Hepatitis C virus (HCV) infection is a major etiology of hepatocellular carcinoma (HCC) around the world. Carcinogenesis may result indirectly from longstanding hepatic inflammation and fibrosis. It also may arise directly from viral proteins and their interaction with the host intracellular machinery. Pegylated interferon plus ribavirin had been the standard antiviral regimen for a decade until recently when the paradigm shifted to the direct-acting antivirals. A large body of evidence has shown undisputedly that antiviral therapy can effectively reduce the occurrence of HCC in patients at any stage of liver fibrosis. Moreover, it is associated with an attenuated risk of recurrence following curative resection of the cancer. Sustained virological eradication is crucial for the effectiveness in clinical outcomes, whereas prolonged interferon maintenance without viral clearance should be regarded as obsolete. Surveillance remains essential after successful antiviral treatment because the risk of HCC is decreased but not eliminated, particularly in older patients or those with liver cirrhosis. In the upcoming interferon-free era, more efficacious and tolerable medications hopefully will further extinguish not only the virus but also the health burden associated with it.
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