SARS-CoV nucleocapsid protein antagonizes IFN-β response by targeting initial step of IFN-β induction pathway, and its C-terminal region is critical for the antagonism.
Identifieur interne : 002047 ( Main/Exploration ); précédent : 002046; suivant : 002048SARS-CoV nucleocapsid protein antagonizes IFN-β response by targeting initial step of IFN-β induction pathway, and its C-terminal region is critical for the antagonism.
Auteurs : Xiaolu Lu [République populaire de Chine] ; Ji'An Pan ; Jiali Tao ; Deyin GuoSource :
- Virus genes [ 1572-994X ] ; 2011.
Descripteurs français
- KwdFr :
- ARN viral (analyse), DEAD-box RNA helicases (immunologie), Délétion de séquence, Facteur-3 de régulation d'interféron (immunologie), Humains, Interféron bêta (immunologie), Interféron bêta (métabolisme), Lignée cellulaire, Poly I-C (immunologie), Protein-Serine-Threonine Kinases (immunologie), Protéines adaptatrices de la transduction du signal (immunologie), Protéines nucléocapside (immunologie), Récepteur de type Toll-3 (immunologie), Régions promotrices (génétique), Virus Sendai (immunologie), Virus du SRAS (immunologie), Virus du SRAS (pathogénicité).
- MESH :
- analyse : ARN viral.
- immunologie : DEAD-box RNA helicases, Facteur-3 de régulation d'interféron, Interféron bêta, Poly I-C, Protein-Serine-Threonine Kinases, Protéines adaptatrices de la transduction du signal, Protéines nucléocapside, Récepteur de type Toll-3, Virus Sendai, Virus du SRAS.
- métabolisme : Interféron bêta.
- pathogénicité : Virus du SRAS.
- Délétion de séquence, Humains, Lignée cellulaire, Régions promotrices (génétique).
English descriptors
- KwdEn :
- Adaptor Proteins, Signal Transducing (immunology), Cell Line, DEAD-box RNA Helicases (immunology), Humans, Interferon Regulatory Factor-3 (immunology), Interferon-beta (immunology), Interferon-beta (metabolism), Nucleocapsid Proteins (immunology), Poly I-C (immunology), Promoter Regions, Genetic, Protein-Serine-Threonine Kinases (immunology), RNA, Viral (analysis), SARS Virus (immunology), SARS Virus (pathogenicity), Sendai virus (immunology), Sequence Deletion, Toll-Like Receptor 3 (immunology).
- MESH :
- chemical , analysis : RNA, Viral.
- chemical , immunology : Adaptor Proteins, Signal Transducing, DEAD-box RNA Helicases, Interferon Regulatory Factor-3, Interferon-beta, Nucleocapsid Proteins, Poly I-C, Protein-Serine-Threonine Kinases, Toll-Like Receptor 3.
- chemical , metabolism : Interferon-beta.
- immunology : SARS Virus, Sendai virus.
- pathogenicity : SARS Virus.
- Cell Line, Humans, Promoter Regions, Genetic, Sequence Deletion.
Abstract
Severe acute respiratory syndrome coronavirus (SARS-CoV) encodes a highly basic nucleocapsid (N) protein which can inhibit the synthesis of type I interferon (IFN), but the molecular mechanism of this antagonism remains to be identified. In this study, we demonstrated that the N protein of SARS-CoV could inhibit IFN-beta (IFN-β) induced by poly(I:C) or Sendai virus. However, we found that N protein could not inhibit IFN-β production induced by overexpression of downstream signaling molecules of two important IFN-β induction pathways, toll-like receptor 3 (TLR3)- and RIG-I-like receptors (RLR)-dependent pathways. These results indicate that SARS-CoV N protein targets the initial step, probably the cellular PRRs (pattern recognition receptors)-RNAs-recognition step in the innate immune pathways, to suppress IFN expression responses. In addition, co-immunoprecipitation assays revealed that N protein did not interact with RIG-I or MDA5. Further, an assay using truncated mutants revealed that the C-terminal domain of N protein was critical for its antagonism of IFN induction, and the N deletion mutant impaired for RNA-binding almost completely lost the IFN-β antagonist activity. These results contribute to our further understanding of the pathogenesis of SARS-CoV.
DOI: 10.1007/s11262-010-0544-x
PubMed: 20976535
Affiliations:
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Le document en format XML
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In this study, we demonstrated that the N protein of SARS-CoV could inhibit IFN-beta (IFN-β) induced by poly(I:C) or Sendai virus. However, we found that N protein could not inhibit IFN-β production induced by overexpression of downstream signaling molecules of two important IFN-β induction pathways, toll-like receptor 3 (TLR3)- and RIG-I-like receptors (RLR)-dependent pathways. These results indicate that SARS-CoV N protein targets the initial step, probably the cellular PRRs (pattern recognition receptors)-RNAs-recognition step in the innate immune pathways, to suppress IFN expression responses. In addition, co-immunoprecipitation assays revealed that N protein did not interact with RIG-I or MDA5. Further, an assay using truncated mutants revealed that the C-terminal domain of N protein was critical for its antagonism of IFN induction, and the N deletion mutant impaired for RNA-binding almost completely lost the IFN-β antagonist activity. These results contribute to our further understanding of the pathogenesis of SARS-CoV.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country><region><li>Hubei</li></region><settlement><li>Wuhan</li></settlement><orgName><li>Université de Wuhan</li></orgName></list><tree><noCountry><name sortKey="Guo, Deyin" sort="Guo, Deyin" uniqKey="Guo D" first="Deyin" last="Guo">Deyin Guo</name><name sortKey="Pan, Ji An" sort="Pan, Ji An" uniqKey="Pan J" first="Ji'An" last="Pan">Ji'An Pan</name><name sortKey="Tao, Jiali" sort="Tao, Jiali" uniqKey="Tao J" first="Jiali" last="Tao">Jiali Tao</name></noCountry><country name="République populaire de Chine"><region name="Hubei"><name sortKey="Lu, Xiaolu" sort="Lu, Xiaolu" uniqKey="Lu X" first="Xiaolu" last="Lu">Xiaolu Lu</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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