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The final paper discussed this month reports that an EBV transcription factor occupies a large number of the MS genetic risk variants and this may at least partly explain how EBV infection and genetic risk intersect to cause MS. To assess whether a confounder could independently lead to EBV infection and MS, seropositivity to CMV was tested, because CMV infection displays very similar epidemiology to EBV infection. The association between Epstein-Barr virus (EBV) and multiple sclerosis (MS) has been known for many years. [Extracted from the article]

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Multiple sclerosis (MS) with onset in childhood offers a unique opportunity to study the infectious background of this disease but the immune reactions against infectious agents in such children have only recently been investigated. These and other epidemiological studies strongly implicate involvement of one or more infectious agents in the aetiology of MS, with Epstein-Barr virus (EBV) being the prime candidate. Rather than being the actual cause of MS, it is more probable that these agents are involved in the development of immunoregulatory pathways. These pathways, if disturbed by hygiene-related factors including an altered sequence of infections, may generate and maintain a deficit within the immunological network that facilitates, to particular early events in the development of MS, preceding the onset of MS disease by years or a decade. A framework that can serve as a guide for further epidemiological, immunologic and molecular biologic investigations is formulated. This approach may shed light on the complex natural history of MS and may lead to rational preventive and therapeutic strategies. It is possible that, in the future, MS could be prevented by vaccination against EBV in early childhood; the framework is of relevance to the design of an appropriate type of vaccine. [ABSTRACT FROM AUTHOR]