Transient virus infection and multiple sclerosis

G J Atkins, S McQuaid, M M Morris-Downes, S E Galbraith, S Amor, S L Cosby, B J Sheahan

Research output: Contribution to journalReview articleAcademicpeer-review

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.

Original languageEnglish
Pages (from-to)291-303
Number of pages13
JournalReviews in Medical Virology
Volume10
Issue number5
Publication statusPublished - 4 Oct 2000

Cite this

Atkins, G. J., McQuaid, S., Morris-Downes, M. M., Galbraith, S. E., Amor, S., Cosby, S. L., & Sheahan, B. J. (2000). Transient virus infection and multiple sclerosis. Reviews in Medical Virology, 10(5), 291-303.
Atkins, G J ; McQuaid, S ; Morris-Downes, M M ; Galbraith, S E ; Amor, S ; Cosby, S L ; Sheahan, B J. / Transient virus infection and multiple sclerosis. In: Reviews in Medical Virology. 2000 ; Vol. 10, No. 5. pp. 291-303.
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Atkins, GJ, McQuaid, S, Morris-Downes, MM, Galbraith, SE, Amor, S, Cosby, SL & Sheahan, BJ 2000, 'Transient virus infection and multiple sclerosis' Reviews in Medical Virology, vol. 10, no. 5, pp. 291-303.

Transient virus infection and multiple sclerosis. / Atkins, G J; McQuaid, S; Morris-Downes, M M; Galbraith, S E; Amor, S; Cosby, S L; Sheahan, B J.

In: Reviews in Medical Virology, Vol. 10, No. 5, 04.10.2000, p. 291-303.

Research output: Contribution to journalReview articleAcademicpeer-review

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AU - Atkins, G J

AU - McQuaid, S

AU - Morris-Downes, M M

AU - Galbraith, S E

AU - Amor, S

AU - Cosby, S L

AU - Sheahan, B J

N1 - Copyright 2000 John Wiley & Sons, Ltd.

PY - 2000/10/4

Y1 - 2000/10/4

N2 - 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.

AB - 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.

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KW - Disease Models, Animal

KW - Encephalomyelitis, Autoimmune, Experimental

KW - Humans

KW - Multiple Sclerosis

KW - Virus Diseases

KW - Viruses

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

KW - Review

M3 - Review article

VL - 10

SP - 291

EP - 303

JO - Reviews in Medical Virology

JF - Reviews in Medical Virology

SN - 1052-9276

IS - 5

ER -

Atkins GJ, McQuaid S, Morris-Downes MM, Galbraith SE, Amor S, Cosby SL et al. Transient virus infection and multiple sclerosis. Reviews in Medical Virology. 2000 Oct 4;10(5):291-303.