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Semliki Forest Virus-induced, Immune-mediated Demyelination: Adoptive Transfer Studies and Viral Persistence in Nude Mice

J. K. Fazakerley

Neurovirology Unit, Rayne Institute, The United Medical and Dental Schools of Guy's and St Thomas' Hospitals, Lambeth Palace Road, London SE1 7EH, U.K.

Adoptive transfer experiments in athymic nude mice demonstrated that the demyelination seen in the central nervous system (CNS) following Semliki Forest virus (SFV) infection was directly dependent upon sensitized T lymphocytes. Antibodies generated during the infection did not seem to be involved in the demyelination, but thymus-dependent antibodies (IgG) were responsible for the reduction of brain virus titres. In the absence of a T cell response and T cell-dependent antibody production, virus persisted in the CNS for several months. Despite persistence of high virus titres for this time, only mice eventually developing a CNS inflammatory response developed lesions of demyelination. In the absence of an inflammatory response no demyelination was apparent even after several months of persistent infection. Administration of anti-SFV hyperimmune serum intracerebrally to both infected and control mice did not produce demyelination but resulted in CNS tissue degeneration with marked pycnosis.

Keywords: SFV, demyelination, autoimmunity, persistence

Present address: Department of Microbiology, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, U.S.A.

Received 7 May 1986; accepted 26 September 1986.

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