Virus–host interactions in hepatitis C virus infection: implications for molecular pathogenesis and antiviral strategies

With a global burden of 170 million chronically infected patients and a major cause of liver cirrhosis and hepatocellular carcinoma, hepatitis C virus (HCV) is a major public health challenge. Recent discoveries of viral and cellular factors mediating virus–host interactions have allowed scientists to uncover the key molecular mechanisms of viral infection and escape from innate and adaptive immune responses. These include the discovery of tight junction proteins as entry factors and microRNA-122, cyclophilins and lipoproteins as host factors for virus translation, replication and production. Furthermore, global genetic analyses have identified IL-28B as a genetic factor associated with the outcome of HCV infection. These discoveries markedly advance the understanding of the molecular pathogenesis of HCV infection and uncover novel targets for urgently needed antiviral strategies.