Abstract

AbstractHepatocellular carcinomas (HCC) are the most common primary liver tumours. They are the second leading cause of cancer-related mortality worldwide. The main etiological factors include viral hepatitis B and C, chronic alcohol intake and metabolic syndromes. We will focus this review on the impact of hepatitis B virus (HBV) infection and the progression of liver damage to HCC. Both direct and indirect mechanisms of HBV infection contribute to the emergence of HCC. We will address these two types of mechanisms by focusing on direct viral effects, explored in numerous in vivo and in vitro studies. Published results can sometimes be contradictory. They vary depending on the study model, the viral sequence, the level of HBV expression, the type of viral genome transferred (partial or complete), the transfer method, generating a stable or transient expression, and many other parameters. Nevertheless, the knowledge acquired recently on the viral cycle, and in particular on the nature of the hepatocyte receptor of HBV, allows today to reproduce in vitro a complete viral cycle in different experimental models and thus, to better appreciate the pro-tumor activities of HBV infection.This review is obviously not exhaustive and the knowledge, particularly on the clinical and therapeutic management of HCC, whether associated with the presence of HBV or not, is currently evolving with the rise of combined immunotherapies.

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