{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T13:28:54Z","timestamp":1787059734604,"version":"build-2736575974"},"reference-count":49,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:00:00Z","timestamp":1787011200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:00:00Z","timestamp":1787011200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["32473013 (J.P.) 32272992 (J.P.) 31772775 (J.P.)"],"award-info":[{"award-number":["32473013 (J.P.) 32272992 (J.P.) 31772775 (J.P.)"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Postgraduate Reaserch and Practice Innovation Program of Jiangsu Province","award":["KYCX25_1012"],"award-info":[{"award-number":["KYCX25_1012"]}]},{"name":"Xinjiang Uygur Autonomous Region Major Science and Technology Project-Xinjiang Animal Disease Prevention and Control System Quality Improvement Project","award":["2023A02007"],"award-info":[{"award-number":["2023A02007"]}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2026,8,18]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>Influenza A viruses (IAVs) pose an ongoing threat to humans and other species because of their zoonotic potential. Accumulating evidence has demonstrated that certain long non-coding RNAs (lncRNAs) exhibit differential expression during viral infection and modulate diverse facets of viral pathogenesis. As key regulatory RNAs, lncRNAs participate in fundamental physiological processes and disease progression via a wide array of functional interactions with DNA, RNA, and proteins. Here, we identified ckATP1A1-AS1 as an antiviral host lncRNA that is induced by IAV infection. Functional analyses demonstrated that ckATP1A1-AS1 overexpression restricted infection by multiple IAV subtypes, whereas ckATP1A1-AS1 knockdown enhanced viral replication. Mechanistically, during IAV infection, the transcription factor JUN transcriptionally activates ckATP1A1-AS1, which further enhances the expression of interferon-\u03b2 and key interferon-stimulated genes, thereby positively regulating type I interferon immune responses. Furthermore, ckATP1A1-AS1 interacts directly with the viral nucleoprotein, competitively disrupting its binding to importin \u03b15, impairing its oligomerization, and blocking the nuclear import of viral ribonucleoprotein complexes. Consequently, ckATP1A1-AS1 suppresses viral ribonucleoprotein assembly and reduces viral polymerase activity. These findings establish ckATP1A1-AS1 as a key antiviral lncRNA that restricts IAV replication by coordinating innate immune signaling and directly targeting several steps in the viral replication cycle.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>Accumulating evidence indicates that host long non-coding RNAs (lncRNAs) play important roles in regulating virus\u2013host interactions during influenza A virus (IAV) infection. However, the functions and mechanisms of action of most IAV-associated lncRNAs remain unclear. This study identifies the novel chicken antisense lncRNA ckATP1A1-AS1 as a key antiviral factor with a unique dual mechanism: it is transcriptionally activated by transcription factor JUN and, in turn, upregulates the expression of interferon-\u03b2 and key interferon-stimulated genes to positively regulate the type I interferon immune response. It directly interacts with viral nucleoprotein, competitively disrupting the binding of nucleoprotein to importin \u03b15 and impairing nucleoprotein oligomerization, thereby suppressing viral ribonucleoprotein assembly and reducing viral polymerase activity.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/jvi.00259-26","type":"journal-article","created":{"date-parts":[[2026,7,24]],"date-time":"2026-07-24T13:00:26Z","timestamp":1784898026000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["LncRNA ckATP1A1-AS1 inhibits influenza A virus replication by mediating innate immune responses and suppressing viral nuclear 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