Hepatitis A virus replication in tamarins and host immune response in relation to pathogenesis of liver cell damage.
Hepatitis A virus (HAV) shedding in the faeces, appearance of HAV-Ag (antigen) in the liver, and development of humoral immunity to HAV have been studied in experimentally infected tamarins. The appearance of liver damage measured by transaminase elevation and histology, in relation to the above variables, suggests that the virus is not cytopathic and the immune system contributes to the production of liver cell damage. Preliminary data suggest that HAV replication may occur in the mucosa of the small intestine and in the liver.
D000818:Animals; D000906:Antibodies / Q000032:analysis; D000956:Antigens, Viral / Q000032:analysis; D002143:Callitrichinae / Q000276:immunology*; D005243:Feces / Q000032:analysis; D005455:Fluorescent Antibody Technique; D035921:Hepatitis A Antigens; D006507:Hepatovirus / Q000145:classification / Q000254:growth & development* / Q000276:immunology / Q000378:metabolism; D000949:Histocompatibility Antigens Class II / Q000009:adverse effects / Q000276:immunology; D007075:Immunoglobulin M / Q000032:analysis; D008099:Liver / Q000166:cytology / Q000276:immunology / Q000473:pathology* / Q000648:ultrastructure; D008854:Microscopy, Electron; D011239:Prednisolone / Q000276:immunology / Q000494:pharmacology; D011863:Radioimmunoassay; D014018:Tissue Distribution; D014779:Virus Replication
D000906:Antibodies; D000956:Antigens, Viral; D035921:Hepatitis A Antigens; D000949:Histocompatibility Antigens Class II; D007075:Immunoglobulin M; D011239:Prednisolone