Severe acute respiratory syndrome coronavirus M protein inhibits type I interferon production by impeding the formation of TRAF3.TANK.TBK1/IKKepsilon complex.
Identifieur interne : 002A21 ( Main/Exploration ); précédent : 002A20; suivant : 002A22Severe acute respiratory syndrome coronavirus M protein inhibits type I interferon production by impeding the formation of TRAF3.TANK.TBK1/IKKepsilon complex.
Auteurs : Kam-Leung Siu [Hong Kong] ; Kin-Hang Kok ; Ming-Him James Ng ; Vincent K M. Poon ; Kwok-Yung Yuen ; Bo-Jian Zheng ; Dong-Yan JinSource :
- The Journal of biological chemistry [ 0021-9258 ] ; 2009.
Descripteurs français
- KwdFr :
- Cellules HeLa, Facteur-3 associé aux récepteurs de TNF (métabolisme), Facteur-3 de régulation d'interféron (métabolisme), Humains, I-kappa B Kinase (métabolisme), Interféron de type I (génétique), Interféron de type I (immunologie), Phosphorylation, Protein-Serine-Threonine Kinases (métabolisme), Protéines adaptatrices de la transduction du signal (métabolisme), Protéines de la matrice virale (immunologie), Protéines de la matrice virale (métabolisme), Rein (cytologie), Régulation de l'expression des gènes (immunologie), Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (virologie), Transduction du signal (immunologie), Virus du SRAS (immunologie).
- MESH :
- cytologie : Rein.
- génétique : Interféron de type I.
- immunologie : Interféron de type I, Protéines de la matrice virale, Régulation de l'expression des gènes, Syndrome respiratoire aigu sévère, Transduction du signal, Virus du SRAS.
- métabolisme : Facteur-3 associé aux récepteurs de TNF, Facteur-3 de régulation d'interféron, I-kappa B Kinase, Protein-Serine-Threonine Kinases, Protéines adaptatrices de la transduction du signal, Protéines de la matrice virale.
- virologie : Syndrome respiratoire aigu sévère.
- Cellules HeLa, Humains, Phosphorylation.
English descriptors
- KwdEn :
- Adaptor Proteins, Signal Transducing (metabolism), Gene Expression Regulation (immunology), HeLa Cells, Humans, I-kappa B Kinase (metabolism), Interferon Regulatory Factor-3 (metabolism), Interferon Type I (genetics), Interferon Type I (immunology), Kidney (cytology), Phosphorylation, Protein-Serine-Threonine Kinases (metabolism), SARS Virus (immunology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (virology), Signal Transduction (immunology), TNF Receptor-Associated Factor 3 (metabolism), Viral Matrix Proteins (immunology), Viral Matrix Proteins (metabolism).
- MESH :
- chemical , genetics : Interferon Type I.
- chemical , immunology : Interferon Type I, Viral Matrix Proteins.
- chemical , metabolism : Adaptor Proteins, Signal Transducing, I-kappa B Kinase, Interferon Regulatory Factor-3, Protein-Serine-Threonine Kinases, TNF Receptor-Associated Factor 3, Viral Matrix Proteins.
- cytology : Kidney.
- immunology : Gene Expression Regulation, SARS Virus, Severe Acute Respiratory Syndrome, Signal Transduction.
- virology : Severe Acute Respiratory Syndrome.
- HeLa Cells, Humans, Phosphorylation.
Abstract
Severe acute respiratory syndrome (SARS) coronavirus is highly pathogenic in humans and evades innate immunity at multiple levels. It has evolved various strategies to counteract the production and action of type I interferons, which mobilize the front-line defense against viral infection. In this study we demonstrate that SARS coronavirus M protein inhibits gene transcription of type I interferons. M protein potently antagonizes the activation of interferon-stimulated response element-dependent transcription by double-stranded RNA, RIG-I, MDA5, TBK1, IKKepsilon, and virus-induced signaling adaptor (VISA) but has no influence on the transcriptional activity of this element when IRF3 or IRF7 is overexpressed. M protein physically associates with RIG-I, TBK1, IKKepsilon, and TRAF3 and likely sequesters some of them in membrane-associated cytoplasmic compartments. Consequently, the expression of M protein prevents the formation of TRAF3.TANK.TBK1/IKKepsilon complex and thereby inhibits TBK1/IKKepsilon-dependent activation of IRF3/IRF7 transcription factors. Taken together, our findings reveal a new mechanism by which SARS coronavirus circumvents the production of type I interferons.
