become chronic carriers is highly age-dependent. It ranges from about 80 to 90 percent for offspring of e-antigen positive mothers to 5 to 10 percent for adults (Francis and Maynard, 1979; Stevens et al., 1975). Chronic infection may result (usually after a period of many years) in cirrhosis or primary hepatocellular carcinoma, either of which can lead to death.
HBV is a small (42 nm) virus particle consisting of an outer coat and a central core with an unusual circular, partially double-stranded DNA (Dane et al., 1970; Gerin and Wai-Kuo Shih, 1978; Robinson, 1978). The central core of the virus contains the core antigen (HBcAg) which, in solution, has a conformational variant, the so-called e antigen (HBeAg). The coat protein is designated the surface antigen (HBsAg) of the virus. In addition to the whole virus particle, the blood of infected individuals contains smaller (20 to 22 nm) spherical and tubular forms that consist entirely of HBsAg. HBsAg has several major antigenic determinants. The a antigen is shared by all known strains of HBV. In addition, there are two sets of mutually exclusive antigenic determinants (d/y and w/r) that, in combination, produce the four major viral subtypes, adw, adr, ayw, and ayr. Additional subtype classifications and variants of each of the above major determinants have been described, but their importance for HBV infection or for immunity to infection is unclear (Gerin et al., 1982).
The immune response to HBV infection involves antibody production to all the HBV antigens: anti-HBc, anti-HBe, and anti-HBs. Anti-HBs usually appears only after resolution of HBV infection and is the antibody that is considered protective (Francis and Maynard, 1979). Anti-HBc and anti-HBe may be present during acute or chronic HBV infection, as well as following resolution. Their contribution to protection against HBV, if any, has not been fully elucidated. Individuals who recover from HBV infection usually develop substantial anti-HBs levels, which probably persist for life. The major humoral immune response following infection is to the common a antigenic component (anti-HBs/a) (McAuliffe et al., 1982). Thus, most individuals who have recovered from infection with one subtype of HBV will have subtype cross-protection. Rarely, anti-HBs/a fails to develop; when this occurs, the patient may remain susceptible to the other subtypes.
Investigations are under way to elucidate the role of the so-called preS region of the surface antigen protein(s). The preS region is removed in the processing of plasma derived vaccines and appears to enhance the protection provided by the s protein (National Institute of Allergy and Infectious Diseases, 1985).