{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T12:57:16Z","timestamp":1792155436255,"version":"4.4.0"},"reference-count":48,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2023,3,18]],"date-time":"2023-03-18T00:00:00Z","timestamp":1679097600000},"content-version":"vor","delay-in-days":17,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Medical Virology"],"published-print":{"date-parts":[[2023,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Increasing evidence suggests that natural antisense transcriptional lncRNAs regulate their adjacent coding genes to mediate diverse aspects of biology. Bioinformatics analysis of the previously identified antiviral gene\n                    <jats:italic>ZNFX1<\/jats:italic>\n                    revealed neighboring lncRNA\n                    <jats:italic>ZFAS1<\/jats:italic>\n                    transcribed on the opposite strand from\n                    <jats:italic>ZNFX1<\/jats:italic>\n                    . Whether\n                    <jats:italic>ZFAS1<\/jats:italic>\n                    exerts antiviral function via regulating the dsRNA sensor ZNFX1 is unknown. Here we found that\n                    <jats:italic>ZFAS1<\/jats:italic>\n                    was upregulated by RNA and DNA viruses and type I IFNs (IFN\u2010I) dependent on Jak\u2010STAT signaling, similar to the transcription regulation of\n                    <jats:italic>ZNFX1<\/jats:italic>\n                    . Knockdown of endogenous\n                    <jats:italic>ZFAS1<\/jats:italic>\n                    partially facilitated viral infection, while\n                    <jats:italic>ZFAS1<\/jats:italic>\n                    overexpression showed opposite effects. In addition, mice were more resistant to VSV infection with the delivery of human\n                    <jats:italic>ZFAS1<\/jats:italic>\n                    . We further observed that\n                    <jats:italic>ZFAS1<\/jats:italic>\n                    knockdown significantly inhibited IFNB1 expression and IFR3 dimerization, whereas\n                    <jats:italic>ZFAS1<\/jats:italic>\n                    overexpression positively regulated antiviral innate immune pathways. Mechanistically,\n                    <jats:italic>ZFAS1<\/jats:italic>\n                    positively regulated ZNFX1 expression and antiviral function by enhancing the protein stability of ZNFX1, thereby establishing a positive feedback loop to enhance antiviral immune activation status. In short,\n                    <jats:italic>ZFAS1<\/jats:italic>\n                    is a positive regulator of antiviral innate immune response via regulating its neighbor gene ZNFX1, adding new mechanistic insight into lncRNA\u2010mediated regulation of signaling in innate immunity.\n                  <\/jats:p>","DOI":"10.1002\/jmv.28637","type":"journal-article","created":{"date-parts":[[2023,3,9]],"date-time":"2023-03-09T07:57:52Z","timestamp":1678348672000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["ZNFX1 antisense RNA1 promotes antiviral innate immune responses via modulating ZNFX1 function"],"prefix":"10.1002","volume":"95","author":[{"given":"Xin","family":"Jia","sequence":"first","affiliation":[{"name":"School of Chinese Materia Medica Beijing University of Chinese Medicine Beijing 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