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The elusive link: EBV in MS
Svetlana P Eckert1,2, Gabriela Funez-DePagnier1, Mark D Hicar3
1Jacobs Comprehensive MS Treatment and Research Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA.
Expert Review of Clinical Immunology
|August 1, 2026
Summary
Epstein-Barr Virus (EBV) infection is linked to Multiple Sclerosis (MS) risk. Understanding EBV
Area of Science:
- Neuroimmunology
- Virology
- Epidemiology
Background:
- The established link between Epstein-Barr Virus (EBV) infection and Multiple Sclerosis (MS) risk necessitates further investigation into the underlying pathogenic mechanisms.
- The complex interplay of EBV subtypes, host immunity, and environmental factors contributes to the unclear relationship between EBV and MS development.
Purpose of the Study:
- To review the molecular mechanisms by which EBV may contribute to MS pathogenesis across relapsing-remitting and progressive disease.
- To explore how MS risk factors and disease-modifying therapies (DMTs) interact with EBV and influence MS pathophysiology.
Main Methods:
- Literature search of PubMed and Medline databases.
- Keywords included 'Epstein-Barr Virus,' 'Multiple Sclerosis,' 'disease-modifying therapies,' and 'EBV activity.'
- Synthesis of evidence to address EBV's role in MS pathophysiology and treatment efficacy.
Main Results:
- EBV's molecular contribution to MS pathogenesis is explored across different MS types.
- The influence of MS risk factors and the efficacy of DMTs are examined in the context of EBV activity.
- The review addresses how EBV may explain the effects of certain risk factors and treatment outcomes.
Conclusions:
- Targeting EBV infection and replication is crucial for discovering an MS cure.
- Suppression of EBV protein expression and targeting viral reservoirs are key strategies to prevent MS disease activity, progression, and neurodegeneration.
- Addressing EBV is vital for managing MS, considering genetic factors and immune-mediated damage.
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