Hepatitis A Virus

Abstract

Hepatitis A virus (HAV), a human picornavirus, is spread by the fecal–oral route, but the site of virus replication is the liver. The symptoms of the disease are heterogeneous depending on the age of infection, ranging from silent infections mainly in young children to classical hepatitis in older age groups, and fatal courses of the disease also occur. Chronic infections are not described, and elimination of the virus is mediated mainly by cytotoxic T lymphocytes. The incidence of acute hepatitis A is decreasing worldwide due to improved hygienic conditions, resulting in a decline of the anti-HAV prevalence, and leaving considerable parts of the population susceptible to infection. Efficacious inactivated vaccines are available. In addition to its high physical stability, HAV has several characteristics that make it unique among the human picornaviruses. Studies in cell culture, including a variety of primate and nonprimate cell lines, demonstrated that HAV exhibits a protracted replication cycle and is normally not cytopathogenic, but establishes a persistent infection. Furthermore, there are significant differences to other picornaviruses with regard to its mechanism of polyprotein processing and virion morphogenesis. In order to evade innate cellular antiviral defense mechanisms, HAV inhibits the induction of both interferon synthesis and apoptosis.