In view of the observations described above, EBV is very likely to have a role in the pathogenesis of MS and, more- over, it might influence also the clinical course of the dis- ease. A number of hypotheses on the mechanism of this re- lationship have been suggested; however, each of these is supported by conflicting evidence (Table 4). Several ob- servations indicate that EBV itself cannot be regarded as the underlying cause of MS, or else the existence of cofac- tors must be presumed between the virus and the disease. These include, for example, the unexplained observation that the incidence of MS is lower among individuals relo- cating from a high-risk region to a lower risk domicile later than childhood. Another example is the MS epidemic that
afflicted the Faroe Islands between 1943 and 1960 – four years after the occupation by the British troops in 1940. Considering that EBV was present already in the population of the island before the arrival of the soldiers, some acti- vating infectious agent, or the introduction of a different strain of EBV could be held responsible for the epidemic. In recent studies of Simon et al. [31], however, findings do indicate that variation in EBNA1 N-terminus, EBNA1 C-terminus or LMP1 contributes to MS risk.