Most hepatitis C virus (HCV) infection results in persistent infection. Significant portion of chronic HCV-infected patients develop hepatocellular carcinoma (HCC). Chronic hepatitis C is also associated with extrahepatic manifestations, including cryoglobulinemia, lymphoma, insulin resistance, type 2 diabetes, and neurological disorders. The molecular mechanisms of how HCV infection causes liver cancer are largely unknown. HCV replication or viral proteins may perturb cellular hemostasis and induce the generation of reactive oxygen species (ROS); viral components or viral replication products act as agonist to trigger innate immune response and cause chronic inflammation. Within the liver, non-hepatocytes such as hepatic stellate cell (HSC) are activated upon HCV infection to provide the major source of extracellular proteins and play important roles in fibrogenesis. With the great achievements of HCV treatment, especially the direct-acting antivirals (DAAs) against HCV, HCV eradication is possible. However, until now there are only very limited data on the effect of DAA-based anti-HCV treatment on HCC patients.
Keywords: Chronic infection; Direct-acting antivirals; Fibrogenesis; Hepatic stellate cells; Hepatitis C virus; Hepatocellular carcinoma; Inflammation; Reactive oxygen species; Steatosis; Transforming growth factor.