{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T20:46:21Z","timestamp":1790196381612,"version":"4.1.0"},"reference-count":40,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T00:00:00Z","timestamp":1770163200000},"content-version":"vor","delay-in-days":3,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,2,1]],"date-time":"2026-02-01T00:00:00Z","timestamp":1769904000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Medical Virology"],"published-print":{"date-parts":[[2026,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Zika virus (ZIKV) infection is known to cause microcephaly in newborns, and its outbreaks have previously emerged as a global public health crisis. The lack of a preventive vaccine or specific antiviral drugs underscores the urgency of investigating the detailed mechanisms of pathogenesis. We identified that interferon\u2010induced protein 44 (IFI44) is significantly upregulated following ZIKV infection, but its role in ZIKV pathogenesis remains unclear. Using A549 and 2FTGH cells, we established ZIKV\u2010infected cell models and employed quantitative real\u2010time PCR and Western blotting to demonstrate that IFI44 overexpression suppressed ZIKV replication, whereas IFI44 knockdown via specific small interfering RNA promoted viral replication. Mechanistically, IFI44 inhibited early\u2010stage ZIKV infection, including viral attachment and entry into host cells. Further analyses revealed that IFI44 promoted IFN\u2010\u03b2 expression, triggering activation of the Jak\/STAT signaling pathway\u2014as evidenced by increased phosphorylated STAT1 (p\u2010STAT1), enhanced interferon\u2010stimulated response element activity, and upregulated the downstream interferon\u2010stimulated genes (MX1, OAS2, IFIT2, and RIG\u2010I). Collectively, these findings demonstrate that ZIKV infection induced IFI44 expression, which acts as a positive feedback regulator of the Jak\/STAT pathway to restrict viral replication. Our results establish IFI44 as a key component of the host antiviral response against ZIKV, highlighting its potential as a therapeutic target.<\/jats:p>","DOI":"10.1002\/jmv.70827","type":"journal-article","created":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T12:45:46Z","timestamp":1770209146000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["IFI44 Functions as a Positive Regulator of Type I Interferon Signaling to Restrict Zika Virus Infection"],"prefix":"10.1002","volume":"98","author":[{"given":"Mingshuang","family":"Lai","sequence":"first","affiliation":[{"name":"The Joint Laboratory on Transfusion\u2010Transmitted Diseases (TTDs) Between Institute of Blood Transfusion Chinese Academy of Medical Sciences and Nanning Blood Center, Nanning Blood Center Nanning China"},{"name":"Institute of Blood Transfusion Chinese Academy of Medical Sciences &amp; Peking Union Medical College Chengdu 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