Abstract
Hepatitis B virus (HBV) is a noncytopathic virus that causes liver disease of variable duration and severity. It is widely assumed that during HBV infection the host immune response is responsible for both hepatocellular damage and viral clearance. Whereas there is considerable evidence that the innate immune response does not play a significant role in these processes, the adaptive immune response, particularly virus-specific cytotoxic T lymphocytes (CTLs), seems to contribute to nearly all of the liver injury associated with HBV infection. By killing infected cells and producing antiviral cytokines capable of purging HBV from viable hepatocytes, CTLs are also thought to eliminate the virus. Although liver damage is initiated and mediated by the CTLs, antigen-nonspecific inflammatory cells can worsen CTL-induced immunopathology and platelets may facilitate the accumulation of CTLs in the liver. The mechanisms responsible for disease pathogenesis and viral clearance during HBV infection are the subject of this review.
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