Fig. (4) Model for the effect of CypI and DAAs on the HCV-dependent activation of IFN-induced PKR. (Left) HCV replication in hepatoma cells leads to an accumulation of dsRNA intermediates. During this established infection, PKR is slightly expressed and activated. In response to IFN, infected cells overexpress the inactive form of PKR, which is subsequently activated/phosphorylated upon the recognition of and binding to viral dsRNA. (Right) The addition of anti-HCV agents either CypI or DAAs stops viral dsRNA accumulation resulting in the prevention of the activation of IFN-induced PKR.