Brain lysosomal glycosidase activity in immunosuppressed mice infected with avirulent Semliki forest virus

Suckling, A.J.; Jagelman, S.; Webb, H. E.

doi:10.1128/iai.15.2.386-391.1977

Cited by 13 publications

(2 citation statements)

References 18 publications

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“…Even though there is a subclinical infection, the brains exhibit an inflammatory spongiform degeneration. Previous studies using an immunosuppressive agent suggest that the brain lesions are immunopathological (27).…”

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confidence: 95%

Humoral and cell-mediated immune mechanisms in the production of pathology in avirulent Semliki Forest virus encephalitis

Berger¹

1980

Infect Immun

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Seven days after peripheral inoculation with an avirulent strain of Semliki Forest virus, the brains of CBA and nude mice exhibited a mononuclear inflammation and spongiform degeneration. Mice that had received cyclophosphamide (150 mg/kg) 24 h after infection showed no pathology until day 11. However, immunofluorescence studies of the brains of immunosuppressed, infected mice demonstrated viral antigen within the soma and processes of neurons at earlier periods. The brain lesions could be reconstituted on day 7 in immunosuppressed, infected recipients with 6-day immune spleen cells. Immune spleen cells depleted of T lymphocytes, the non-immunoglobulin-bearing population deficient in B lymphocytes, or immune sera plus nonimmune bone marrow cells could also reconstitute the lesions. However, inflammation and spongiform changes were reduced when donor immune cells were depleted of either T or B lymphocytes. When both T and B lymphocytes were removed from the donor immune population, recipient brains did not show pathology. The results demonstrate that either antibody or immune T cells can trigger pathology, but there is also participation of nonimmune bone marrow-derived mononuclear cells, probably of the monocyte-macrophage lineage.

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confidence: 95%

Humoral and cell-mediated immune mechanisms in the production of pathology in avirulent Semliki Forest virus encephalitis

Berger¹

1980

Infect Immun

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“…Antiviral cytotoxic T cells are present from 5 to 17 days postinfection (2). Immunosuppression, using total body irradiation, antithymo-cyte serum, cyclophosphamide, or cycloleucine, can delay or prevent the lesions of demyelination (1,10,24). In athymic nu/nu mice, the virus establishes a persistent infection with no CNS damage and no lesions of demyelination.…”

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In vivo depletion of CD8+ T cells prevents lesions of demyelination in Semliki Forest virus infection

Subak-Sharpe

Dyson

Fazakerley

1993

J Virol

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Following intraperitoneal infection of BALB/c mice with the A7(74) strain of Semliki Forest virus, the virus spreads to the central nervous system (CNS) and initiates an acute inflammatory reaction which includes lesions of primary demyelination. This demyelination is dependent upon activated T lymphocytes. To determine whether CD4+ or CD8+ T cells are involved in the pathogenesis of the demyelination, we have investigated the course of infection in animals treated with monoclonal anti-CD4 or anti-CD8 antibodies. In the normal course of infection, virus was detectable in the brain by infectivity assay and in situ hybridization for up to 14 days. Antiviral immunoglobulin M (IgM) and all subclasses of IgG were produced. From day 10 to 21 postinfection lesions of inflammatory demyelination were present, most notably in the cerebellum and corpus callosum but also in other white matter tracts. Administration of anti-CD4 antibodies removed CD4+ cells from the spleen, prevented production of antiviral IgG, increased virus titers in the brain, and increased demyelination. Administration of anti-CD8 antibodies depleted CD8+ cells from the spleen and did not affect antiviral IgG synthesis or spread of brain virus but reduced CNS inflammatory responses and virtually abolished lesions of demyelination. Administration of both antibodies depleted both T-cell subsets from the spleen, prevented IgG antibody production, increased brain virus, and abrogated both CNS inflammation and lesions of demyelination. In conclusion, the CNS demyelination induced by Semliki Forest virus can be prevented by in vivo depletion of CD8+ T lymphocytes.

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Ross river virus‐induced demyelination: I. Pathogenesis and histopathology

Seay

Wolinsky

1982

Annals of Neurology

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Ross River virus (strain T48) infection in mice causes an encephalomyelitis characterized by focal, primary demyelination in the cerebellum, brain stem, and spinal cord. Maximal serum and brain content of virus occurs on days 2 and 4, respectively. Virus is not detectable in serum after day 3 or in brain after day 9. Histopathological lesions are present by day 2 and consist of perivascular macrophage and polymorphonuclear leukocyte infiltration, focal necrosis in the internal granule cell layer, and myelin disruption. Mononuclear cell infiltrates are present by day 5. Foci of demyelination in the presence of preserved axons become more widespread by day 8, and early partial remyelination occurs by day 13. Immunosuppression reduces the mononuclear cell infiltration but does not alter the demyelination . Although the mechanism of Ross River virus-induced demyelination is not known, these findings suggest that it is not immune mediated.

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Brain lysosomal glycosidase activity in immunosuppressed mice infected with avirulent Semliki forest virus

Abstract: The pathogenesis of WEE in adult hamsters with special reference to the long and shortterm effects on the CNS of the attenuated Clone 15 variant. Br.

Cited by 13 publications

References 18 publications

Humoral and cell-mediated immune mechanisms in the production of pathology in avirulent Semliki Forest virus encephalitis

Humoral and cell-mediated immune mechanisms in the production of pathology in avirulent Semliki Forest virus encephalitis

In vivo depletion of CD8+ T cells prevents lesions of demyelination in Semliki Forest virus infection

Ross river virus‐induced demyelination: I. Pathogenesis and histopathology

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