Abstract: The occurrence and development of hepatocellular carcinoma （HCC） induced by chronic infection of hepatitis B virus （HBV） is a typical process of Cancer Evolution-development. Viral replication， viral mutation， and viral integration are three major mechanisms by which HBV promotes evolution of HCC. The replication of HBV induces and maintains chronic inflammatory microenvironment， that induces the generation of somatic mutation and viral mutation and provides selective pressure. HBV mutation helps cells to get stem-ness characteristics by activating key signaling pathways. HBV integration activates oncogenes， participates in the mechanism underlying the male predilection of HCC， and promotes the maintenance of chronic infection. Biomarkers related with HBV are effective predictive and prognostic markers of HCC. Anti-viral treatment significantly reduces the risk of HCC occurrence. High risk HBV mutations can be applied for predicting the effect of anti-viral treatment on improving HCC survival. Continuing to exploring mechanisms of HBV induced hepatocarcinogenesis can improve the specific prophylaxis of HCC by providing more effective biomarkers and therapeutic targets.