Viral infections, particularly Epstein-Barr virus, promote autoimmunity in multiple sclerosis, whereas parasitic infections appear to exert neuroprotective immunoregulatory effects.
This review highlights the contrasting roles of infectious agents in MS, where viral pathogens like EBV trigger autoimmunity and parasitic infections may offer neuroprotective immunomodulation.
Multiple sclerosis (MS) is a chronic immune-mediated disease of the central nervous system characterized by demyelination, neuroinflammation, and progressive neurodegeneration. While there is a small component of genetic susceptibility to MS risk, environmental factors, including infectious exposures, are gaining increased recognition as playing a critical role in MS initiation and progression. Viral infections, especially by Epstein–Barr virus (EBV), have emerged as strong candidates and triggers of MS symptoms, through antibody-mediated molecular mimicry and B-cell dysregulation. In contrast, parasitic infections, including helminths and select protozoa, appear to exert neuroprotective effects by skewing immune responses toward regulation and tolerance. In this review, we examine antibody-driven mechanisms by which viral pathogens promote autoimmunity in MS and contrast these with parasite-induced immunoregulatory pathways that suppress pathogenic inflammation. We further discuss diagnostic and therapeutic implications, highlighting how insights from infectious immunology may inform novel strategies for MS treatment.
Frohman et al. (Thu,) conducted a review in Multiple sclerosis. Viral and parasitic infections was evaluated. Viral infections, particularly Epstein-Barr virus, promote autoimmunity in multiple sclerosis, whereas parasitic infections appear to exert neuroprotective immunoregulatory effects.