DOI: 10.1074/jbc.M109.008227
PubMed: 19380580
Affiliations:
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Le document en format XML
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Poon</name></author><author><name sortKey="Yuen, Kwok Yung" sort="Yuen, Kwok Yung" uniqKey="Yuen K" first="Kwok-Yung" last="Yuen">Kwok-Yung Yuen</name></author><author><name sortKey="Zheng, Bo Jian" sort="Zheng, Bo Jian" uniqKey="Zheng B" first="Bo-Jian" last="Zheng">Bo-Jian Zheng</name></author><author><name sortKey="Jin, Dong Yan" sort="Jin, Dong Yan" uniqKey="Jin D" first="Dong-Yan" last="Jin">Dong-Yan Jin</name></author></analytic><series><title level="j">The Journal of biological chemistry</title><idno type="ISSN">0021-9258</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptor Proteins, Signal Transducing (metabolism)</term><term>Gene Expression Regulation (immunology)</term><term>HeLa Cells</term><term>Humans</term><term>I-kappa B Kinase (metabolism)</term><term>Interferon Regulatory Factor-3 (metabolism)</term><term>Interferon Type I (genetics)</term><term>Interferon Type I (immunology)</term><term>Kidney (cytology)</term><term>Phosphorylation</term><term>Protein-Serine-Threonine Kinases (metabolism)</term><term>SARS Virus (immunology)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (virology)</term><term>Signal Transduction (immunology)</term><term>TNF Receptor-Associated Factor 3 (metabolism)</term><term>Viral Matrix Proteins (immunology)</term><term>Viral Matrix Proteins (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Cellules HeLa</term><term>Facteur-3 associé aux récepteurs de TNF (métabolisme)</term><term>Facteur-3 de régulation d'interféron (métabolisme)</term><term>Humains</term><term>I-kappa B Kinase (métabolisme)</term><term>Interféron de type I (génétique)</term><term>Interféron de type I (immunologie)</term><term>Phosphorylation</term><term>Protein-Serine-Threonine Kinases (métabolisme)</term><term>Protéines adaptatrices de la transduction du signal (métabolisme)</term><term>Protéines de la matrice virale (immunologie)</term><term>Protéines de la matrice virale (métabolisme)</term><term>Rein (cytologie)</term><term>Régulation de l'expression des gènes (immunologie)</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Syndrome respiratoire aigu sévère (virologie)</term><term>Transduction du signal (immunologie)</term><term>Virus du SRAS (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interferon Type I</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Interferon Type I</term><term>Viral Matrix Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term><term>I-kappa B Kinase</term><term>Interferon Regulatory Factor-3</term><term>Protein-Serine-Threonine Kinases</term><term>TNF Receptor-Associated Factor 3</term><term>Viral Matrix Proteins</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Rein</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Kidney</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Interféron de type I</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Interféron de type I</term><term>Protéines de la matrice virale</term><term>Régulation de l'expression des gènes</term><term>Syndrome respiratoire aigu sévère</term><term>Transduction du signal</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Gene Expression Regulation</term><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur-3 associé aux récepteurs de TNF</term><term>Facteur-3 de régulation d'interféron</term><term>I-kappa B Kinase</term><term>Protein-Serine-Threonine Kinases</term><term>Protéines adaptatrices de la transduction du signal</term><term>Protéines de la matrice virale</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>HeLa Cells</term><term>Humans</term><term>Phosphorylation</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules HeLa</term><term>Humains</term><term>Phosphorylation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) coronavirus is highly pathogenic in humans and evades innate immunity at multiple levels. It has evolved various strategies to counteract the production and action of type I interferons, which mobilize the front-line defense against viral infection. In this study we demonstrate that SARS coronavirus M protein inhibits gene transcription of type I interferons. M protein potently antagonizes the activation of interferon-stimulated response element-dependent transcription by double-stranded RNA, RIG-I, MDA5, TBK1, IKKepsilon, and virus-induced signaling adaptor (VISA) but has no influence on the transcriptional activity of this element when IRF3 or IRF7 is overexpressed. M protein physically associates with RIG-I, TBK1, IKKepsilon, and TRAF3 and likely sequesters some of them in membrane-associated cytoplasmic compartments. Consequently, the expression of M protein prevents the formation of TRAF3.TANK.TBK1/IKKepsilon complex and thereby inhibits TBK1/IKKepsilon-dependent activation of IRF3/IRF7 transcription factors. Taken together, our findings reveal a new mechanism by which SARS coronavirus circumvents the production of type I interferons.</div></front></TEI><affiliations><list><country><li>Hong Kong</li></country></list><tree><noCountry><name sortKey="Jin, Dong Yan" sort="Jin, Dong Yan" uniqKey="Jin D" first="Dong-Yan" last="Jin">Dong-Yan Jin</name><name sortKey="Kok, Kin Hang" sort="Kok, Kin Hang" uniqKey="Kok K" first="Kin-Hang" last="Kok">Kin-Hang Kok</name><name sortKey="Ng, Ming Him James" sort="Ng, Ming Him James" uniqKey="Ng M" first="Ming-Him James" last="Ng">Ming-Him James Ng</name><name sortKey="Poon, Vincent K M" sort="Poon, Vincent K M" uniqKey="Poon V" first="Vincent K M" last="Poon">Vincent K M. Poon</name><name sortKey="Yuen, Kwok Yung" sort="Yuen, Kwok Yung" uniqKey="Yuen K" first="Kwok-Yung" last="Yuen">Kwok-Yung Yuen</name><name sortKey="Zheng, Bo Jian" sort="Zheng, Bo Jian" uniqKey="Zheng B" first="Bo-Jian" last="Zheng">Bo-Jian Zheng</name></noCountry><country name="Hong Kong"><noRegion><name sortKey="Siu, Kam Leung" sort="Siu, Kam Leung" uniqKey="Siu K" first="Kam-Leung" last="Siu">Kam-Leung Siu</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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