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The underlying molecular mechanisms are unclear. Here, we examined mediation through differential DNA methylation (DNAm) to better understand possible epigenetic programming.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n Two case\u2010control studies (Ausimmune Study, Australia\u2009=\u2009206 cases\u2009+\u2009348 controls; and Epidemiologic Investigations of MS [EIMS], Sweden\u2009=\u2009140 cases\u2009+\u2009139 controls). DNAm was measured using Illumina arrays. Dimension\u2010reduction methods generated MS\u2010associated DNAm modules. Pathway enrichment analyses were used to describe DNAm modules\u2019 system\u2010level biological characteristics. Individual and joint associations with MS risk were assessed using logistic regression. DNAm module mediation of risk factor\u2010outcome associations were assessed using mediation analysis. A range of temporality analyses were used.<\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n EBV indices (infectious mononucleosis history and anti\u2010EBNA IgG titer), lower 25(OH)D, low sun exposure, and\n HLA\u2010DRB1*1501<\/jats:italic>\n risk variant were individually and jointly associated with MS risk. In each study, 2 DNAm modules were found which mediated multiple exposure\u2010MS associations. Proportions mediated ranged from 21 to 47% in Ausimmune and 25 to 53% in EIMS. Results were robust to sensitivity analyses. Top\u2010ranked genomewide association study (GWAS) MS risk\u2010associated genes were over\u2010represented in both Ausimmune DNAm modules, A1 3.5\u2010fold (\n p<\/jats:italic>\n \u2009=\u20090.004) and A2 3\u2010fold (\n p<\/jats:italic>\n \u2009=\u20090.015). Reactome pathways enriched for DNAm had cross\u2010study overlap \u2013 45% of pathways enriched in Ausimmune DNAm modules were also enriched in EIMS (4.82\u2010fold,\n p<\/jats:italic>\n \u2009<\u20090.001).\n <\/jats:p>\n <\/jats:sec>\n \n Interpretation<\/jats:title>\n \n EBV, lower vitamin D, low sun exposure, and\n HLA\u2010DRB1*1501<\/jats:italic>\n risk variant act in concert and through common epigenetic pathways to impact MS onset risk. ANN NEUROL 2026;99:341\u2013355\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/ana.78043","type":"journal-article","created":{"date-parts":[[2025,10,10]],"date-time":"2025-10-10T11:21:08Z","timestamp":1760095268000},"page":"341-355","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Epstein\u2013Barr Virus, Lower Vitamin D, Low Sun Exposure, and\n \n HLA<\/scp>\n \u2010\n DRB1<\/scp>\n *1501\n <\/i>\n Risk Variant Share Common Epigenetic Pathways Leading to Multiple Sclerosis Onset"],"prefix":"10.1002","volume":"99","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6521-3056","authenticated-orcid":false,"given":"Steve","family":"Simpson\u2010Yap","sequence":"first","affiliation":[{"name":"The Florey Institute of Neuroscience and Mental Health, The University of Melbourne Parkville VIC Australia"},{"name":"Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne Carlton VIC 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