http://purl.uniprot.org/citations/17977974 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/17977974 | http://www.w3.org/2000/01/rdf-schema#comment | "RIG-I and MDA5, two related pathogen recognition receptors (PRRs), are known to be required for sensing various RNA viruses. Here we investigated the roles that RIG-I and MDA5 play in eliciting the antiviral response to West Nile virus (WNV). Functional genomics analysis of WNV-infected fibroblasts from wild-type mice and RIG-I null mice revealed that the normal antiviral response to this virus occurs in two distinct waves. The initial response to WNV resulted in the expression of interferon (IFN) regulatory factor 3 target genes and IFN-stimulated genes, including several subtypes of alpha IFN. Subsequently, a second phase of IFN-dependent antiviral gene expression occurred very late in infection. In cells lacking RIG-I, both the initial and the secondary responses to WNV were delayed, indicating that RIG-I plays a critical role in initiating innate immunity against WNV. However, another PRR(s) was able to trigger a response to WNV in the absence of RIG-I. Disruption of both MDA5 and RIG-I pathways abrogated activation of the antiviral response to WNV, suggesting that MDA5 is involved in the host's defense against WNV infection. In addition, ablation of the function of IPS-1, an essential RIG-I and MDA5 adaptor molecule, completely disabled the innate antiviral response to WNV. Our data indicate that RIG-I and MDA5 are responsible for triggering downstream gene expression in response to WNV infection by signaling through IPS-1. We propose a model in which RIG-I and MDA5 operate cooperatively to establish an antiviral state and mediate an IFN amplification loop that supports immune effector gene expression during WNV infection."xsd:string |
http://purl.uniprot.org/citations/17977974 | http://purl.org/dc/terms/identifier | "doi:10.1128/jvi.01305-07"xsd:string |
http://purl.uniprot.org/citations/17977974 | http://purl.uniprot.org/core/author | "Gale M. Jr."xsd:string |
http://purl.uniprot.org/citations/17977974 | http://purl.uniprot.org/core/author | "Katze M.G."xsd:string |
http://purl.uniprot.org/citations/17977974 | http://purl.uniprot.org/core/author | "Fredericksen B.L."xsd:string |
http://purl.uniprot.org/citations/17977974 | http://purl.uniprot.org/core/author | "Keller B.C."xsd:string |
http://purl.uniprot.org/citations/17977974 | http://purl.uniprot.org/core/author | "Fornek J."xsd:string |
http://purl.uniprot.org/citations/17977974 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
http://purl.uniprot.org/citations/17977974 | http://purl.uniprot.org/core/name | "J Virol"xsd:string |
http://purl.uniprot.org/citations/17977974 | http://purl.uniprot.org/core/pages | "609-616"xsd:string |
http://purl.uniprot.org/citations/17977974 | http://purl.uniprot.org/core/title | "Establishment and maintenance of the innate antiviral response to West Nile Virus involves both RIG-I and MDA5 signaling through IPS-1."xsd:string |
http://purl.uniprot.org/citations/17977974 | http://purl.uniprot.org/core/volume | "82"xsd:string |
http://purl.uniprot.org/citations/17977974 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17977974 |
http://purl.uniprot.org/citations/17977974 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/17977974 |
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http://purl.uniprot.org/uniprot/#_Q3U0Y5-mappedCitation-17977974 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17977974 |
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