Middle East respiratory syndrome coronavirus M protein suppresses type I interferon expression through the inhibition of TBK1-dependent phosphorylation of IRF3.
Identifieur interne : 000F85 ( Main/Exploration ); précédent : 000F84; suivant : 000F86Middle East respiratory syndrome coronavirus M protein suppresses type I interferon expression through the inhibition of TBK1-dependent phosphorylation of IRF3.
Auteurs : Pak-Yin Lui [République populaire de Chine] ; Lok-Yin Roy Wong [République populaire de Chine] ; Cheuk-Lai Fung [République populaire de Chine] ; Kam-Leung Siu [République populaire de Chine] ; Man-Lung Yeung [République populaire de Chine] ; Kit-San Yuen [République populaire de Chine] ; Chi-Ping Chan [République populaire de Chine] ; Patrick Chiu-Yat Woo [République populaire de Chine] ; Kwok-Yung Yuen [République populaire de Chine] ; Dong-Yan Jin [République populaire de Chine]Source :
- Emerging microbes & infections [ 2222-1751 ] ; 2016.
Descripteurs français
- KwdFr :
- Alignement de séquences, Arabie saoudite, Cellules HEK293, Coronavirus du syndrome respiratoire du Moyen-Orient (génétique), Coronavirus du syndrome respiratoire du Moyen-Orient (immunologie), Coronavirus du syndrome respiratoire du Moyen-Orient (pathogénicité), Coronavirus du syndrome respiratoire du Moyen-Orient (physiologie), Facteur-3 associé aux récepteurs de TNF (génétique), Facteur-3 associé aux récepteurs de TNF (immunologie), Facteur-3 de régulation d'interféron (génétique), Facteur-3 de régulation d'interféron (immunologie), Facteur-3 de régulation d'interféron (métabolisme), Humains, Immunité innée, Interféron de type I (antagonistes et inhibiteurs), Interféron de type I (biosynthèse), Interféron de type I (génétique), Interféron de type I (immunologie), Phosphorylation, Phosphotransferases, Protein-Serine-Threonine Kinases (génétique), Protein-Serine-Threonine Kinases (immunologie), Protein-Serine-Threonine Kinases (métabolisme), Protéine-58 à domaine DEAD (génétique), Protéines de la matrice virale (génétique), Protéines de la matrice virale (physiologie), Régulation de l'expression des gènes, Virus Sendai (génétique), Virus Sendai (immunologie), Virus du SRAS (génétique), Virus du SRAS (immunologie), Virus du SRAS (pathogénicité), Échappement immunitaire.
- MESH :
- antagonistes et inhibiteurs : Interféron de type I.
- biosynthèse : Interféron de type I.
- génétique : Coronavirus du syndrome respiratoire du Moyen-Orient, Facteur-3 associé aux récepteurs de TNF, Facteur-3 de régulation d'interféron, Interféron de type I, Protein-Serine-Threonine Kinases, Protéine-58 à domaine DEAD, Protéines de la matrice virale, Virus Sendai, Virus du SRAS.
- immunologie : Coronavirus du syndrome respiratoire du Moyen-Orient, Facteur-3 associé aux récepteurs de TNF, Facteur-3 de régulation d'interféron, Interféron de type I, Protein-Serine-Threonine Kinases, Virus Sendai, Virus du SRAS.
- métabolisme : Facteur-3 de régulation d'interféron, Protein-Serine-Threonine Kinases.
- pathogénicité : Coronavirus du syndrome respiratoire du Moyen-Orient, Virus du SRAS.
- physiologie : Coronavirus du syndrome respiratoire du Moyen-Orient, Protéines de la matrice virale.
- Alignement de séquences, Arabie saoudite, Cellules HEK293, Humains, Immunité innée, Phosphorylation, Phosphotransferases, Régulation de l'expression des gènes, Échappement immunitaire.
English descriptors
- KwdEn :
- DEAD Box Protein 58 (genetics), Gene Expression Regulation, HEK293 Cells, Humans, Immune Evasion, Immunity, Innate, Interferon Regulatory Factor-3 (genetics), Interferon Regulatory Factor-3 (immunology), Interferon Regulatory Factor-3 (metabolism), Interferon Type I (antagonists & inhibitors), Interferon Type I (biosynthesis), Interferon Type I (genetics), Interferon Type I (immunology), Middle East Respiratory Syndrome Coronavirus (genetics), Middle East Respiratory Syndrome Coronavirus (immunology), Middle East Respiratory Syndrome Coronavirus (pathogenicity), Middle East Respiratory Syndrome Coronavirus (physiology), Phosphorylation, Phosphotransferases, Protein-Serine-Threonine Kinases (genetics), Protein-Serine-Threonine Kinases (immunology), Protein-Serine-Threonine Kinases (metabolism), SARS Virus (genetics), SARS Virus (immunology), SARS Virus (pathogenicity), Saudi Arabia, Sendai virus (genetics), Sendai virus (immunology), Sequence Alignment, TNF Receptor-Associated Factor 3 (genetics), TNF Receptor-Associated Factor 3 (immunology), Viral Matrix Proteins (genetics), Viral Matrix Proteins (physiology).
