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EBV Infection and Multiple Sclerosis: Lessons from a Marmoset Model.
Bert A 'tHart1, Yolanda S Kap2, Elena Morandi3
1Department of Immunobiology, Biomedical Primate Research Centre (BPRC), Rijswijk, The Netherlands; University of Groningen, University Medical Center, Department of Neuroscience, Groningen, The Netherlands.
Trends in Molecular Medicine
|November 13, 2016
Summary
Epstein-Barr virus (EBV) infection may trigger multiple sclerosis (MS) by altering how the immune system processes antigens. This mechanism explains how a common virus contributes to this autoimmune disease.
Area of Science:
- Neuroimmunology
- Virology
- Autoimmunity
Background:
- Multiple sclerosis (MS) pathogenesis involves genetic and environmental factors.
- Epstein-Barr virus (EBV) is a significant infectious risk factor for MS.
- The link between high EBV prevalence and low MS incidence requires explanation.
Purpose of the Study:
- To investigate the mechanism by which EBV infection may contribute to MS pathogenesis.
- To explore the role of EBV in initiating autoimmune responses in the central nervous system.
Main Methods:
- Utilized marmosets with experimental autoimmune encephalomyelitis (EAE), a primate model for MS.
- Analyzed the interaction between EBV infection, antigen processing, and immune cell activation.
Main Results:
- EBV infection induces peptide citrullination and autophagy during antigen processing.
- This process enables B cells to cross-present autoantigen to specific T cells.
Conclusions:
- EBV infection can equip B cells to initiate an autoimmune attack on the central nervous system.
- This mechanism provides a potential explanation for EBV's role in MS progression.
