Linked Life Data

20130065

Source:http://linkedlifedata.com/resource/pubmed/id/20130065

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2010-3-22
pubmed:abstractText
The rabies virus Ni-CE strain causes nonlethal infection in adult mice after intracerebral inoculation, whereas the parental Nishigahara (Ni) strain kills mice. We previously reported that the chimeric CE(NiN) strain with the N gene from the Ni strain in the genetic background of the Ni-CE strain kills adult mice, indicating that the N gene is related to the different pathogenicities of Ni and Ni-CE strains. In the present study, to obtain an insight into the mechanism by which the N gene determines viral pathogenicity, we compared the effects of Ni, Ni-CE, and CE(NiN) infections on host gene expressions using a human neuroblastoma cell line. Microarray analysis of these infected cells revealed that the expression levels of particular genes in Ni- and CE(NiN)-infected cells, including beta interferon (IFN-beta) and chemokine genes (i.e., CXCL10 and CCL5) were lower than those in Ni-CE-infected cells. We also demonstrated that Ni-CE infection activated the interferon regulatory factor 3 (IRF-3)-dependent IFN-beta promoter and induced IRF-3 nuclear translocation more efficiently than did Ni or CE(NiN) infection. Furthermore, we showed that Ni-CE infection, but not Ni or CE(NiN) infection, strongly activates the IRF-3 pathway through activation of RIG-I, which is known as a cellular sensor of virus infection. These findings indicate that the N protein of rabies virus (Ni strain) has a function to evade the activation of RIG-I. To our knowledge, this is the first report that the Mononegavirales N protein functions to evade induction of host IFN and chemokines.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/CCL5 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/CXCL10 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL5, http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL10, 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/Interferon Regulatory Factor-3, http://linkedlifedata.com/resource/pubmed/chemical/Interferon-beta, http://linkedlifedata.com/resource/pubmed/chemical/Nucleoproteins, http://linkedlifedata.com/resource/pubmed/chemical/Viral Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Virulence Factors
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1098-5514
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4002-12
pubmed:dateRevised
2010-10-4
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Rabies virus nucleoprotein functions to evade activation of the RIG-I-mediated antiviral response.
pubmed:affiliation
Laboratory of Zoonotic Diseases, Faculty of Applied Biological Sciences, Gifu University, 1-1 Yanagido, Gifu 501-1193, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't