Lymphoreticular and myeloid pathogenesis of Venezuelan equine encephalitis in hamsters.
Ultrastructural, histopathologic, and virologic studies of adult hamsters infected with virulent Venezuelan equine encelphalomyelitis (VEE) virus (Subtype I-B) demonstrated precise chronologic and topographic progression of lesions and viral replication in extraneural sites. Thymus contained the earliest lesions and the highest initial and subsequent viral titers. No particular cytotropism was observed as highly efficient viral replication and severe cytonecrosis proceded. Early cortical necrosis of splenic periarteriolar lymphocytic sheath was followed by lymphoblastoid repopulation of the peripheral zone. Massive bone marrow necrosis was accompained by ultrastructural evidence of VEE viral particle production in reticulum cells, rubricytes, myeloid cells, lymphoblastoid cells, and megakaryocytes. Speed, efficiency, destructiveness, and relative sensitivity of virtually all lymphoreticular and hematopoetic cells were hallmarks of virulent VEE infection in the hamster.
D000818:Animals; D001853:Bone Marrow / Q000473:pathology; D006224:Cricetinae; D003588:Cytopathogenic Effect, Viral; D004683:Encephalomyelitis, Equine / Q000473:pathology*; D004685:Encephalomyelitis, Venezuelan Equine / Q000473:pathology*; D007082:Ileum / Q000473:pathology; D007181:Inclusion Bodies, Viral; D008198:Lymph Nodes / Q000473:pathology; D008208:Lymphatic System / Q000473:pathology*; D008297:Male; D013154:Spleen / Q000473:pathology; D013950:Thymus Gland / Q000473:pathology; D014779:Virus Replication