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. 2000 Sep 28;10(5):291–303. doi: 10.1002/1099-1654(200009/10)10:5<291::AID-RMV278>3.0.CO;2-U

Transient virus infection and multiple sclerosis

G J Atkins 1,✉, S McQuaid 2, M M Morris‐Downes 1, S E Galbraith 1, S Amor 3, S L Cosby 2, B J Sheahan 4
PMCID: PMC7169221  PMID: 11015741

Abstract

Multiple sclerosis (MS) is a chronic, demyelinating disease of the CNS in which autoimmunity to myelin plays a role in pathogenesis. The epidemiology of MS indicates that it may be triggered by a virus infection before the age of adolescence, but attempts to associate a specific virus with MS have produced equivocal results. Many studies of the aetiology of MS have postulated that a persistent virus infection is involved, but transient virus infection may provide a plausible alternative mechanism that could explain many of the inconsistencies in MS research. The most studied animal model of MS is chronic relapsing experimental autoimmune encephalomyelitis (CREAE), which is induced in susceptible animals following injection of myelin components. While CREAE cannot provide information on the initiating factor for MS, it may mimic disease processes occurring after an initial trigger that may involve transient virus infection. The disease process may comprise separate triggering and relapse phases. The triggering phase may involve sensitisation to myelin antigens as a result of damage to oligodendrocytes or molecular mimicry. The relapse phase could be similar to CREAE, or alternatively relapses may be induced by further transient virus infections which may not involve infection of the CNS, but which may involve the recrudescence of anti‐myelin autoimmunity. Although current vaccines have a high degree of biosafety, it is suggested that the measles‐mumps‐rubella vaccine in particular could be modified to obviate any possibility of triggering anti‐myelin autoimmunity. Copyright © 2000 John Wiley & Sons, Ltd.

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