Abstract
Jaundice has been historically noted in association with both sporadic and epidemic disease, but it was not until 1839 that it was recognized to be a result of hepatocellular necrosis. The series of experimental inoculations into humans with infectious sera and subsequent transmission in animal models (marmosets and chimpanzees) established the existence of two distinct hepatotropic viruses. Hepatitis A virus (HAV) and hepatitis B virus (HBV) produce clinically indistinguishable acute hepatocellular necrosis. Viral hepatitides negative for the serologic markers of HAV or HBV infection have been termed non-A non-B (NANB). Among the heterogeneous etiologies, a proportion of such NANB disease may be ascribed to antigenically distinct agents that share nuclei acid homology with HBV (7). Because of the lack of a reliable laboratory test, the NANB virus continues to be enigmatic and a major cause of posttransfusion hepatitis (4,25). The epidemic NANB hepatitis prevalent in India and Russia is due to a distinct etiologic agent. We assess here the current concepts and information about biology (genes and antigens) of the HBV and current vaccines, and the future prospects in worldwide control of HBV infection.
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Roy, S., Vyas, G.N. (1989). Molecular Immunology of Viral Antigens in Hepatitis B Vaccination. In: Talwar, G.P. (eds) Progress in Vaccinology. Progress in Vaccinology, vol 2. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-3508-8_9
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DOI: https://doi.org/10.1007/978-1-4612-3508-8_9
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