Medicine

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This repository contains the published and unpublished research of the Faculty of Medicine by the staff members of the faculty

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    Pathogenesis of murine gammaherpesvirus infection in mice deficient in CD4 and CD8 T cells
    (American Society for Microbiology., 1993) Ehtisham, S.; Sunil-Chandra, N.P.; Nash, A.A.
    Murine gammaherpesvirus is a natural pathogen of wild mice. The virus infects alveolar cells and spleen cells during the primary infection and establishes a latent/persistent infection in B lymphocytes. Little is known about the immunological response to gammaherpesviruses during a primary infection. To address this issue, we investigated the pathogenesis of murine herpesvirus 68 (MHV-68) infection in mice deficient in CD4 or CD8 T-cell populations. Infection of the lung and spleen were greatly exacerbated in CD8-deficient mice, reflected by elevated virus titers in the lung and an increase in the number of infected splenocytes located around germinal centers. This finding contrasts with clearance of virus from the lung and spleen by day 12 postinfection in CD4-depleted animals. These data clearly indicate a major role for CD8 T cells in recovery from an acute MHV-68 infection. Whereas CD4 T cells fail to influence the course of infection in the lung, they do contribute to lymphoproliferation seen in the spleen (splenomegaly) during the primary infection. The significance of these results are discussed in relation to the immune response to other herpesviruses, in particular Epstein-Barr virus, with which MHV-68 shares similar molecular and biological properties.
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    Virological and pathological features of mice infected with murine gamma-herpesvirus 68
    (Society for General Microbiology; Microbiology Society, 1992) Sunil-Chandra, N.P.; Efstathiou, S.; Arno, J.; Nash, A.A.
    The primary infection of BALB/c mice with murine herpesvirus 68 (MHV-68) was investigated. When the virus was introduced intranasally, the lung was the main tissue infected, the virus being associated with alveolar epithelium and mononuclear cells. A productive infection lasted for 10 days, after which viral DNA could be detected by in situ hybridization up to 30 days after infection. At that time lymphoproliferative accumulations were also observed in the lung, with formation of germinal centres. Virus could also be recovered from the heart, kidney, adrenal gland and spleen during the primary infection. In addition, the spleen appeared to be the major site of virus persistence, with latently infected cells detected up to 90 days post-infection. During the primary infection, there was atrophy of the thymus and spleen of clinically sick animals. In contrast, lymphoproliferative responses, typified by splenomegaly, were frequently seen in asymptomatic animals. The pattern of infection observed in MHV-68-infected mice is similar to that seen in infectious mononucleosis of man following Epstein-Barr virus infection. The model described in this paper may prove to be useful in studying natural gamma-herpesvirus infections of man and domestic animals.
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    Interactions of the murine gammaherpesvirus with the immune system
    (Current Science; Elsevier, 1994) Nash, A.A.; Sunil-Chandra, N.P.
    Our understanding of the host response to gammaherpesviruses comes largely from studies on Epstein-Barr virus. A recent addition to this family is murine herpesvirus-68 which, like Epstein-Barr virus, establishes a latent infection in B lymphocytes and is associated with lymphoproliferative disease. This virus provides a unique opportunity to explore the relationship between gammaherpesviruses and the immune system.
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