Abstract

Hepatitis B virus (HBV) is a small enveloped DNA virus, which primarily infects hepatocytes and causes acute and persistent liver disease. Chronic HBV infection is a major risk factor for the development of hepatocarcinoma. The role of HBV in carcinogenesis appears to be complex and may involve both direct and indirect mechanisms. Chronic liver inflammation and hepatic regeneration induced by cellular immune responses may favor the accumulation of genetic alterations. Also important is the role of integration of HBV DNA into host cellular DNA, which could disrupt or promote the expression of cellular genes that are important in cell growth and differentiation. In addition, prolonged expression of HBx protein and PreS2 activators may contribute to deregulating the control of the cellular transcriptional program and proliferation, and sensitize cells to carcinogens. Recent genetic studies have provided insight into the mechanisms underlying viralassociated hepatocarcinogenesis showing that the rate of chromosomal alterations is significantly increased in HBV-related tumors compared with tumors associated with other risk factors. HBV might therefore play a role in enhancing genomic instability. Together, these data strongly support the notion that chronic HBV infection triggers oncogenic pathways, thus playing a role beyond stimulation of host immune responses and chronic necroinflammatory liver disease.

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