{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T21:00:59Z","timestamp":1788382859449,"version":"build-2803163510"},"reference-count":62,"publisher":"National Academy of Sciences","issue":"32","license":[{"start":{"date-parts":[[2026,8,6]],"date-time":"2026-08-06T00:00:00Z","timestamp":1785974400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000057","name":"HHS | NIH | National Institute of General Medical Sciences","doi-asserted-by":"publisher","award":["GM159612"],"award-info":[{"award-number":["GM159612"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["AI166116"],"award-info":[{"award-number":["AI166116"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2026,8,11]]},"abstract":"<jats:p>\n                    Innate immune recognition shapes infection outcomes by linking microbial detection to host defense. Although pattern recognition receptors are classified by the ligands they detect (lipids, peptidoglycans, or nucleic acids) cross-talk between these pathways is increasingly recognized.\n                    <jats:italic toggle=\"yes\">Staphylococcus aureus<\/jats:italic>\n                    , a major cause of skin and soft tissue infections, can persist intracellularly, evading immunity and antibiotics. Here, we describe a lipid-based immune evasion strategy in which the\n                    <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                    enzyme oleate hydratase (OhyA) converts host fatty acids into hydroxylated lipids that antagonize TLR3\u2013TRIF\u2013IRF7 signaling, a pathway activated by double-stranded RNA. Deletion of\n                    <jats:italic toggle=\"yes\">ohyA<\/jats:italic>\n                    unleashed this pathway, triggering rapid bacterial clearance, whereas loss of TLR3, TRIF, or IRF7 restored bacterial persistence, establishing a noncanonical antibacterial role for an antiviral signaling pathway. These findings identify a previously unrecognized interface between bacterial lipid metabolism and antiviral immune machinery, highlighting how pathogens manipulate cross-kingdom signaling to evade intracellular immunity.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2620143123","type":"journal-article","created":{"date-parts":[[2026,8,6]],"date-time":"2026-08-06T17:49:18Z","timestamp":1786038558000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":1,"title":["A bacterial fatty acid enzyme hijacks nucleic acid\u2013sensing Toll-like receptor signaling"],"prefix":"10.1073","volume":"123","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-9452-357X","authenticated-orcid":false,"given":"William A.","family":"Lathram","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02k3smh20","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology, Immunology, and Molecular Genetics, University of 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