Epstein–Barr virus infection and Human Leukocyte Antigen Class II allele DRB1*1501 increase the risk of developing multiple sclerosis, an autoimmune disease of the central nervous system. Human endogenous retroviral envelope proteins, molecular mimicry and neuroinflammation have been linked to multiple sclerosis. While the pathology of multiple sclerosis has been well-studied, the molecular and cellular mechanisms underlying interactions between the different predisposing factors in its etiology are unclear and are addressed here in an overarching hypothesis. Besides advancing understanding of multiple sclerosis etiology and promoting further research, this may generate new approaches for treating multiple sclerosis.
Ranjan Ramasamy (Mon,) studied this question.