- MESH :
- chemical , antagonists & inhibitors : Interferon Type I.
- chemical , biosynthesis : Interferon Type I.
- chemical , genetics : DEAD Box Protein 58, Interferon Regulatory Factor-3, Interferon Type I, Protein-Serine-Threonine Kinases, TNF Receptor-Associated Factor 3, Viral Matrix Proteins.
- chemical , immunology : Interferon Regulatory Factor-3, Interferon Type I, Protein-Serine-Threonine Kinases, TNF Receptor-Associated Factor 3.
- chemical , metabolism : Interferon Regulatory Factor-3, Protein-Serine-Threonine Kinases.
- genetics : Middle East Respiratory Syndrome Coronavirus, SARS Virus, Sendai virus.
- immunology : Middle East Respiratory Syndrome Coronavirus, SARS Virus, Sendai virus.
- pathogenicity : Middle East Respiratory Syndrome Coronavirus, SARS Virus.
- physiology : Middle East Respiratory Syndrome Coronavirus, Viral Matrix Proteins.
- Gene Expression Regulation, HEK293 Cells, Humans, Immune Evasion, Immunity, Innate, Phosphorylation, Phosphotransferases, Saudi Arabia, Sequence Alignment.
Abstract
Middle East respiratory syndrome coronavirus (MERS-CoV) infection has claimed hundreds of lives and has become a global threat since its emergence in Saudi Arabia in 2012. The ability of MERS-CoV to evade the host innate antiviral response may contribute to its severe pathogenesis. Many MERS-CoV-encoded proteins were identified to have interferon (IFN)-antagonizing properties, which correlates well with the reduced IFN levels observed in infected patients and ex vivo models. In this study, we fully characterized the IFN-antagonizing property of the MERS-CoV M protein. Expression of MERS-CoV M protein suppressed type I IFN expression in response to Sendai virus infection or poly(I:C) induction. This suppressive effect was found to be specific for the activation of IFN regulatory factor 3 (IRF3) but not nuclear factor-κB. MERS-CoV M protein interacted with TRAF3 and disrupted TRAF3-TBK1 association leading to reduced IRF3 activation. M proteins from MERS-CoV and SARS-CoV have three highly similar conserved N-terminal transmembrane domains and a C-terminal region. Using chimeric and truncation mutants, the N-terminal transmembrane domains of the MERS-CoV M protein were found to be sufficient for its inhibitory effect on IFN expression, whereas the C-terminal domain was unable to induce this suppression. Collectively, our findings suggest a common and conserved mechanism through which highly pathogenic MERS-CoV and SARS-CoV harness their M proteins to suppress type I IFN expression at the level of TBK1-dependent phosphorylation and activation of IRF3 resulting in evasion of the host innate antiviral response.
DOI: 10.1038/emi.2016.33
PubMed: 27094905
Affiliations:
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first="Man-Lung" last="Yeung">Man-Lung Yeung</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Yuen, Kit San" sort="Yuen, Kit San" uniqKey="Yuen K" first="Kit-San" last="Yuen">Kit-San Yuen</name><affiliation wicri:level="1"><nlm:affiliation>School of Biomedical Sciences, The University of Hong Kong, Pokfulam Hong Kong, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Biomedical Sciences, The University of Hong Kong, Pokfulam Hong Kong</wicri:regionArea><wicri:noRegion>Pokfulam Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Chan, Chi Ping" sort="Chan, Chi Ping" uniqKey="Chan C" first="Chi-Ping" last="Chan">Chi-Ping Chan</name><affiliation wicri:level="1"><nlm:affiliation>School of Biomedical Sciences, The University of Hong Kong, Pokfulam Hong Kong, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Biomedical Sciences, The University of Hong Kong, Pokfulam Hong Kong</wicri:regionArea><wicri:noRegion>Pokfulam Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Woo, Patrick Chiu Yat" sort="Woo, Patrick Chiu Yat" uniqKey="Woo P" first="Patrick Chiu-Yat" last="Woo">Patrick Chiu-Yat Woo</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Yuen, Kwok Yung" sort="Yuen, Kwok Yung" uniqKey="Yuen K" first="Kwok-Yung" last="Yuen">Kwok-Yung Yuen</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Jin, Dong Yan" sort="Jin, Dong Yan" uniqKey="Jin D" first="Dong-Yan" last="Jin">Dong-Yan Jin</name><affiliation wicri:level="1"><nlm:affiliation>School of Biomedical Sciences, The University of Hong Kong, Pokfulam Hong Kong, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Biomedical Sciences, The University of Hong Kong, Pokfulam Hong Kong</wicri:regionArea><wicri:noRegion>Pokfulam Hong Kong</wicri:noRegion></affiliation></author></analytic><series><title level="j">Emerging microbes & infections</title><idno type="eISSN">2222-1751</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>DEAD