Published online Apr 7, 2015. doi: 10.3748/wjg.v21.i13.3786
Peer-review started: November 28, 2014
First decision: January 8, 2015
Revised: January 21, 2015
Accepted: February 12, 2015
Article in press: February 13, 2015
Published online: April 7, 2015
Processing time: 131 Days and 5 Hours
Hepatitis C virus (HCV) is a major human pathogen of chronic hepatitis and related liver diseases. Innate immunity is the first line of defense against invading foreign pathogens, and its activation is dependent on the recognition of these pathogens by several key sensors. The interferon (IFN) system plays an essential role in the restriction of HCV infection via the induction of hundreds of IFN-stimulated genes (ISGs) that inhibit viral replication and spread. However, numerous factors that trigger immune dysregulation, including viral factors and host genetic factors, can help HCV to escape host immune response, facilitating viral persistence. In this review, we aim to summarize recent advances in understanding the innate immune response to HCV infection and the mechanisms of ISGs to suppress viral survival, as well as the immune evasion strategies for chronic HCV infection.
Core tip: The complex interaction between hepatitis C virus (HCV) and its host determines which side the balance tends to be tipped between antiviral innate response and viral immune evasion. The development of new cell culture systems and small animal models for HCV research permits increased understanding of how the host responds to viral infection and what leads to HCV evasion of innate immunity. Recent discoveries in these areas reveal many pivotal factors imparting the control of viral-induced innate immunity, and facilitate the development of novel drugs and effective vaccines for HCV infection.