There is abundant evidence that HHV-6A has an etiopathologic role in MS [for review, see Ref. (74)]. HHV-6A infects astrocytes via the CD46, thereby interfering with complement regulation (13, 14), in much the same way as is proposed here for RPE cells. Furthermore, it has recently been postulated that HHV-6A also interacts with Epstein–Barr virus in the CNS of MS patients leading to B-cell transformation and production of oligoclonal immunoglobulins that are typical for MS (12). This evidence concerns the gene CD46 and myeloid sarcoma.