Different mechanisms related to EBV and HHV-6 replication may explain the onset and relapsing of MS, including TLR-4 activation, inflammation, expansion of M1 macrophages and Th-17 cells, molecular mimicry, infiltration of autoreactive T cells and antibodies, neuroinflammation, and breakdown of myelin sheaths. This evidence concerns the gene TLR4 and myeloid sarcoma.