HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Gates, M. C. Articles by Atkins, G. J. Search for Related Content PubMed PubMed Citation Articles by Gates, M. C. Articles by Atkins, G. J. Agricola Articles by Gates, M. C. Articles by Atkins, G. J.

The Pathogenicity of the M9 Mutant of Semliki Forest Virus in Immune-compromised Mice

Department of Microbiology, Moyne Institute, Trinity College, Dublin 2
and¹ Faculty of Veterinary Medicine, University College, Dublin 4, Ireland

The role of immune mechanisms in the pathogenicity of the M9 mutant of Semliki Forest virus (SFV) has been examined by the use of immune-deficient and immune-suppressed mice. In immune-competent BALB/c and C57BL/6 mice, the lesions in the central nervous system (CNS) were characterized by acute demyelinating meningo-encephalomyelitis. Myelin vacuolation and demyelination were more severe in BALB/c mice than in mice with a C57BL background. The mortality was 12% and 29% respectively. Treatment with cyclophosphamide or sodium aurothiomalate did not greatly alter the type of lesion produced, although mortality was increased. Lesions were less severe in nude (T-lymphocyte-deficient) mice and more severe in beige (natural killer cell-deficient) mice than in most immune-competent mice. Mortality was marginally increased in nude mice but not in beige mice. Demyelination in nude mice was followed rapidly by remyelination. Immune modification did not significantly alter the titres of virus in the brain at 7 days post-infection and infectious virus had been cleared from the brain by 14 days in all cases. Degenerating oligodendrocytes were detected in the CNS of all immune-modified mice examined at day 7. This study therefore suggests that both immune mechanisms and destruction of oligodendrocytes play a role in the production of demyelination by M9.

Keywords: SFV, demyelination, immune suppression

Received 13 June 1983; accepted 22 September 1983.

This article has been cited by other articles:

				A. A. Dandekar and S. Perlman Virus-Induced Demyelination in Nude Mice Is Mediated by {gamma}{delta} T Cells Am. J. Pathol., October 1, 2002; 161(4): 1255 - 1263. [Abstract] [Full Text] [PDF]

				G. J. Atkins, B. J. Sheahan, and P. Liljeström The molecular pathogenesis of Semliki Forest virus: a model virus made useful? J. Gen. Virol., September 1, 1999; 80(9): 2287 - 2297. [Full Text]