Box Protein 58 (genetics)</term><term>Gene Expression Regulation</term><term>HEK293 Cells</term><term>Humans</term><term>Immune Evasion</term><term>Immunity, Innate</term><term>Interferon Regulatory Factor-3 (genetics)</term><term>Interferon Regulatory Factor-3 (immunology)</term><term>Interferon Regulatory Factor-3 (metabolism)</term><term>Interferon Type I (antagonists & inhibitors)</term><term>Interferon Type I (biosynthesis)</term><term>Interferon Type I (genetics)</term><term>Interferon Type I (immunology)</term><term>Middle East Respiratory Syndrome Coronavirus (genetics)</term><term>Middle East Respiratory Syndrome Coronavirus (immunology)</term><term>Middle East Respiratory Syndrome Coronavirus (pathogenicity)</term><term>Middle East Respiratory Syndrome Coronavirus (physiology)</term><term>Phosphorylation</term><term>Phosphotransferases</term><term>Protein-Serine-Threonine Kinases (genetics)</term><term>Protein-Serine-Threonine Kinases (immunology)</term><term>Protein-Serine-Threonine Kinases (metabolism)</term><term>SARS Virus (genetics)</term><term>SARS Virus (immunology)</term><term>SARS Virus (pathogenicity)</term><term>Saudi Arabia</term><term>Sendai virus (genetics)</term><term>Sendai virus (immunology)</term><term>Sequence Alignment</term><term>TNF Receptor-Associated Factor 3 (genetics)</term><term>TNF Receptor-Associated Factor 3 (immunology)</term><term>Viral Matrix Proteins (genetics)</term><term>Viral Matrix Proteins (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Alignement de séquences</term><term>Arabie saoudite</term><term>Cellules HEK293</term><term>Coronavirus du syndrome respiratoire du Moyen-Orient (génétique)</term><term>Coronavirus du syndrome respiratoire du Moyen-Orient (immunologie)</term><term>Coronavirus du syndrome respiratoire du Moyen-Orient (pathogénicité)</term><term>Coronavirus du syndrome respiratoire du Moyen-Orient (physiologie)</term><term>Facteur-3 associé aux récepteurs de TNF (génétique)</term><term>Facteur-3 associé aux récepteurs de TNF (immunologie)</term><term>Facteur-3 de régulation d'interféron (génétique)</term><term>Facteur-3 de régulation d'interféron (immunologie)</term><term>Facteur-3 de régulation d'interféron (métabolisme)</term><term>Humains</term><term>Immunité innée</term><term>Interféron de type I (antagonistes et inhibiteurs)</term><term>Interféron de type I (biosynthèse)</term><term>Interféron de type I (génétique)</term><term>Interféron de type I (immunologie)</term><term>Phosphorylation</term><term>Phosphotransferases</term><term>Protein-Serine-Threonine Kinases (génétique)</term><term>Protein-Serine-Threonine Kinases (immunologie)</term><term>Protein-Serine-Threonine Kinases (métabolisme)</term><term>Protéine-58 à domaine DEAD (génétique)</term><term>Protéines de la matrice virale (génétique)</term><term>Protéines de la matrice virale (physiologie)</term><term>Régulation de l'expression des gènes</term><term>Virus Sendai (génétique)</term><term>Virus Sendai (immunologie)</term><term>Virus du SRAS (génétique)</term><term>Virus du SRAS (immunologie)</term><term>Virus du SRAS (pathogénicité)</term><term>Échappement immunitaire</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Interferon Type I</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Interferon Type I</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DEAD Box Protein 58</term><term>Interferon Regulatory Factor-3</term><term>Interferon Type I</term><term>Protein-Serine-Threonine Kinases</term><term>TNF Receptor-Associated Factor 3</term><term>Viral Matrix Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Interferon Regulatory Factor-3</term><term>Interferon Type I</term><term>Protein-Serine-Threonine Kinases</term><term>TNF Receptor-Associated Factor 3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Interferon Regulatory Factor-3</term><term>Protein-Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Interféron de type I</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Interféron de type I</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Middle East Respiratory Syndrome Coronavirus</term><term>SARS Virus</term><term>Sendai virus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Coronavirus du syndrome respiratoire du Moyen-Orient</term><term>Facteur-3 associé aux récepteurs de TNF</term><term>Facteur-3 de régulation d'interféron</term><term>Interféron de type I</term><term>Protein-Serine-Threonine Kinases</term><term>Protéine-58 à domaine DEAD</term><term>Protéines de la matrice virale</term><term>Virus Sendai</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Coronavirus du syndrome