SrasV1, PubMed, Checkpoint, bibRecord, 001432

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 : 001432 ( PubMed/Checkpoint ); précédent : 001431; suivant : 001433

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.

Auteurs : Xiaolu Lu [République populaire de Chine] ; Ji'An Pan ; Jiali Tao ; Deyin Guo

Source :

Virus genes [ 1572-994X ] ; 2011.

RBID : pubmed:20976535

Descripteurs français

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:

Links toward previous steps (curation, corpus...)

to stream PubMed, to step Corpus: 001603
to stream PubMed, to step Curation: 001603

Links to Exploration step

pubmed:20976535

Le document en format XML

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<front><div type="abstract" xml:lang="en">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.</div>
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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.

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.

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