Innate Immunity in Hepatitis C Virus Infection

Activation and viral control of the innate immune response are hallmarks of hepatitis C virus (HCV) infection and are major determinants of spontaneous clearance or progression to chronic infection and liver disease. In this review, we provide a contemporary overview of how HCV is sensed by the host cell to trigger innate immune activation and the mechanisms deployed by the virus to evade this response. Type I and III interferons (IFNs) are crucial mediators of antiviral innate immunity against HCV, and we specifically highlight the importance of IFN-lambda host genetics for the outcome of HCV infection. Last, we focus on the proinflammatory responses elicited by HCV infection and describe our current understanding of how interleukin (IL)-1 beta signaling and cross talk betweenthe IL-1 beta and IFN signaling pathways lead to sustained inflammation and increased risk of liver pathology.

Automated summary

This review discusses the activation of the innate immune response by HCV infection and how the virus evades this response. Type I and III interferons play a crucial role in antiviral innate immunity against HCV, with the host genetics of IFN-lambda being highlighted. Furthermore, the interactions between IL-1 beta signaling and IFN signaling pathways contribute to sustained inflammation and increased risk of liver pathology in HCV infection.