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Biomedical subjects

O Narayan

Publications and source records attributed to O Narayan.

233 records · Page 13Linked to original sources
PubMed1972

Effects of viral infection on nervous system development. II. Attempts to modify bluetongue-virus-induced malformations with cyclophosphamide and antithymocyte serum.

Treatment with cyclophosphamide and antithymocyte serum (ATS) did not significantly increase the susceptibility of mice to bluetongue virus infections of the nervous system. Cyclophosphamide actually inhibited virus growth in newborn and 2-week-old mice and, in newborn mice, diminished the severity of virus-induced pathologic sequelae. Autoradiographic studies suggested this inhibition resulted from the effect of cyclophosphamide on the immature cells of the subventricular zone which were the cell population selectively infected by bluetongue virus. In newborn mice ATS inhibited the inflammatory reaction and development of antibody, but did not result in alterations in mortality, initial virus growth and localization or early necrosis of cells in the subventricular zone. Antithymocyte serum only caused longer persistence of virus and slight extension of late pathologic lesions. The failure of cyclophosphamide and ATS treatment to induce more extensive lesions in older mice show that the age-dependency of bluetongue lesions is not determined by the immaturity of immune responses.

Age Factors↗
PubMed1972

Effects of viral infection on nervous system development. I. Pathogenesis of bluetongue virus infection in mice.

Bluetongue vaccine virus was adapted to mice by serial intracerebral passage. The adapted virus was found to multiply selectively in immature cells of the subventricular zone of the forebrain and spread along cell migratory pathways to the olfactory bulbs, caudate/putamen, hippocampus and areas of cerebral cortex. Symmetrical, mineralized, partially cavitated lesions developed in these areas as a sequela of the infection. Infection of fetal mice led to more severe cerebral malformation, and infection of 2-week-old mice resulted in very limited multiplication without sequelae. The pattern of infection correlated with the maturation and migration of cells within the developing telencephalon.

Age Factors↗
PubMed1971

A new influenza A virus infection in turkeys. VII. Comparative immunology.

Four influenza A strains isolated from turkeys in Ontario as well as strain Chicken/Scotland/59 were found to immunize turkeys against the lethal disease caused by virus Turkey/Ontario 7732/66 (V7732). These viruses form the avian influenza A serotype 5 (AA5). Immunoprotection against V7732 was not obtained with influenza viruses of other serotypes. Immunoprotective relationships among AA5 viruses were not always demonstrable in hemagglutination-inhibition (HI) and serum-neutralization (SN) tests, especially with turkey and mammalian antisera; better correlation between immunoprotection and these in vitro tests was seen with chicken antisera. The implications of these findings relative to virus classification, serodiagnosis and vaccination are discussed.

Animals↗
PubMed1970

A new influenza A virus infection in turkeys. VI. Artificial immunization against the malignant virus strain turkey-Ontario 7732-66.

The immune reaction of turkeys and chickens to inactivated preparations of a virulent strain of avian influenza A virus has been examined. In both species any level of antibody detectable by the hemagglutination inhibition or serum neutralization tests was protective against the challenge exposure. However, some vaccinated birds were protected in the absence of detectable antibody. Chickens responded with higher and longer lasting antibody titers than turkeys to identical antigen preparations. Whereas the vaccine induced protection in chickens for at least 84 days, the immune protection in turkeys barely lasted 42 days. Immune birds responded to the live virus challenge with a marked rise in serologic titers which suggest that they were still susceptible to subclinical infection. These findings are discussed in their relationship to available data on classical fowl plague and influenza in mammals.

Animals↗
PubMedDate not supplied

Immunopathology of lentiviral infections in ungulate animals.

The immunopathogenesis of lentiviral lesions in sheep and goats requires continuous replication of the virus in tissues of the animal. This entails escape from various defense mechanisms of the host. Viral expression occurs mainly in tissue-specific macrophage populations and viral proteins produced by the cells induce and combine with antibodies to form immune complexes. These may be pathogenic locally. Infected macrophages also present lentiviral antigens to T lymphocytes and this results in a cascade of cellular responses including proliferation and accumulation of CD8 cells. Cytokines including interferon(s) are produced by lymphocytes and these enhance the antigen-presenting capacity of the macrophages. These lymphoproliferative cellular responses vary from those in human immunodeficiency virus- and simian immunodeficiency virus-infected hosts, mainly because CD4 cells of sheep and goats are not killed by the viruses. These cells, therefore, respond immunologically to viral antigens and this leads to active-chronic inflammation.

Animals↗
PubMedDate not supplied

Lentiviral diseases of sheep and goats: chronic pneumonia leukoencephalomyelitis and arthritis.

This review describes the pathogenesis of a slowly progressive disease complex caused by naturally occurring nononcogenic retroviruses in sheep and goats. In nature, infections are usually clinically silent, but disease may manifest itself after prolonged incubation periods. Clinically, this is seen as dyspnea, progressive paralysis, and/or progressive arthritis. In all organs the basic lesion is inflammatory with infiltration and proliferation of lymphocytes, plasma cells, and macrophages. Other organ-specific pathologic changes such as primary demyelination in the central nervous system and degeneration of cartilaginous structures in joints accompany inflammation. The viruses infect tissue-specific macrophage populations in vivo. Viral replication in these cells is restricted to minimal levels but continues indefinitely in the animal as a result of either failure to induce specific neutralizing antibodies or antigenic drift when neutralizing antibodies develop. Consistent low-grade viral replication sets the pace for disease by providing continuous antigenic stimulation for the inflammatory cellular immune response or antibodies that localize in the target tissues. These cells and immune complexes may have adverse effects on indigenous cell populations.

Animals↗
PubMedDate not supplied

Studies of cultured human and simian fetal brain cells. II. Infections with human (BK) and simian (SV40) papovaviruses.

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.

Animals↗
PubMedDate not supplied

Early activation of PBMC and appearance of antiviral CD8+ cells influence the prognosis of SIV-induced disease in rhesus macaques.

We studied 15 macaques inoculated with SIV and identified three phases of infection. Phase 1 was characterized by activated lymphocytes in blood and infected cells in the CSF. In phase 2, activated cells were not detected but virus was recovered from mitogen-stimulated PBMC, while in phase 3, virus was recovered from mitogen-stimulated PBMC only after depletion of CD8+ lymphocytes, indicating effective control of the virus in peripheral blood. Early development of phase 3 status correlated with a longer period of clinical normalcy.

Animals↗
PubMedDate not supplied

Chimeric SHIV that causes CD4+ T cell loss and AIDS in rhesus macaques.

By animal to animal passage in rhesus and pig-tailed macaques, we developed a rhesus model of HIV-1 disease in humans. Rhesus macaques infected with a cell-free stock of SHIVKU-2 developed CD4+ T cell loss, primary lentiviral encephalitis and pneumonia, and AIDS. Six of nine rhesus macaques died within eight months post-inoculation, while the remaining three are at five, five, and eight months post-inoculation, respectively. Animals infected by either mucosal or parenteral routes of infection had a similar course of infection.

Acquired Immunodeficiency Syndrome↗