Although hepatitis-like illnesses have been known to physicians since antiquity and recognized as an infectious disease with potential for occurrence in large outbreaks (epidemic jaundice) for about a century, it was not until the 1940s that transmission studies in human and epidemiologic observations provided evidence for the existence of the presently recognized two distinct forms of viral hepatitis, A and B. Unlike that of hepatitis B, research on hepatitis A progressed slowly until the 1970s when hepatitis A virus could be visualized and immunologic assays to detect virus antigen and antibody were effectively developed, thus could HAV be identified unequivocally as the causative agent of sporadic and epidemic cases of hepatitis. Among the hepatitis viruses, hepatitis A virus is uniquely and primarily transmitted by the fecal-oral route and thus possesses an unequaled potential for epidemic spread. Although relatively benign and never progressing into chronic hepatitis infection, the hepatitis A virus (HAV) nevertheless remain an important cause of morbidity and occasional mortality (Lemon, 1985; Hoffman, 1991). In Shanghai, China, over 1 million people were infected by HAV in a major outbreak (Yang et al., 1988). Some aspects of the pathogenesis of hepatitis A virus disease are discussed below.
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