Abstract
The last decade has borne witness to accelerated expansion of our understanding of hepatitis A virus. The agent of type A hepatitis is an RNA virus with a mean diameter of 27 nm. and biochemical-biophysical properties of an enterovirus. A variety of sensitive specific serologic techniques have been developed with which to identify hepatitis A virus and antibody, and both chimpanzees and marmosets have been studied extensively as experimental animal models. As a result of these studies, in vitro cultivation of hepatitis A virus has finally been accomplished, and a commercial radioimmunoassay for IgM antibody to hepatitis A virus has been developed for the rapid diagnosis of hepatitis A virus infection during acute illness. Clinically the illness caused by hepatitis A virus is relatively mild, often subclinical, and of limited duration and does not progress to chronic liver disease. This relative clinical benignity is reflected, according to preliminary histologic observations, in the sparing of the centrozonal area of the liver lobule. Rarely, however, hepatitis A virus can cause fulminant hepatitis. Type A hepatitis is transmitted almost exclusively by the fecal-oral route, and its spread is enhanced by epidemiologic settings favoring dissemination of enteric infections. Hepatitis A virus does not contribute to transfusion associated or other types of percutaneously transmitted hepatitis. Exposure to the virus increases as a function of age and decreasing socioeconomic class, but the incidence of hepatitis A virus infection in urbanized societies is decreasing. There is no evidence for the existence of chronic hepatitis A virus carriage; natural perpetuation of hepatitis A virus in urban communities appears to depend on a reservoir of nonepidemic, clinically inapparent cases. Until a vaccine, now being developed, becomes available, prevention of hepatitis A virus infection will continue to depend on maintenance of high standards of environmental and personal hygiene and on timely administration of immune serum globulin. Such prophylaxis may confer long lasting passive-active immunity but more frequently prevents infection entirely.
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