Source:http://linkedlifedata.com/resource/pubmed/id/17641046
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2007-7-20
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pubmed:abstractText |
Sin Nombre virus (SNV) is a highly pathogenic New World virus and etiologic agent of hantavirus cardiopulmonary syndrome. We have previously shown that replication-defective virus particles are able to induce a strong IFN-stimulated gene (ISG) response in human primary cells. RNA viruses often stimulate the innate immune response by interactions between viral nucleic acids, acting as a pathogen-associated molecular pattern, and cellular pattern-recognition receptors (PRRs). Ligand binding to PRRs activates transcription factors which regulate the expression of antiviral genes, and in all systems examined thus far, IFN regulatory factor 3 (IRF3) has been described as an essential intermediate for induction of ISG expression. However, we now describe a model in which IRF3 is dispensable for the induction of ISG transcription in response to viral particles. IRF3-independent ISG transcription in human hepatoma cell lines is initiated early after exposure to SNV virus particles in an entry- and replication-independent fashion. Furthermore, using gene knockdown, we discovered that this activation is independent of the best-characterized RNA- and protein-sensing PRRs including the cytoplasmic caspase recruitment domain-containing RNA helicases and the TLRs. SNV particles engage a heretofore unrecognized PRR, likely located at the cell surface, and engage a novel IRF3-independent pathway that activates the innate immune response.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DDX58 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/DEAD-box RNA Helicases,
http://linkedlifedata.com/resource/pubmed/chemical/IRF3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/IRF7 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Regulatory Factor-3,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Regulatory Factor-7,
http://linkedlifedata.com/resource/pubmed/chemical/Interferons,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Virus,
http://linkedlifedata.com/resource/pubmed/chemical/TLR3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 3,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
179
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1796-802
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17641046-Carcinoma, Hepatocellular,
pubmed-meshheading:17641046-Cell Line, Tumor,
pubmed-meshheading:17641046-DEAD-box RNA Helicases,
pubmed-meshheading:17641046-Gene Expression Regulation, Viral,
pubmed-meshheading:17641046-Humans,
pubmed-meshheading:17641046-Immunity, Innate,
pubmed-meshheading:17641046-Interferon Regulatory Factor-3,
pubmed-meshheading:17641046-Interferon Regulatory Factor-7,
pubmed-meshheading:17641046-Interferons,
pubmed-meshheading:17641046-Receptors, Virus,
pubmed-meshheading:17641046-Sin Nombre virus,
pubmed-meshheading:17641046-Toll-Like Receptor 3,
pubmed-meshheading:17641046-Toll-Like Receptors,
pubmed-meshheading:17641046-Ultraviolet Rays,
pubmed-meshheading:17641046-Virion,
pubmed-meshheading:17641046-Virus Internalization,
pubmed-meshheading:17641046-Virus Replication
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pubmed:year |
2007
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pubmed:articleTitle |
Early innate immune responses to Sin Nombre hantavirus occur independently of IFN regulatory factor 3, characterized pattern recognition receptors, and viral entry.
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pubmed:affiliation |
Department of Pathology, Center for Infectious Diseases and Immunity, School of Medicine, University of New Mexico, Albuquerque, NM 87131, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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