they generate mutant strains are a matter of degree. Moreover, these two differences are two sides of the same coin; i.e. protease inhibitors stress the HCV virus to a greater degree than polymerase inhibitors, and this is why they generate mutant strains at a faster rate and are more susceptible to viral breakthrough than polymerase inhibitors.
Ideally, a cocktail of direct antiviral agents for HCV will include one or more agents that induce high viral stress and have a low barrier to resistance*and* one or more agents that induce low viral stress and have a high barrier to resistance. This approach has worked well in HIV, and the INFORM-1 study in HCV is starting down the same path. Regards, Dew
“The efficient-market hypothesis may be the foremost piece of B.S. ever promulgated in any area of human knowledge!”