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Volume 4
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10.3390/sclerosis4020014
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This is an early access version, the complete PDF, HTML, and XML versions will be available soon.
Perspective

Oligodendrocyte Dysfunction to Immune Pathology in Multiple Sclerosis: A Conspiracy of Herpesviruses?

by
Richard C. Cipian
1,†,
Bert A. ’t Hart
2,*,†,
Christine Masztak
3,
Abbas Karimi
4,
Mohammad Taghizadeh
4 and
Moses Rodriguez
5
1
Department of Philosophy, California State University, Los Angeles, CA 90032, USA
2
Department of Anatomy and Neurosciences, Amsterdam University Medical Center (VUMC), de Boelelaan 1108, 1081HZ Amsterdam, The Netherlands
3
Department of Neurology, Mercy St. Vincent Hospital, 2213 Cherry St., Toledo, OH 43608, USA
4
Molecular Medicine Department, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz 5165665931, Iran
5
Department of Neurology and Immunology, Mayo Clinic Medical and Graduate School, Rochester, MN 55905, USA
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Sclerosis 2026, 4(2), 14; https://doi.org/10.3390/sclerosis4020014 (registering DOI)
Submission received: 30 March 2026 / Revised: 23 May 2026 / Accepted: 17 June 2026 / Published: 21 June 2026
Versions Notes

Abstract

Multiple sclerosis is an immune-driven neurological disease that affects myelinated axons in the central nervous system. However, the trigger of the (dysregulated) immune reactions is not known. According to Wilkin’s primary lesion theory, myelin-reactive T cells present in the immune repertoire hyper-react to myelin antigens that are released from idiopathic lesions within the central nervous system. However, neither the cause of the primary lesion nor the cause of the immune hyper-reactivity is known. We investigated whether these unknown activation signals may be relayed by common herpesviruses. In this concept paper, we propose the novel paradigm that the trigger of autoimmunity in MS comprises a conspiracy of three common herpesviruses: human herpesvirus-6A as a potential trigger of primary lesions due to its proven capacity to cause oligodendrogliopathy, cytomegalovirus as a trigger for the formation of effector memory cytotoxic T cells with proven capacity to induce multiple sclerosis pathology in a non-human primate MS model and Epstein−Barr Virus due to its capacity to render B cells capable to effectively present a critical myelin antigen to these effector memory cytotoxic T cells.
Keywords: EBV; CMV; HHV-6; oligodendrogliopathy; autoimmunity EBV; CMV; HHV-6; oligodendrogliopathy; autoimmunity

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MDPI and ACS Style

Cipian, R.C.; ’t Hart, B.A.; Masztak, C.; Karimi, A.; Taghizadeh, M.; Rodriguez, M. Oligodendrocyte Dysfunction to Immune Pathology in Multiple Sclerosis: A Conspiracy of Herpesviruses? Sclerosis 2026, 4, 14. https://doi.org/10.3390/sclerosis4020014

AMA Style

Cipian RC, ’t Hart BA, Masztak C, Karimi A, Taghizadeh M, Rodriguez M. Oligodendrocyte Dysfunction to Immune Pathology in Multiple Sclerosis: A Conspiracy of Herpesviruses? Sclerosis. 2026; 4(2):14. https://doi.org/10.3390/sclerosis4020014

Chicago/Turabian Style

Cipian, Richard C., Bert A. ’t Hart, Christine Masztak, Abbas Karimi, Mohammad Taghizadeh, and Moses Rodriguez. 2026. "Oligodendrocyte Dysfunction to Immune Pathology in Multiple Sclerosis: A Conspiracy of Herpesviruses?" Sclerosis 4, no. 2: 14. https://doi.org/10.3390/sclerosis4020014

APA Style

Cipian, R. C., ’t Hart, B. A., Masztak, C., Karimi, A., Taghizadeh, M., & Rodriguez, M. (2026). Oligodendrocyte Dysfunction to Immune Pathology in Multiple Sclerosis: A Conspiracy of Herpesviruses? Sclerosis, 4(2), 14. https://doi.org/10.3390/sclerosis4020014

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