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However, IFN levels must be fine-tuned to achieve antiviral efficacy while limiting hyperinflammatory and tissue-damaging effects. Here, we report that NAT10, a histone and cytidine acetyltransferase, regulates the production of type I IFNs and RNA virus infections. Depletion of NAT10 increased the expression of IFN-\u03b2 and IFN-stimulated genes, and correspondingly impaired viral replication. Mechanistically, NAT10 dynamically associated with the IFN-\u03b2 promoter and also negatively regulated IRF3\u2019s chromatin associations through modulation of long noncoding RNAs that inhibit IRF3. Treatment of cells with Remodelin, a NAT10 inhibitor, similarly increased IFN-\u03b2 expression and inhibited viral infections. Overall, our findings reveal NAT10 is a potential host-directed target for antiviral treatment via regulation of type I IFN.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>Type I interferons (IFNs) signaling pathway is critical to cellular defense and innate immunity against evading pathogens, including viruses. However, induction of type I IFNs is fine-tuned to achieve the antiviral consequence while maintaining host cellular homeostasis. This paper presents a novel mechanism for the NAT10 protein to silence IFN-\u03b2 induction through modulation of IRF3 activity at the promoter of IFN-\u03b2, and further demonstrates the therapeutic potential of the NAT10 inhibitor Remodelin to restrict viral infection while inducing IFN-\u03b2.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.01452-26","type":"journal-article","created":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T13:03:20Z","timestamp":1785848600000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":1,"title":["NAT10 is critical to block RNA sensing-induced IFN-\u03b2 transactivation in viral infection"],"prefix":"10.1128","volume":"17","author":[{"given":"Youngmin","family":"Park","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00rs6vg23","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Pathology, College of Medicine, The Ohio State 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