ArticleProceedings of the National Academy of Sciences of the United States of America2026
Multiple molecular mimics in Epstein Barr Nuclear Antigen-1, and the pathogenesis of multiple sclerosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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Who cites it
5 citing papers in PubMed.
- "Home": How Immune Cells Enter the Central Nervous System.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- The EBNA-1 Conundrum: Does Epstein-Barr Virus Invoke Autoimmune Pathology in a Population Subset by Poorly Purine-Loading Its Major Latency-Maintaining Transcript?Scandinavian journal of immunology · 2026Review
- Decoding the association between microorganisms and autoimmunity: a multifaceted review of evidence on specific pathogens that trigger autoimmune diseases.Clinical and experimental medicine · 2026Review
- Infectious Agents in Multiple Sclerosis: Viral Triggers, Antibody-Mediated Autoimmunity, and Parasitic Immunomodulation.Biomolecules · 2026Review
- Aquaporin-5-specific heavy chain VDJ knock-in (A5H) mice reveal molecular mimicry-driven initiation and diversification of autoreactive B-cell responses.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The Epstein-Barr virus (EBV) infects greater than 95% of humans and is associated with initiating and perpetuating multiple sclerosis (MS). Antibody to Epstein-Barr Nuclear Antigen-1 (EBNA1) is present in nearly 100% of patients with MS before the development of clinical symptoms. Infection with EBV is necessary, but not sufficient, for causation of disease. Within the EBNA1 transcription factor is a stretch of 47 amino acids containing three regions with shared linear sequences of portions of three molecules, Glialcell adhesion molecule (CAM), alpha Crystallin-B, and Anoctamin-2. These cross-reactive linear sequences between EBNA1 and each of these three molecules are termed "molecular mimics." Cross-reactive adaptive immunity to these three molecules mimicking regions of EBNA1 each play distinct roles in the pathogenesis of MS. Antibodies to each of these molecules greatly increase the chance of developing MS. Analysis of the cellular landscape of MS lesions reveals EBNA1 in B cells, glial cells, and neurons. Here, we provide commentary on recent publications on the molecular and cellular landscape of EBV infection in studies on the blood, cerebrospinal fluid, and brain specimens of individuals with MS. The published studies reveal perspectives on the pathology of MS in detail ranging from the atomic level using crystallography to multiplexed anatomical imaging of lesions in the brain.
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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.