MersV1, Main, Exploration, bibRecord, 001123

Middle East respiratory syndrome coronavirus M protein suppresses type I interferon expression through the inhibition of TBK1-dependent phosphorylation of IRF3

Identifieur interne : 001123 ( Main/Exploration ); précédent : 001122; suivant : 001124

Middle East respiratory syndrome coronavirus M protein suppresses type I interferon expression through the inhibition of TBK1-dependent phosphorylation of IRF3

Source :

Emerging Microbes & Infections [ 2222-1751 ] ; 2016.

RBID : PMC:4855074

Descripteurs français

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.

Emerging Microbes and Infections (2016) 5, e39; doi:10.1038/emi.2016.33; published online 20 April 2016

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4855074

DOI: 10.1038/emi.2016.33
PubMed: 27094905
PubMed Central: 4855074

Affiliations:

République populaire de Chine

Le document en format XML

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 Hong Kong,<country>China</country>
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 Hong Kong,<country>China</country>
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 Hong Kong,<country>China</country>
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<country xml:lang="fr">République populaire de Chine</country>
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 Hong Kong,<country>China</country>
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 Hong Kong,<country>China</country>
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 Hong Kong,<country>China</country>
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<author><name sortKey="Chan, Chi Ping" sort="Chan, Chi Ping" uniqKey="Chan C" first="Chi-Ping" last="Chan">Chi-Ping Chan</name>
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 Hong Kong,<country>China</country>
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<country xml:lang="fr">République populaire de Chine</country>
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<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>
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, Hong Kong,<country>China</country>
</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Yuen, Kwok Yung" sort="Yuen, Kwok Yung" uniqKey="Yuen K" first="Kwok-Yung" last="Yuen">Kwok-Yung Yuen</name>
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,<addr-line>Pokfulam</addr-line>
, Hong Kong,<country>China</country>
</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Jin, Dong Yan" sort="Jin, Dong Yan" uniqKey="Jin D" first="Dong-Yan" last="Jin">Dong-Yan Jin</name>
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,<addr-line>Pokfulam</addr-line>
 Hong Kong,<country>China</country>
</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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<term>Interferon Regulatory Factor-3 (genetics)</term>
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<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>
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<term>Phosphotransferases</term>
<term>Protein-Serine-Threonine Kinases (genetics)</term>
<term>Protein-Serine-Threonine Kinases (immunology)</term>
<term>Protein-Serine-Threonine Kinases (metabolism)</term>
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<term>Protéines de la matrice virale (génétique)</term>
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<term>Virus Sendai (génétique)</term>
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<term>Virus du SRAS (génétique)</term>
<term>Virus du SRAS (immunologie)</term>
<term>Virus du SRAS (pathogénicité)</term>
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<term>TNF Receptor-Associated Factor 3</term>
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<term>Virus Sendai</term>
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<term>Protein-Serine-Threonine Kinases</term>
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<term>Virus du SRAS</term>
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<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"><p>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 <italic>ex vivo</italic> 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.</p>
<p><italic>Emerging Microbes and Infections</italic>
 (2016) <bold>5,</bold> e39;
doi:<ext-link ext-link-type="doi" xlink:href="10.1038/emi.2016.33">10.1038/emi.2016.33</ext-link>
; published online 20 April 2016</p>
</div>
</front>
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</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>
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Serveur d'exploration MERS

Middle East respiratory syndrome coronavirus M protein suppresses type I interferon expression through the inhibition of TBK1-dependent phosphorylation of IRF3

Middle East respiratory syndrome coronavirus M protein suppresses type I interferon expression through the inhibition of TBK1-dependent phosphorylation of IRF3

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