ArticleGenome medicine2019
Evidence from genome wide association studies implicates reduced control of Epstein-Barr virus infection in multiple sclerosis susceptibility.
Article in Genome medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 56 citations in OpenAlex.
- Why Is MS a More Frequent Complication of EBV Infection in Females?Immunological reviews · 2026Review
- CRISPR Screens Reveal Epstein-Barr Virus-activated JunB as a Key Lymphoblastoid B cell Dependency Factor that Represses Cyclin Dependent Kinase Inhibitor P18INK4c.bioRxiv : the preprint server for biology · 2026Article
- Epstein-Barr Virus Transformed B Cells From Systemic Lupus Erythematosus and Multiple Sclerosis Patients Differ in EBV Lytic and Latency Marker Expression.Immunity, inflammation and disease · 2026Article
- Incorporation of Epstein-Barr viral variation implicates significance of Latent Membrane Protein 1 in survival prediction and prognostic subgrouping in Burkitt lymphoma.International journal of cancer · 2025Article
- Clinical features and risk factors for Epstein-Barr virus-associated encephalitis: a retrospective cohort study.Virology journal · 2025Article
- A disease-specific convergence of host and Epstein-Barr virus genetics in multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Exploring the role of EBV in multiple sclerosis pathogenesis through EBV interactome.Frontiers in immunology · 2025Article
- New insights on the link between Epstein‑Barr virus infection and cognitive decline in neurodegenerative diseases (Review).Experimental and therapeutic medicine · 2024Review
- Genetics of immune response to Epstein-Barr virus: prospects for multiple sclerosis pathogenesis.Brain : a journal of neurology · 2024Article
- Adverse Childhood Experiences and the Risk of Multiple Sclerosis Development: A Review of Potential Mechanisms.International journal of molecular sciences · 2024Review
- Role of 14-3-3 protein family in the pathobiology of EBV in immortalized B cells and Alzheimer's disease.Frontiers in molecular biosciences · 2024Article
- Epstein-Barr Virus and Multiple Sclerosis: A Convoluted Interaction and the Opportunity to Unravel Predictive Biomarkers.International journal of molecular sciences · 2023Review
- The interaction between Epstein-Barr virus and multiple sclerosis genetic risk loci: insights into disease pathogenesis and therapeutic opportunities.Clinical & translational immunology · 2023Review
- Comprehensive Investigations Relationship Between Viral Infections and Multiple Sclerosis Pathogenesis.Current microbiology · 2022Review
- KARAJ: An Efficient Adaptive Multi-Processor Tool to Streamline Genomic and Transcriptomic Sequence Data Acquisition.International journal of molecular sciences · 2022Article
- The low abundance of CpG in the SARS-CoV-2 genome is not an evolutionarily signature of ZAP.Scientific reports · 2022Article
- Prevention of MS Requires Intervention on the Causes of the Disease: Reconciling Genes, Epigenetics, and Epstein Barr Virus.Frontiers in neurology · 2022Article
- Antibodies from Multiple Sclerosis Brain Identified Epstein-Barr Virus Nuclear Antigen 1 & 2 Epitopes which Are Recognized by Oligoclonal Bands.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Article
- SMAD1 as a biomarker and potential therapeutic target in drug-resistant multiple myeloma.Biomarker research · 2021Article
- The Interaction of Human andInternational journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGenome wide association studies have identified > 200 susceptibility loci accounting for much of the heritability of multiple sclerosis (MS). Epstein-Barr virus (EBV), a memory B cell tropic virus, has been identified as necessary but not sufficient for development of MS. The molecular and immunological basis for this has not been established. Infected B cell proliferation is driven by signalling through the EBV produced cell surface protein LMP1, a homologue of the MS risk gene CD40.
methodsWe have investigated transcriptomes of B cells and EBV-infected B cells at Latency III (LCLs) and identified MS risk genes with altered expression on infection and with expression levels associated with the MS risk genotype (LCLeQTLs). The association of LCLeQTL genomic burden with EBV phenotypes in vitro and in vivo was examined. The risk genotype effect on LCL proliferation with CD40 stimulation was assessed.
resultsThese LCLeQTL MS risk SNP:gene pairs (47 identified) were over-represented in genes dysregulated between B and LCLs (p < 1.53 × 10
conclusionsThese data indicate targeting EBV may be of therapeutic benefit in MS.
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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.