Viral Hepatitis

Hepatitis A is a viral infection of the liver that may occur sporadically or in epidemics. The liver involvement is part of a generalized infection but dominates the clinical picture. Although transmission of the virus may occur by contaminated needles, it is usually by the fecal-oral route. The excretion of hepatitis A virus (HAV) as determined by immune electron microscopy of stool occurs up to 2 weeks prior to illness. HAV is rarely demonstrated in feces after the third week of illness. There is no known carrier state with HAV. Blood and stools are infectious during the incubation period (2 to 6 weeks) and early illness until peak transaminase levels are achieved. Although theoretically possible, the short duration of viremia makes posttransfusion hepatitis unlikely. In fact, posttransfusion hepatitis due to HAV has not been documented. Although the mortality rate with hepititis A is low, it may cause fulminant disease. The mortality rate (as with hepatitis B) appears to be age-related. Marmoset monkeys and chimpanzees appear to be the only susceptible animals; livers of infected marmoset monkeys have revealed the 27-nm particles.

An unequivocal diagnosis of HAV is established by demonstrating the hepatitis A virus antigen (HAAg) in the stool or the IgM antibody to hepatitis A in serum. The absence of HAAg in the stool does not rule out HAV infection.

Antibodies to type A hepatitis appear early in the course of the illness and tend to persist in the serum. Immune electron microscopy and radioimmunoassay detect both IgM and IgG antibodies and are positive soon after the onset of the illness.

Immune adherence hemagglutination reflects an IgG response and is positive later in the course of the disease. Peak titers of IgG antibodies occur after 1 month of disease and may persist for years. Peak titers of IgG antibodies occur during the first week of clinical disease and disappear within an 8-week period; therefore measurement of these antibodies is an excellent test for demonstrating acute hepatitis A infection. The presence of anti-HAV activity indicates: (1) previous exposure to HAV; (2) nonin fectivity; and (3) immunity to recurring HAV infection. It does not imply previous clinically apparent hepatitis, nor does it establish a relationship to ongoing liver disease unless seroconversion has been demonstrated.

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