ArticleProceedings of the National Academy of Sciences of the United States of America2025
Antibody reactivity against EBNA1 and GlialCAM differentiates multiple sclerosis patients from healthy controls.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Elusive B Cell Antigen in Multiple Sclerosis: Time to Rethink CNS B Cell Functions.International journal of molecular sciences · 2025Pooled it
- EBNA1Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- The Impact of Antigen Presentation on BBB Disruption and Neuroinflammation.Physiology (Bethesda, Md.) · 2026Review
- HLA-dependent association between EBNA1 antibody levels and disability progression in multiple sclerosis.Journal of neurology, neurosurgery, and psychiatry · 2026Article
- Viral subversion of B-cell tolerance: mechanisms linking infection to autoimmunity.EMBO reports · 2026Review
- "Home": How Immune Cells Enter the Central Nervous System.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Proinflammatory Epstein-Barr Virus Antibody Functions Track with Disease Activity in Multiple Sclerosis.Annals of neurology · 2026Article
- Epstein-Barr Virus and Multiple Sclerosis: Mechanistic Insights into Virus-Driven Autoimmunity.Microorganisms · 2026Review
- CD4Science translational medicine · 2026Article
- Infectious Agents in Multiple Sclerosis: Viral Triggers, Antibody-Mediated Autoimmunity, and Parasitic Immunomodulation.Biomolecules · 2026Review
- Viral associations in multiple sclerosis: pathogenetic mechanisms and therapeutic implications.Virology journal · 2026Review
- Memory Impairments: Type, Causes, and Molecular Players-Memory Dysfunction Across Neurologic Insults.Cells · 2026Review
- Detection of Diagnostic Antibodies in Immune-Mediated Diseases: A Focus on Antigens and Technologies.Chembiochem : a European journal of chemical biology · 2026Review
- Why Is MS a More Frequent Complication of EBV Infection in Females?Immunological reviews · 2026Review
- Epstein-Barr Virus and Multiple Sclerosis: A Narrative Review on Prevention and the Concept of an Infection-Driven Disease.Biomedicines · 2026Review
- Article
- EBV genome analysis in multiple sclerosis shows extensive viral diversity and links to autoimmunity.NAR molecular medicine · 2026Article
- 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 · 2026Article
- EBV Dysregulation Is Associated With Immune Imbalance in Multiple Sclerosis: Evidence From Integrated Viral and Host Analyses.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- EBV reprograms autoreactive anti-CNS B cells as antigen presenting cells in multiple sclerosis.bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Multiple sclerosis (MS) is an autoimmune demyelinating disorder of the central nervous system (CNS), which is linked to Epstein-Barr virus (EBV) infection, preceding the disease. The molecular mechanisms underlying this connection are only partially understood. We previously described molecular mimicry between the EBV transcription factor EBV nuclear antigen 1 (EBNA1) and three human CNS proteins: anoctamin-2 (ANO2), alpha-B crystallin (CRYAB), and glial cellular adhesion molecule (GlialCAM). Here, we investigated antibody responses against EBNA1 and GlialCAM in a large cohort of 650 MS patients and 661 matched population controls and compared them to responses against CRYAB and ANO2. We confirmed that elevated IgG responses against EBNA1 and all three CNS-mimic antigens associate with increased MS risk. Blocking experiments confirmed the presence of cross-reactive antibodies and molecular mimicry between EBNA1 and GlialCAM, and accompanying antibody responses against adjacent peptide regions of GlialCAM suggest epitope spreading. Antibody responses against EBNA1, GlialCAM, CRYAB, and ANO2 are elevated in MS patients carrying the main risk allele
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Registered trials
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 OpenQuestion graph.