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Epstein-Barr virus and multiple sclerosis: Updating Pender's hypothesis
Martin Laurence1, Julián Benito-León2
1Shipshaw Labs, Montreal, Quebec, Canada.
Multiple Sclerosis and Related Disorders
|July 31, 2017
Summary
Epstein-Barr virus (EBV) infection is linked to multiple sclerosis (MS). EBV may trigger MS by enabling B cells to recognize self-antigens, even after the virus is cleared from the central nervous system.
Area of Science:
- Neuroimmunology
- Virology
- Epidemiology
Background:
- Substantial epidemiological evidence links Epstein-Barr virus (EBV) to multiple sclerosis (MS).
- EBV is typically acquired in childhood but MS develops in adulthood, with EBV latent for decades.
- Latent EBV resides in a small fraction of memory B cells.
Purpose of the Study:
- To review proposed mechanisms linking EBV to MS pathogenesis.
- To explore how EBV might contribute to the autoimmune response in MS.
Main Methods:
- Review of epidemiological and mechanistic studies on EBV and MS.
- Analysis of EBV latency, reactivation, and B cell interactions in the context of MS.
Main Results:
- EBV reactivation in the CNS is a proposed MS cause.
- EBV in B cells may induce recognition of 'forbidden' self-antigens.
- EBV absence in MS lesions is noted, challenging direct reactivation hypotheses.
Conclusions:
- EBV-free B cells, descended from EBV-infected precursors, may mediate MS autoimmunity.
- This mechanism explains MS development even without detectable EBV in CNS lesions.
- B cell involvement in MS supports EBV-related autoimmune triggers.
