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Previous EBV infection is associated with autoimmune and neoplastic disease\n                    <jats:sup>4<\/jats:sup>\n                    . Still, the biological basis of host control during EBV persistence remains unclear. Here we report the identification of non-genetic and genetic factors that are associated with EBV control during persistent infection. Using blood-based genome sequence data from 486,315 UK Biobank and\u00a0336,123 All of Us participants, we identified short-read pairs mapping to the EBV genome in 16.2% and 21.8% of individuals, respectively. EBV read detection (EBVread\n                    <jats:sup>+<\/jats:sup>\n                    ) reflects increased viral load in blood cells, as shown by orthogonal measurements, and was associated with HIV infection, immunosuppressive drug\u00a0intake and current smoking. Genome-wide analyses of EBVread\n                    <jats:sup>+<\/jats:sup>\n                    identified strong associations at the major histocompatibility complex (MHC), including 54\u00a0independent human leukocyte antigen (HLA) alleles of MHC classes I and II, and\u00a0at 27 genomic regions outside MHC. Epistasis with distinct HLA alleles of MHC\u00a0class I was observed at the\n                    <jats:italic>ERAP2<\/jats:italic>\n                    locus. Analysis of individuals with EBV-associated diseases\n                    <jats:sup>4<\/jats:sup>\n                    revealed a higher polygenic burden of EBVread\n                    <jats:sup>+<\/jats:sup>\n                    for HLA alleles at MHC class I in multiple sclerosis (driven by HLA-A*02:01) and at MHC class II in rheumatoid arthritis. Phenome-wide analyses identified a polygenic overlap of EBVread\n                    <jats:sup>+<\/jats:sup>\n                    with inflammatory bowel disease, hypothyroidism and type 1 diabetes. Our study establishes by-products of human genome sequencing as a surrogate marker of EBV viral load. This will facilitate investigation and treatment for EBV and other persistent viral infections.\n                  <\/jats:p>","DOI":"10.1038\/s41586-026-10274-4","type":"journal-article","created":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T16:02:14Z","timestamp":1771516934000},"page":"444-454","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Host control of persistent Epstein\u2013Barr virus infection"],"prefix":"10.1038","volume":"653","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9780-7243","authenticated-orcid":false,"given":"Axel","family":"Schmidt","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T. 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