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Infectious Agents in Multiple Sclerosis: Viral Triggers, Antibody-Mediated Autoimmunity, and Parasitic

Dafni F T Frohman1, Stella E Tsirka2

  • 1Department of Neurology, Mount Sinai Morningside/West, New York, NY 10019, USA.

Biomolecules
|June 26, 2026
PubMed

Insights

Viral infections like Epstein-Barr virus may trigger multiple sclerosis (MS) through immune responses. Conversely, parasitic infections show potential neuroprotective effects, offering new avenues for MS treatment strategies.

Area of Science:

  • Neuroimmunology
  • Infectious Immunology
  • Central Nervous System Disorders

Background:

  • Multiple sclerosis (MS) is a chronic immune-mediated central nervous system disease.
  • Environmental factors, particularly infections, are increasingly recognized as key players in MS.
  • Epstein-Barr virus (EBV) is implicated in MS pathogenesis via molecular mimicry and B-cell issues.

Purpose of the Study:

  • To review antibody-driven mechanisms of viral-induced autoimmunity in MS.
  • To contrast these with parasite-induced immunoregulatory pathways.
  • To explore diagnostic and therapeutic implications for MS treatment.

Main Methods:

  • Review of scientific literature on infectious agents and MS.
  • Analysis of immune mechanisms involved in viral and parasitic infections.
  • Examination of antibody-mediated autoimmunity and immune tolerance.

Main Results:

  • Viral infections, notably EBV, can promote MS autoimmunity through specific immune responses.
  • Parasitic infections demonstrate neuroprotective potential by inducing immune tolerance.
  • Contrasting these pathogen-host interactions offers insights into MS pathogenesis.

Conclusions:

  • Understanding infectious triggers and protective mechanisms is crucial for MS.
  • Novel therapeutic strategies for MS may emerge from studying host-pathogen immune interactions.
  • Targeting immune pathways informed by infectious immunology holds promise for MS treatment.
Keywords:
Epstein–Barr virusantibodieshelminthshygiene hypothesisimmune regulationmolecular mimicrymultiple sclerosisneuroinflammation

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