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HAV, a 27-nm RNA agent classified as a picornavirus, can produce either asymptomatic or symptomatic infection in humans after an average incubation period of 28 days range, 1550 days) (3). The illness caused by HAV infection typically has an abrupt onset of symptoms that can include fever, malaise, anorexia, nausea, abdominal discomfort, dark urine, and jaundice. The likelihood of having symptoms with HAV infection is related to the person´s age. In children <6 years of age, most (70%) infections are asymptomatic; if illness does occur, it is not usually accompanied by jaundice (4). Among older children and adults, infection is usually symptomatic, with jaundice occurring in >70% of patients (5). Signs and symptoms usually last <2 months, although 10%15% of symptomatic persons have prolonged or relapsing disease lasting up to 6 months (6). In infected persons, HAV replicates in the liver, is excreted in bile, and is shed in the stool. Peak infectivity of infected persons occurs during the 2-week period before onset of jaundice or elevation of liver enzymes, when the concentration of virus in stool is highest (7,8). The concentration of virus in stool declines after jaundice appears (7,8). Children and infants can shed HAV for longer periods than adults, up to several months after the onset of clinical illness (9). Chronic shedding of HAV in feces does not occur; however, shedding can occur in persons who have relapsing illness (10). Viremia occurs soon after infection and persists through the period of liver enzyme elevation (11,12). Hepatitis A cannot be differentiated from other types of viral hepatitis on the basis of clinical or epidemiologic features alone. Serologic testing to detect immunoglobulin M (IgM) antibody to the capsid proteins of HAV (IgM anti-HAV) is required to confirm a diagnosis of acute HAV infection. In most persons, IgM anti-HAV becomes detectable 510 days before the onset of symptoms and can persist for up to 6 months after infection (12,13). Immunoglobulin G (IgG) anti-HAV, which appears early in the course of infection, remains detectable for the person´s lifetime and confers lifelong protection against the disease (14). Commercial diagnostic tests are available for the detection of IgM and total (IgM and IgG) anti-HAV in serum. HAV RNA can be detected in the blood and stool of most persons during the acute phase of infection by using nucleic acid amplification methods, and nucleic acid sequencing has been used to determine the relatedness of HAV isolates (15). However, these methods, available in only a limited number of research laboratories, generally are not used for diagnostic purposes.
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