Transient virus infection and multiple sclerosis

Multiple sclerosis (MS) is a chronic, demyelinating disease of the CNS in w hich autoimmunity to myelin plays a role in pathogenesis. The epidemiology of MS indicates that it map be triggered by a virus infection before the ag e of adolescence, but attempts to associate a specific virus with MS have p roduced equivocal results. Many studies of the aetiology of MS have postula ted that a persistent virus infection is involved, but transient virus infe ction 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), wh ich is induced in susceptible animals following injection of myelin compone nts. While CREAE provide information on the initiating initial trigger that may involve transient virus infection. The disease process may comprise se parate triggering and relapse phases. The triggering phase may involve sens itisation to myelin antigens as a result of damage to oligodendrocytes or m olecular mimicry. The relapse phase could be similar to CREAE, or alternati vely relapses may be induced by further transient virus infections which ma p 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 par ticular could be modified to obviate any possibility of triggering anti-mye lin autoimmunity. Copyright (C) 2000 John Wiley & Sons, Ltd.