Аннотация:Significance Understanding how viruses interact with their hosts, especially the mechanisms that restrict virus replication, will provide a molecular basis for vaccine development. However, the search for restriction factors is oftentimes difficult if the virus has already evolved to counteract the restriction. Here, we describe a systematic approach to identify such restriction and counterrestriction mechanisms. We constructed a library of mutant hepatitis C viruses, where each mutant has a 15-nt stretch randomly inserted on the genome. We aimed to identify mutations that lose the anti-IFN function, but maintain replication capacity. We have identified p7 as an immune evasion protein and further characterize the antiviral function of IFI6-16 against hepatitus C virus (HCV) replication.
