Category: Antiviral Innate Immunity
My thesis research focuses on understanding how RNA viruses, in particular hepatitis C virus (HCV), avoids detection by the antiviral innate immune system, a host defense program. Human cells normally activate this antiviral defense during RNA virus infection to limit viral replication. However, many viruses have evolved ways to circumvent detection by this innate immune program, allowing them to establish infection. One of the major antiviral sensor proteins of RNA virus infection is RIG-I. When RIG-I senses virus infection, it activates a signaling pathway through the adaptor protein MAVS to induce the production of type I interferon. Interestingly, HCV can avoid this sensing pathway through the actions of its NS3-NS4A protein. My research focuses on how the NS3-NS4A protein blocks antiviral innate immune signaling of the RIG-I pathway. I’m studying (1) the molecular features that regulate the localization of NS3-NS4A and (2) how the factors that are regulated by NS3-NS4A are important for antiviral innate immune signaling.