The etiology of MS is unknown, although epidemiological studies have implicated an infective agent as a probable initiating factor (Acheson, 1977; Gilden, 2001). An epidemiological survey reported the increased risk of developing MS was associated with late infection with mumps, measles, and Epstein-Barr virus (Miguel et al., 2001). In addition, exacerbations of MS are frequently preceded by viral infections (Sibley et al., 1985). It is also intriguing that the antiviral agent IFN-ß has been reported to have a beneficial effect on relapsing/remitting MS (IFN-ß Multiple Sclerosis Study Group, 1993). A number of different viral agents have been isolated from the brains of MS patients, including measles, mumps, parainfluenza type I (Allen and Brankin, 1993), and human herpes simplex type 6 (HHSV6) (Challoner et al., 1995). In common with other autoimmune diseases, stressful life events may precipitate the onset and clinical relapses in MS patients (Whitacre et al., 1994). One mechanism of stress-induced exacerbation might be via increased glucocorticoid levels resulting in immunosuppres-sion and reactivation of latent viruses such as herpes virus.
Viruses are also known to cause demyelination in animals: measles virus in rats; JHM mouse hepatitis virus, Semliki Forest virus, and Theiler's virus in mice; visna in sheep; herpes simplex in rabbits (Dal Canto and Rabinowitz, 1982). Therefore, in order to understand the pathogenesis of MS, it is most appropriate to study an animal model of virus-induced demyelination such as Theiler's virus infection. Theiler's virus infection in mice represents not only an excellent model for the study of the patho-genesis of MS but also a model system for studying disease susceptibility factors, mechanisms of viral persistence within the CNS, and mechanisms of virus-induced autoimmune disease.
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