Only three pathogens bearing the two homologies on the same protein, which is postulated to be optimal for a co-operation of the corresponding T-cells, have been identified, namely, herpes simplex (1 and 2) virus (tegument protein), measles (nucleoprotein), and varicella (tegument). The MS-association of the serology of these pathogens (higher specific antibody concentration) [16] was confirmed in a recent study: herpes simplex-2, P \ 0.0001; measles, P \ 0.0001 and varicella, P \ 0.0001 [12] . The epidemiological evidence for the MS-association of the majority of the other pathogens in Table 3 is only weak and inconsistent. Moreover, a simultaneous occurrence of homologies to epitopes 1 and 2 was also found in a diverse range of pathogens causing respiratory and gastrointestinal infections and which have also been associated, beneficially and Specific T-cells directed against this region were found to be expanded in MS patients as compared to control individuals [36] ; the region with homologies in HHV-6 and CP proteins extends to EBNA1 amino acid position 640 * for identical amino acid; ? = conserved amino acid exchange; / = missing amino acid; arabic numbers for additional amino acids: 1 = DKK; 2 = PF; 3 = D detrimentally, with the risk of MS [48] [49] [50] . Likewise, unknown parasitic infections have recently been found to be associated with a reduced risk of MS [51] , and some parasitic organisms share the two homologies (Table 3 , footnote). In addition, preliminary studies indicate that parasite infections in MS patients lead to fewer exacerbations and this has been linked to the emergence of T reg s [52] . The relatively widespread occurrence of these two homologies explains, at least in part, why the infectious background of MS has proved so complex and difficult to define.