HBV is a small DNA virus of 3000 base pairs. Primary infection produces either acute hepatitis B or a subclinical infection. The majority of infections resolve with clearance of virus and lifelong immunity; 5% fail to clear the virus and go on to develop a lifelong persistent hepatic infection, resulting in a spectrum of hepatocellular injury and the development of chronic persistent hepatitis or chronic active hepatitis. Chronic HBV infection is associated with a 100-fold increase in hepatocellular carcinoma (HCC) risk.
Hepatocellular injury is thought to trigger a proliferative response in the liver. This response increases the chance for cellular mutations to occur over time and for cells to consequently escape normal cellular growth control. However, cases of HHC do arise in non-cirrhotic livers, so raising the possibility of another mechanism, such as the existence of a specific HBV oncogene. Unproven candidates include ORF X that encodes for a small regulatory protein that may bind to and inactivate p53. Alternative molecular mechanisms may involve viral genome integration. However, no one common integrated viral encoding site has been demonstrated.
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