Liver reprogramming toward hepatocellular carcinoma following hepatitis C sustained virologic response: a narrative review

and Objective: Despite direct-acting antiviral (DAA) therapies achieving sustained virologic response (SVR) rates exceeding 95%, hepatocellular carcinoma (HCC) risk persists in cured hepatitis C virus (HCV) patients, particularly those with advanced fibrosis or concurrent metabolic dysfunction-associated steatotic liver disease (MASLD). This clinical paradox implies that HCV induces durable oncogenic molecular alterations independent of active viral replication, fundamentally challenging the notion that virologic cure equates to biological liver cure. This review aims to delineate the molecular mechanisms underlying this residual risk and to identify rational targets for chemoprevention in the post-SVR era.