Axonal damage is T cell mediated and occurs concomitantly with demyelination in mice infected with a neurotropic coronavirus

A. A. Dandekar, G. F. Wu, L. Pewe, S. Perlman

Research output: Contribution to journalArticle

57 Scopus citations

Abstract

Mice infected with mouse hepatitis virus (MHV) strain JHM develop primary demyelination. Herein we show that axonal damage occurred in areas of demyelination and also in adjacent areas devoid of myelin damage. Immunodeficient MHV-infected RAG1-/- mice (mice defective in recombinase activating gene 1 expression) do not develop demyelination unless they receive splenocytes from a mouse previously immunized against MHV (G. F. Wu, A. Dandekar, L. Pewe, and S. Perlman, J. Immunol. 165:2278-2286, 2000). In the present study, we show that adoptive transfer oft cells was also required for the majority of the axonal injury observed in these animals. Both demyelination and axonal damage were apparent by 7 days posttransfer. Recent data suggest that axonal injury is a major factor in the long-term disability observed in patients with multiple sclerosis. Our data demonstrate that immune system-mediated damage to axons is also a common feature in mice with MHV-induced demyelination. Remarkably, there appeared to be a minimal, if any, interval of time between the appearance of demyelination and that of axonal injury.

Original languageEnglish
Pages (from-to)6115-6120
Number of pages6
JournalJournal of virology
Volume75
Issue number13
DOIs
StatePublished - Jul 3 2001
Externally publishedYes

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