In most clinically apparent cases of hepatitis B virus (HBV) disease, it is recognized that hepatocellular necrosis is followed by virus elimination and complete recovery. In a small proportion of infected individuals unable to clear the virus from their hepatocytes viral replication continues. These patients exhibit a spectrum of chronic liver disease varying from chronic active hepatitis (CAH) with severe liver inflammation to asymptomatic chronic hepatitis B infection with normal or almost-normal hepatic morphology. The existence of the asymptomatic chronic carrier state is suggestive of HBV being an indirect cytopathic agent with liver cell necrosis possibly attributable to an attack by the hosts’ immune system on hepatocytes altered by the hepatocytes (Edgington and Chisari, 1975). This hypothesis is based on the close proximity of lymphoid cells to necrotic hepatocytes in acute and chronic hepatitis B and although widely favored, it hasn’t been validated yet. Available evidence, nevertheless, substantiates for a contribution by the host immune system to the varied outcomes of acute HBV infection. Despite wide recognition of the importance of host response in the determination of the pattern and outcome of acute hepatitis B and a relative failure in this response underlies the carrier state, the precise nature of the tissue damaging response and location of the defect remains obscure.
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