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Adv."],"published-print":{"date-parts":[[2026,6,5]]},"abstract":"<jats:p>\n                    Do viral infections accelerate aging, and does this acceleration scale with pathogenicity? Using transcriptomic aging clocks, we measured biological age in\n                    <jats:italic toggle=\"yes\">Drosophila melanogaster<\/jats:italic>\n                    infected with four enteric RNA viruses spanning a broad pathogenicity range (i.e., reduction of host lifespan). All pathogenic infections accelerated aging and the magnitude of acceleration tracked pathogenicity. This pattern held across oral and systemic infection routes and was conserved in\n                    <jats:italic toggle=\"yes\">Caenorhabditis elegans<\/jats:italic>\n                    where the nonpathogenic Orsay virus produced negligible aging acceleration. Pathway analysis indicated a systemic impact across aging hallmarks with virus- and tissue-specific signatures. Acceleration was comparable in females and males, but host context modulated the acceleration: The bacterial symbiont\n                    <jats:italic toggle=\"yes\">Wolbachia<\/jats:italic>\n                    mitigated the virus-induced aging. Notably, biological age remained elevated even after viral clearance. These results demonstrate that viruses act as age-distorters and link infection severity to lasting aging consequences, providing a quantitative framework for predicting long-term health effects of viral disease.\n                  <\/jats:p>","DOI":"10.1126\/sciadv.aec1735","type":"journal-article","created":{"date-parts":[[2026,6,5]],"date-time":"2026-06-05T17:59:36Z","timestamp":1780682376000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":1,"title":["Enteric viral infections promote systemic accelerated aging in\n                    <i>Drosophila<\/i>"],"prefix":"10.1126","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9588-1127","authenticated-orcid":true,"given":"Rub\u00e9n","family":"Gonz\u00e1lez","sequence":"first","affiliation":[{"name":"Institut Pasteur, Viruses and RNA Interference Unit, Universit\u00e9 Paris Cit\u00e9, Paris, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-7732-046X","authenticated-orcid":true,"given":"Mauro","family":"Castell\u00f3-Sanju\u00e1n","sequence":"additional","affiliation":[{"name":"Institut Pasteur, Viruses and RNA Interference Unit, Universit\u00e9 Paris Cit\u00e9, Paris, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8593-4117","authenticated-orcid":true,"given":"Maria-Carla","family":"Saleh","sequence":"additional","affiliation":[{"name":"Institut Pasteur, Viruses and RNA Interference Unit, Universit\u00e9 Paris Cit\u00e9, Paris, France."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"221","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.78.11.7124"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1093\/gerona\/gls233"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/acel.12601"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.3389\/fgene.2019.00263"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1007\/s11357-022-00613-4"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1002850"},{"key":"e_1_3_2_8_2","doi-asserted-by":"crossref","first-page":"e0127511","DOI":"10.1371\/journal.pone.0127511","article-title":"Chronic hepatitis B virus infection: The relation between hepatitis b antigen expression, telomere length, senescence, inflammation and fibrosis","volume":"10","author":"Tachtatzis P. 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