| http://purl.uniprot.org/citations/16501100 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16501100 | http://www.w3.org/2000/01/rdf-schema#comment | "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."xsd:string |
| http://purl.uniprot.org/citations/16501100 | http://purl.org/dc/terms/identifier | "doi:10.1128/jvi.80.6.2913-2923.2006"xsd:string |
| http://purl.uniprot.org/citations/16501100 | http://purl.uniprot.org/core/author | "Gale M. Jr."xsd:string |
| http://purl.uniprot.org/citations/16501100 | http://purl.uniprot.org/core/author | "Fredericksen B.L."xsd:string |
| http://purl.uniprot.org/citations/16501100 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
| http://purl.uniprot.org/citations/16501100 | http://purl.uniprot.org/core/name | "J Virol"xsd:string |
| http://purl.uniprot.org/citations/16501100 | http://purl.uniprot.org/core/pages | "2913-2923"xsd:string |
| http://purl.uniprot.org/citations/16501100 | http://purl.uniprot.org/core/title | "West Nile virus evades activation of interferon regulatory factor 3 through RIG-I-dependent and -independent pathways without antagonizing host defense signaling."xsd:string |
| http://purl.uniprot.org/citations/16501100 | http://purl.uniprot.org/core/volume | "80"xsd:string |
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