Epstein-Barr virus and multiple sclerosis.

@article{Robinson2022EpsteinBarrVA,
  title={Epstein-Barr virus and multiple sclerosis.},
  author={William H. Robinson and Lawrence Steinman},
  journal={Science},
  year={2022},
  pages={
          eabm7930
        }
}
Infection with Epstein-Barr virus is the trigger for the development of multiple sclerosis. 
Epstein-Barr virus as a driver of multiple sclerosis
  • L. Sollid
  • Medicine, Psychology
    Science Immunology
  • 2022
TLDR
If EBV is a “driver” of MS by inducing antiviral immunity with associated autoimmunity, elimination of EBV may be a rational therapy for MS.
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Role of Helical Structure in MBP Immunodominant Peptides for Efficient IgM Antibody Recognition in Multiple Sclerosis
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TLDR
The presence of ANO2 reactivity associates with a high MS risk, in particular together with HLA risk variants and high EBNA1 antibody titers, which is considered a strong argument for its relevance in MS ethiopathogenesis.
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The persistence of these viral genomes in all malignant cells, yet with the expression of limited latent genes, is consistent with the notion that EBV latent genes are important for malignant cell growth.
Epstein-Barr Functional Mimicry: Pathogenicity of Oncogenic Latent Membrane Protein-1 in Systemic Lupus Erythematosus and Autoimmunity
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Examination of the expression of LMP1 in the context of EBNA-1 may interact to increase immune dysregulation that leads to pathogenic, autoantigen-specific lupus inflammation, suggesting that a combination of EBV and genetic factors may be required to drive l upus-associated renal disease.
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The hypothesis that some humoral autoimmunity in human lupus arises through molecular mimicry between EBNA-1 and l upus autoantigens is supported and further evidence to suspect an etiologic role for Epstein-Barr virus in SLE is provided.
Autoantibodies from patients with systemic lupus erythematosus bind a shared sequence of SmD and Epstein‐Barr virus‐encoded nuclear antigen EBNA I
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Sera from immunized animals displayed the same pattern of reactivity of spontaneously produced anti‐SmD antibodies, suggesting that molecular mimicry may play a role in the induction of anti-SmD autoantibodies.
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TLDR
It is shown that whereas EBV stands out as the only infectious agent that can explain many of the key features of MS epidemiology, by itself the link between EBV and MS cannot explain the decline in risk among migrants from high to low MS prevalence areas, which implies that either EBV strains in low‐risk areas have less propensity to cause MS, or that other infectious or noninfectious factors modify the host response to EBV or otherwise contribute to determine MS risk.
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TLDR
Rabbit central nervous system tissue taken from these rabbits had a histologic picture reminiscent of experimental allergic encephalomyelitis, indicating that viral infection may trigger the production of antibodies and mononuclear cells that cross-react with self proteins by a mechanism termed molecular mimicry.
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