Recovery from hepatitis B virus (HBV) disease is dependent on the integrated activities of the patient’s interferon and immune systems. Chronic HBV infection arises because of defects in these defenses. It was demonstrated that interferon alpha production is reduced in chronic hepatitis B virus infection, reinforcing the views that this cytokine is important in the clearance of HBV. In contrast, the interferon alpha messenger RNA transcripts and the immunoreactive protein were abundant in hepatocytes from patients with acute HBV infection who subsequently recovered (Nouri-Aria et al., 1991). Therapeutic measure available thus, far are unable to suppress inflammatory activity, stimulate liver regeneration, or enhance virus elimination and hence the natural course of acute hepatitis B cannot be influenced. In the early stages of acute HBV infection, however, following the production of alpha-interferon, major histocompatability antigen (MHC) expression on hepatocytes have been found to increase and coincidentally transaminases rise. Interferon also activates a series of enzyme incuding the 2–5A synthetase system leading to the inhibition of viral protein syntheses. It is believed that these changes will produce an anti-viral state of uninfected regenerating liver cells, preventing reinfection, which together with the virus neutralizing antibodies developed, would prevent short and long term relapse or reinfection (Hoofnagle and Di Bisceglie, 1988; Thomas, 1988).
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