ANTIVIRAL THERAPY IN HEPATITIS B INFECTION

Studies of the mechanism of elimination of infected hepatocytes during the course of acute type B hepatitis suggest that early in the infection, interferon is produced which stimulates an increase in HLA class 1 protein display on the hepatocytes. This results in increased lysis of these cells by cytotoxic T cells and natural killer cells. In chronic hepatitis B virus infection, examination of the liver reveals that, although there is some evidence of interferon activation of the infected cells. HLA class 1 protein display is not increased. This appears to be related to a relative deficiency of interferon production and is supported by the observation that the peripheral blood lymphocytes of these patients do not produce normal amounts of interferon-α when stimulated with Sendai virus. These patients with the deficiency of interferon -α production have developed the infection during adult life and they show a significant response rate to treatment with lymphoblastoid interferon. In recent studies, 70% of Caucasian patients receiving a 3-month course of thrice-weekly interferon, seroconverted from HBe antigen to HBe antibody and showed a reduction in the level of inflammatory activity in their liver. In contrast, Chinese patients with chronic hepatitis B virus infection showed no response to this form of treatment. This suggests that these patients, who are predominantly infected at birth, are carriers for different reasons to those operative in Caucasian (predominantly homosexual) patients infected in adult life.