Recent Advances in the Pathogenesis of Hepatitis C Virus-Related Non-Alcoholic Fatty Liver Disease and Its Impact on Patients Cured of Hepatitis C

Abstract

Patients with chronic hepatitis C infection frequently develop non-alcoholic fatty liver disease (NAFLD), which confers a risk of hepatocellular carcinoma (HCC). Although direct-acting antivirals allow the majority of patients to achieve a sustained virologic response (SVR), post-SVR patients still carry a non-negligible risk of HCC. This review summarizes recent findings regarding the pathogenesis of hepatitis C virus (HCV)-related NAFLD and its impact on post-SVR patients. The recently discovered HCV-induced steatosis mechanisms include the upregulation of microRNA-27 expression and the formation of HCV-lipoviral particles, which suppress β-oxidation and triglyceride hydrolysis, respectively. Recent studies also revealed the incidence of NAFLD even among post-SVR patients, as well as an association of steatosis with hepatic inflammation and hepatocarcinogenesis. HCV induces changes in microRNA expression and lipoviral particles to directly promote the development of steatosis. In post-SVR patients, NAFLD is an important pathological condition related to hepatic inflammation and hepatocarcinogenesis.