Epstein-Barr virus and multiple sclerosis.

  title={Epstein-Barr virus and multiple sclerosis.},
  author={William H. Robinson and Lawrence Steinman},
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
If EBV is a “driver” of MS by inducing antiviral immunity with associated autoimmunity, elimination of EBV may be a rational therapy for MS.
Herpesvirus Vaccines
The Special Issue titled "Herpesvirus Vaccines" contains different articles and a review regarding veterinary and human herpesviruses [...].
Involvement of age-associated B cells in EBV-triggered autoimmunity
This commentary highlights the involvement of age-associated B cells, a B cell population defined as CD19+CD11c+CD21−T-bet+, in the process of EBV-triggered autoimmunity, and modifies ABCs, so as to function pathogenically in autoimmune diseases Apart from EBV elimination, targeting of ABCs may also bring therapeutic benefits to autoimmune patients.
Immune Privilege Furnishes a Niche for Latent Infection
This review summarises how immune privilege in the CNS may be permissive for latent infection and allow the eye and the brain to act as a reservoir of pathogens which often remain undetected for the lifetime of the host but in states of immune deficiency may be activated to cause sight- and life-threatening inflammation.
Role of Helical Structure in MBP Immunodominant Peptides for Efficient IgM Antibody Recognition in Multiple Sclerosis
This work investigates the importance of the helical structure in antibody recognition by MBP peptides of different lengths and synthesized the peptide MBP (81–106) and observed that its elongation at both N- and C-termini improves IgM antibody recognition in SP-ELISA, but destabilizes the helicals structure.
The Human Myelin Proteome and Sub-Metalloproteome Interaction Map: Relevance to Myelin-Related Neurological Diseases
The presented PPI dataset could provide a useful resource to the scientific community to further the understanding of human myelin biology and serve as a basis for future studies of myelin-related neurological diseases and particular autoimmune diseases such as multiple sclerosis where myelin epitopes are implicated.
The Potential for EBV Vaccines to Prevent Multiple Sclerosis
Assessment of vaccine efficacy with MS being a delayed consequence of EBV infection with the average age of onset being approximately 30 years of age represents multiple challenges.


Molecular mimicry between Anoctamin 2 and Epstein-Barr virus nuclear antigen 1 associates with multiple sclerosis risk
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.
Epstein–Barr virus latent genes
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
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.
Early events in lupus humoral autoimmunity suggest initiation through molecular mimicry
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
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.
Environmental risk factors for multiple sclerosis. Part I: The role of infection
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.
Amino acid homology between the encephalitogenic site of myelin basic protein and virus: mechanism for autoimmunity.
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.