respiratoire du Moyen-Orient</term><term>Facteur-3 associé aux récepteurs de TNF</term><term>Facteur-3 de régulation d'interféron</term><term>Interféron de type I</term><term>Protein-Serine-Threonine Kinases</term><term>Virus Sendai</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Middle East Respiratory Syndrome Coronavirus</term><term>SARS Virus</term><term>Sendai virus</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur-3 de régulation d'interféron</term><term>Protein-Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Middle East Respiratory Syndrome Coronavirus</term><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Coronavirus du syndrome respiratoire du Moyen-Orient</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Coronavirus du syndrome respiratoire du Moyen-Orient</term><term>Protéines de la matrice virale</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Middle East Respiratory Syndrome Coronavirus</term><term>Viral Matrix Proteins</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Gene Expression Regulation</term><term>HEK293 Cells</term><term>Humans</term><term>Immune Evasion</term><term>Immunity, Innate</term><term>Phosphorylation</term><term>Phosphotransferases</term><term>Saudi Arabia</term><term>Sequence Alignment</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Alignement de séquences</term><term>Arabie saoudite</term><term>Cellules HEK293</term><term>Humains</term><term>Immunité innée</term><term>Phosphorylation</term><term>Phosphotransferases</term><term>Régulation de l'expression des gènes</term><term>Échappement immunitaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Middle East respiratory syndrome coronavirus (MERS-CoV) infection has claimed hundreds of lives and has become a global threat since its emergence in Saudi Arabia in 2012. The ability of MERS-CoV to evade the host innate antiviral response may contribute to its severe pathogenesis. Many MERS-CoV-encoded proteins were identified to have interferon (IFN)-antagonizing properties, which correlates well with the reduced IFN levels observed in infected patients and ex vivo models. In this study, we fully characterized the IFN-antagonizing property of the MERS-CoV M protein. Expression of MERS-CoV M protein suppressed type I IFN expression in response to Sendai virus infection or poly(I:C) induction. This suppressive effect was found to be specific for the activation of IFN regulatory factor 3 (IRF3) but not nuclear factor-κB. MERS-CoV M protein interacted with TRAF3 and disrupted TRAF3-TBK1 association leading to reduced IRF3 activation. M proteins from MERS-CoV and SARS-CoV have three highly similar conserved N-terminal transmembrane domains and a C-terminal region. Using chimeric and truncation mutants, the N-terminal transmembrane domains of the MERS-CoV M protein were found to be sufficient for its inhibitory effect on IFN expression, whereas the C-terminal domain was unable to induce this suppression. Collectively, our findings suggest a common and conserved mechanism through which highly pathogenic MERS-CoV and SARS-CoV harness their M proteins to suppress type I IFN expression at the level of TBK1-dependent phosphorylation and activation of IRF3 resulting in evasion of the host innate antiviral response. </div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Lui, Pak Yin" sort="Lui, Pak Yin" uniqKey="Lui P" first="Pak-Yin" last="Lui">Pak-Yin Lui</name></noRegion><name sortKey="Chan, Chi Ping" sort="Chan, Chi Ping" uniqKey="Chan C" first="Chi-Ping" last="Chan">Chi-Ping Chan</name><name sortKey="Fung, Cheuk Lai" sort="Fung, Cheuk Lai" uniqKey="Fung C" first="Cheuk-Lai" last="Fung">Cheuk-Lai Fung</name><name sortKey="Jin, Dong Yan" sort="Jin, Dong Yan" uniqKey="Jin D" first="Dong-Yan" last="Jin">Dong-Yan Jin</name><name sortKey="Siu, Kam Leung" sort="Siu, Kam Leung" uniqKey="Siu K" first="Kam-Leung" last="Siu">Kam-Leung Siu</name><name sortKey="Wong, Lok Yin Roy" sort="Wong, Lok Yin Roy" uniqKey="Wong L" first="Lok-Yin Roy" last="Wong">Lok-Yin Roy Wong</name><name sortKey="Woo, Patrick Chiu Yat" sort="Woo, Patrick Chiu Yat" uniqKey="Woo P" first="Patrick Chiu-Yat" last="Woo">Patrick Chiu-Yat Woo</name><name sortKey="Yeung, Man Lung" sort="Yeung, Man Lung" uniqKey="Yeung M" first="Man-Lung" last="Yeung">Man-Lung Yeung</name><name sortKey="Yuen, Kit San" sort="Yuen, Kit San" uniqKey="Yuen K" first="Kit-San" last="Yuen">Kit-San Yuen</name><name sortKey="Yuen, Kwok Yung" sort="Yuen, Kwok Yung" uniqKey="Yuen K" first="Kwok-Yung" last="Yuen">Kwok-Yung Yuen</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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