Viral hepatitis, type B.

INTRODUCTION Hepatitis B virus (HBV) is a DNA virus which is highly host and organ specific; to date it has only been found to infect hepatocytes of man and of a few nonhuman primate species. Despite the continuing failure of virologists to find an in vitro system for propagating HBV, it has been possible to gain a great deal of information about the agent and about viral hepatitis, type B, as a result of the discovery of the Australia antigen, now termed hepatitis B surface antigen (HB,Ag), and the recognition of its significance (1-4). The presumptive infectious form of HBV is a 40-42-nm particle, known as the Dane particle (5), which consists of an inner nucleocapsid core, termed hepatitis B core antigen (HBCAg) (6), and an outer lipoprotein coat composed of HB,Ag. The respective antibodies for the inner and outer components of HBV are called anti-HB, and anti-HB,. In the last several years a number of tests have been developed for detecting these antigens and antibodies (7). The most sensitive methods are radioimmunoassays (RIA), which use solid phase or double antibody techniques for separating specifically bound from free radiolabeled proteins. Almost as sensitive and avoiding the requirements for working with radioactive isotopes are the following hemagglutination techniques: passive hemagglutination (PHA) for anti-HB, detection, reversed passive hemagglutination (RPHA) for HB,Ag detection, and immune adherence hemagglutination (IAHA) for anti-HB, detection. A number of less sensitive methods, including agar gel diffusion, counterelectrophoresis, complement fixation, and reversed passive latex agglutination, are valuable for certain specific applications, but the more sensitive methods have vastly increased our understanding of the clinical disease, epidemiology, and approaches to prevention of type B hepatitis.