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Transient virus infection and multiple sclerosis
G J Atkins1, S McQuaid, M M Morris-Downes
1Department of Microbiology, Moyne Institute of Preventive Medicine, Trinity College, Dublin 2, Ireland. gatkins@tcd.ie
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.
Insights
Multiple sclerosis (MS) may be triggered by transient viral infections, offering an alternative explanation for disease inconsistencies. Research suggests modifying vaccines like the measles-mumps-rubella (MMR) vaccine to prevent triggering anti-myelin autoimmunity.
Area of Science:
- Neuroimmunology
- Viral Immunology
- Demyelinating Diseases
Background:
- Multiple sclerosis (MS) is a chronic CNS demyelinating disease with autoimmune involvement.
- Epidemiological data suggests viral infections may trigger MS, but specific causative viruses remain elusive.
- Persistent viral infection theories for MS etiology have yielded inconsistent results.
Purpose of the Study:
- To explore transient viral infections as a plausible alternative mechanism for MS initiation.
- To investigate the potential role of transient infections in explaining inconsistencies in MS research.
- To evaluate the relationship between viral infections, autoimmunity, and MS pathogenesis.
Main Methods:
- Review of epidemiological studies on MS triggers.
- Analysis of the chronic relapsing experimental autoimmune encephalomyelitis (CREAE) animal model.
- Examination of proposed mechanisms for MS triggering and relapse phases.
- Consideration of molecular mimicry and oligodendrocyte damage in MS etiology.
Main Results:
- Transient viral infections present a viable alternative to persistent infections in explaining MS etiology.
- The CREAE model may mimic MS processes following an initial trigger, potentially involving transient infections.
- MS pathogenesis may involve distinct triggering and relapse phases, with relapses possibly induced by further transient infections.
- The measles-mumps-rubella (MMR) vaccine is specifically mentioned as a potential candidate for modification.
Conclusions:
- Transient viral infections offer a unifying hypothesis for MS pathogenesis and research inconsistencies.
- Further research into transient viral triggers and their interaction with myelin autoimmunity is warranted.
- Vaccine modifications, particularly for the MMR vaccine, could potentially mitigate the risk of triggering anti-myelin autoimmunity in susceptible individuals.