Lymphoreticular and myeloid pathogenesis of Venezuelan equine encephalitis in hamsters

Ultrastructural, histopathologic, and virologic studies of adult hamsters infected with virulent Venezuelan equine encephalomyelitis (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 proceeded. Early cortical necrosis of splenic periarteriolar lymphocytic sheath was followed by lymphoblastoid repopulation of the peripheral zone. Massive bone marrow necrosis was accompanied 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 hematopoietic cells were hallmarks of virulent VEE infection in the hamster.