Abstract
The virus responsible for hepatitis A--hepatitis A virus (HAV)--is a small, spherical, and exceptionally resistant RNA-virus. It is transmitted preferentially by the faecal-oral route and apparently replicates exclusively in the liver. The damage of the liver ensuing from HAV infection most likely does not stem directly from virus replication but is the result of an interaction of cell mediated virus-specific immunity with infected hepatocytes. Infection is usually self limiting, yet, in individual cases may also take a protracted and even relapsing course. True chronic infections, however, are not observed. HAV has a world-wide distribution. In countries where inadequate sanitary conditions prevail, the virus persists in the environment and almost 100% of the population acquires infection in childhood. At that age, infection causes no or only minimal clinical symptoms. Infected individuals nevertheless develop protective, long lasting immunity, probably persisting for entire life. In developed, industrialized countries HAV has ceased to circulate in the environment and the general population. Here, infections predominantly occur in adults travelling to endemic areas or exposed at home to thus infected individuals or members of high risk groups (e.g. children in day care centres, i.v. drug users). With increasing age infections become more and more clinically manifest and at and beyond of adolescence more than 80% of patients develop icteric, in some cases even fulminant and fatal hepatitis. Acute hepatitis A infection can be diagnosed by demonstrating the presence of anti-HAV-IgM antibodies. Immunity following either infection or successful vaccination is assessed by measuring anti-HAV-IgG. Preventive measures rely on strict personal and alimentary hygiene as well as on vaccination with inactivated (killed) hepatitis A vaccines. These vaccines are safe, highly immunogenetic and induce long lasting (> 20 years) protection against hepatitis A. Specific antiviral therapy is not yet available.
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