Establishment of chronic hepatitis C virus infection: Translational evasion of oxidative defence

Core Tip

Core tip: Oxidative stress inhibits canonical translation, however, emerging evidence suggests that oxidative stress can actually stimulate alternative translation from select internal ribosome entry site (IRES) elements including that involved in redox regulation and in persistent virus infection e.g., human immunodeficiency virus and hepatitis C virus (HCV). We postulate a novel role of oxidative stress-activated IRES-mediated translation in redox homeostasis and virus persistence. In the case of HCV, we explore the idea that HCV exploits oxidative stress to activate its own translation as a novel means of evading the host oxidative defence to establish chronicity.