While it is clear that HCV is generally sensitive to IFN and cannot overcome the antiviral state in the context of de novo infection, it highly efficiently blunts interferon signaling and thereby innate antiviral immune responses in actively replicating cells (Figure 2C) (Gale et al., 1997; Blindenbacher et al., 2003; Lin et al., 2006; Chandra et al., 2014). Here, IFNA1 is linked to infection.