The document summarizes hepatitis A and E viruses. Hepatitis A virus is a picornavirus transmitted through the fecal-oral route. It has worldwide distribution and causes self-limited infection. Hepatitis E virus is an enterically transmitted RNA virus that causes acute hepatitis, predominantly affecting those aged 15-40 years in developing countries. Both viruses present with acute hepatitis symptoms like jaundice and elevated liver enzymes. Diagnosis involves IgM antibody testing. Treatment is supportive and prevention focuses on sanitation and hygiene.

1. Viral hepatitides A and E Sorokhan MD, PhD Bukovinian State Medical University Department of the infectious diseases and epidemiology

6. Epidemiology Hepatitis A. Time course of infection.

7. Its resilience is demonstrated by its resistance to denaturation by ether, acid (pH 3.0), drying, and temperatures as high as 56°C and as low as -20°C. The hepatitis A virus can remain viable for many years. Boiling water is an effective means of destroying it, and chlorine and iodine are similarly effective. Various genotypes of the hepatitis A virus exist; however, there appears to be only 1 serotype. Virion proteins 1 and 3 are the primary sites of antibody recognition and subsequent neutralization. No antibody cross-reactivity has been identified with other viruses causing acute hepatitis. Epidemiology

8. Most patients have no defined risk factors for hepatitis A. Risk factors for acquisition of hepatitis A include the following: Personal contacts; Institutionalization; Occupation (eg, daycare); Foreign travel; Male homosexuality; Illicit parenteral drug use; Persons in high-risk populations (eg, sewage workers, childcare workers, aid workers, male homosexuals). Epidemiology

9. In humans, viral replication depends on hepatocyte uptake and synthesis, and assembly occurs exclusively in liver cells. Hepatocyte uptake involves a receptor, identified by Kaplan et al, on the plasma membrane of the cell, and viral replication is believed to occur exclusively in hepatocytes. The demonstration of the hepatitis A virus in saliva has raised questions about this exclusivity. After entry into the cell, viral RNA is uncoated, and host ribosomes bind to form polysomes. Viral proteins are synthesized, and the viral genome is copied by a viral RNA polymerase. Assembled virus particles are shed into the biliary tree and excreted in the feces Pathogenesis

10. Pathogenesis Hepatitis A.

11. Minimal cellular morphologic changes result from hepatocyte infection. The development of an immunologic response to infection is accompanied by a predominantly portal and periportal lymphocytic infiltrate and varying degree of necrosis. Many authorities believe that hepatocyte injury is secondary to the host's immunologic response. This hypothesis is supported by the lack of cytotoxic activity in tissue culture and correlations between immunologic response and manifestations of hepatocyte injury. Pathogenesis

27. Hepatitis E

30. Patho genesis

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