Résumé
@#Abstract: Chronic infection of hepatitis B virus (HBV) is the major cause of hepatocellular carcinoma (HCC) in China. The occurrence of HCC through chronic inflammation follows the Darwinian evolutionary law, known as "mutation-selection-adaptation". Inflammatory mutagenic molecules promote the generation of somatic mutations, and the most mutant cells are eliminated by inflammatory microenvironment. However, a minority of mutant cells survive the selective pressure and develop to tumor initial cells by activating oncogenic signaling pathway and acquiring "stemness" characteristics. Alongside this process, HBV also evolves under the pressure of inflammatory microenvironment, which is characterized by the accumulation of cancer-promoting viral mutations, reducing the ability to infect new individuals. The high-risk mutant strains are eliminated with the death of hosts, leading to a phenomenon termed as "dead-end evolution". HBV evolution contributes to cancer evolution by maintaining the inflammatory microenvironment, activating oncogenic pathways, inducing somatic cell mutations, and altering metabolic patterns. The combo mutations of HBV and HBV integrations can be applied to predict the occurrence and prognosis of HCC. Anti-viral treatment reduces the risk of HCC by relieving inflammation. This article reviews the molecular epidemiological evidence and mechanistic advances related to the co-evolution of HBV and HCC. Clarifying the co-evolutionary pattern of virus and cancer and the key molecular events involved, is beneficial for identifying new biomarkers and therapeutic targets, thus improving the prevention and treatment strategies for HCC.