{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T23:09:58Z","timestamp":1793315398675,"version":"4.5.0"},"reference-count":55,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2006,3,15]],"date-time":"2006-03-15T00:00:00Z","timestamp":1142380800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2006,3,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>The ability of viruses to control and\/or evade the host antiviral response is critical to the establishment of a productive infection. We have previously shown that West Nile virus NY (WNV-NY) delays activation of interferon regulatory factor 3 (IRF-3), a transcription factor critical to the initiation of the antiviral response. Here we demonstrate that the delayed activation of IRF-3 is essential for WNV-NY to achieve maximum virus production. Furthermore, WNV-NY utilizes a unique mechanism to control activation of IRF-3. In contrast to many other viruses that impose a nonspecific block to the IRF-3 pathway, WNV-NY eludes detection by the host cell at early times postinfection. To better understand this process, we assessed the role of the pathogen recognition receptor (PRR) retinoic acid-inducible gene I (RIG-I) in sensing WNV-NY infection. RIG-I null mouse embryo fibroblasts (MEFs) retained the ability to respond to WNV-NY infection; however, the onset of the host response was delayed compared to wild-type (WT) MEFs. This suggests that RIG-I is involved in initially sensing WNV-NY infection, while other PRRs sustain and\/or amplify the host response later in infection. The delayed initiation of the host response correlated with an increase in WNV-NY replication in RIG-I null MEFs compared to WT MEFs. Our data suggest that activation of the host response by RIG-I early in infection is important for controlling replication of WNV-NY. Furthermore, pathogenic strains of WNV may have evolved to circumvent stimulation of the host response until after replication is well under way.<\/jats:p>","DOI":"10.1128\/jvi.80.6.2913-2923.2006","type":"journal-article","created":{"date-parts":[[2006,2,24]],"date-time":"2006-02-24T20:47:54Z","timestamp":1140814074000},"page":"2913-2923","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":172,"title":["West Nile Virus Evades Activation of Interferon Regulatory Factor 3 through RIG-I-Dependent and -Independent Pathways without Antagonizing Host Defense Signaling"],"prefix":"10.1128","volume":"80","author":[{"given":"Brenda L.","family":"Fredericksen","sequence":"first","affiliation":[{"name":"Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, 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