Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-7-20
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
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
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
179
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1796-802
pubmed:dateRevised
2009-11-19
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
pubmed:year
2007
pubmed:articleTitle
Early innate immune responses to Sin Nombre hantavirus occur independently of IFN regulatory factor 3, characterized pattern recognition receptors, and viral entry.
pubmed:affiliation
Department of Pathology, Center for Infectious Diseases and Immunity, School of Medicine, University of New Mexico, Albuquerque, NM 87131, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural