Evidence mapPaperPMID 39390260Full record

ReviewNature reviews. Rheumatology2024

Epstein-Barr virus as a potentiator of autoimmune diseases.

William H Robinson, Shady Younis, Zelda Z Love, Lawrence Steinman, Tobias V Lanz

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

70 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. EBV Triggers a Distinct Antiviral Response in HMC3 Cells.bioRxiv : the preprint server for biology · 2026
    Article
  13. EBV Genome Variations and Association With Diseases.Journal of medical virology · 2026
    Review
  14. Review
  15. Review
  16. Article
  17. Multiple molecular mimics in Epstein Barr Nuclear Antigen-1, and the pathogenesis of multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  18. Review
  19. Article
  20. Article

10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

William H RobinsonDivision of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA, USA. wrobins@stanford.edu.ORCID http://orcid.org/0000-0003-4385-704X
Shady YounisDivision of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA, USA.
Zelda Z LoveDivision of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA, USA.
Lawrence SteinmanDepartment of Neurology and Neurological Sciences and Paediatrics, Stanford University School of Medicine, Stanford, CA, USA.
Tobias V LanzDivision of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Epstein-Barr virus (EBV) is epidemiologically associated with development of autoimmune diseases, including systemic lupus erythematosus, Sjögren syndrome, rheumatoid arthritis and multiple sclerosis. Although there is well-established evidence for this association, the underlying mechanistic basis remains incompletely defined. In this Review, we discuss the role of EBV infection as a potentiator of autoimmune rheumatic diseases. We review the EBV life cycle, viral transcription programmes, serological profiles and lytic reactivation. We discuss the epidemiological and mechanistic associations of EBV with systemic lupus erythematosus, Sjögren syndrome, rheumatoid arthritis and multiple sclerosis. We describe the potential mechanisms by which EBV might promote autoimmunity, including EBV nuclear antigen 1-mediated molecular mimicry of human autoantigens; EBV-mediated B cell reprogramming, including EBV nuclear antigen 2-mediated dysregulation of autoimmune susceptibility genes; EBV and host genetic factors, including the potential for autoimmunity-promoting strains of EBV; EBV immune evasion and insufficient host responses to control infection; lytic reactivation; and other mechanisms. Finally, we discuss the therapeutic implications and potential therapeutic approaches to targeting EBV for the treatment of autoimmune disease.

Indexed as

Autoimmune DiseasesEpstein-Barr Virus InfectionsHerpesvirus 4, HumanHumansLupus Erythematosus, SystemicSjogren's Syndrome

Identifiers

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.