Pathogenesis of viral infections of the nervous system.
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Biomedical subjects
Publications and source records attributed to R T Johnson.
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Hydrocephalus developed as a sequela of mumps virus infections of suckling hamsters. The initial infection after intracerebral inoculation was limited largely to ependymal cells lining the ventricles. This infection was clinically inapparent but later resulted in a noninflammatory stenosis or occlusion of the aqueduct of Sylvius.
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Progression of weakness and muscle atrophy may be seen years after paralytic poliomyelitis. This paralysis probably results from physiologic and aging changes rather than from persistent infection. Nevertheless, persistent neural infection with polioviruses can occur in animals and humans.
The effectiveness of a conflict resolution training program was examined in an American midwestern suburban elementary school. Participants were 80 kindergartners randomly assigned to an experimental or control condition in morning or afternoon time blocks. Children in the experimental condition received 9 hr of conflict resolution training integrated into a curriculum unit on friendship taught daily for 4 consecutive weeks. Children in the control condition were taught the identical friendship unit for the same period of time without conflict resolution training. Teachers rotated equally across conditions. Significant differences between trained and untrained children occurred in their knowledge and retention of the conflict resolution procedure, willingness and ability to use the procedure in conflict situations, and conceptual understanding of friendship.
Both simian virus 40 (SV40) and BK viruses infected and lysed not only oligodendroblasts and astrocytes, but also neuroblasts and epithelioid or mesenchymal cells in cultures of fetal brain cells derived from human, rhesus, and cynomolgus hosts. Lytic infections of these four cell types differed ultrastructurally in the amount and arrangement of virions in the nucleus, the extent of nuclear membrane redundancy, the presence of nuclear virion arrays, and the amounts of virions in the cytoplasm. However, major differences were not noted between SV40 and BK viruses, nor between different species of origin or region of brain explanted. Modified astrocytic cells persisted in cultures from all three sources after infection by either virus. These cells stained for glial fibrillary acidic protein (GFAP) and polyomavirus tumour (T) antigen, but did not subculture indefinitely.
The development of murine retrovirus induced spongiform polioencephalomyelopathy was studied sequentially by electron microscopy. During the initial 30 days, viral infection of the central nervous system, as evidenced by viral budding from membranes, was limited to the endothelial cells and pericytes. Viral particles were observed in the lumen of blood vessels, extracellular spaces and astrocytic endfeet surrounding blood vessels, but no morphological evidence of productive infection was found in astrocytes or neurons during early development of vacuolation. The earliest lesions in the neuropil consisted of swelling of astroglia followed by vacuolation, initially in axons and dendrites and later in neuronal and astrocytic soma, where vacuoles appeared to arise from dilated cisternae of the Golgi apparatus. Vacuoles contained only amorphous debris and fragments of membranes. Virions budding aberrantly into vacuoles were seen only in mice surviving beyond 35 days. Numerous reactive astrocytes were observed, but inflammatory cells were absent. The ultrastructural changes were remarkably similar to those described in scrapie, Kuru, and Creutzfeldt-Jakob disease.