Treatment of Chronic Hepatitis B Infection with Alpha (Lymphoblastoid) Interferon: Responses in Different Social And Ethnic Groups in Comparision to Adenine Arabinoside Monophosphate

There are approximately 200 million carriers of hepatitis B virus world-wide. This carriage rate is associated with a high incidence of chronic liver disease and a two hundred fold increased incidence of hepat-cellular carcinoma. These patients are those in whom acute infection has not been associated with clearance of the virus and development of immunity, but in whom this mechanism has broken down to produce the chronic carrier state. There are probably many reasons for the chronic carrier state. Approximately 5–10% of patients infected in adult life in the Western World (1) become chronic carriers whereas 90% of those in the Far East, infected around the time of birth, become carriers.(2). The hepatitis virus is not cytopathic and elimination depends on mobilisation of host defense mechanisms to lyse virus infected cells and to clear circulating virions (3). Lysis of virus infected cells requires recognition of viral proteins in association with HLA class I antigens on the surface of the cell and it is known that on both uninfected liver and in the chronic carrier state there is very little HLA protein display on the surface of the hepatocyte (4). In the animal model of acute viral hepatitis, this HLA display rises following the detection of interferon., in the circulation and the rise corresponds with biochemical evidence of liver damage.