Accessory proteins 8b and 8ab of severe acute respiratory syndrome coronavirus suppress the interferon signaling pathway by mediating ubiquitin-dependent rapid degradation of interferon regulatory factor 3
Identifieur interne : 000E78 ( Main/Exploration ); précédent : 000E77; suivant : 000E79Accessory proteins 8b and 8ab of severe acute respiratory syndrome coronavirus suppress the interferon signaling pathway by mediating ubiquitin-dependent rapid degradation of interferon regulatory factor 3
Auteurs : Hui Hui Wong [République populaire de Chine, Singapour] ; To Sing Fung [République populaire de Chine] ; Shouguo Fang [Singapour, République populaire de Chine] ; Mei Huang [Singapour] ; My Tra Le [Singapour] ; Ding Xiang Liu [République populaire de Chine, Singapour]Source :
- Virology [ 0042-6822 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux, Domaines protéiques, Facteur-3 de régulation d'interféron (), Facteur-3 de régulation d'interféron (génétique), Facteur-3 de régulation d'interféron (métabolisme), Humains, Liaison aux protéines, Lignée cellulaire, Proteasome endopeptidase complex (génétique), Proteasome endopeptidase complex (métabolisme), Protéines virales régulatrices ou accessoires (génétique), Protéines virales régulatrices ou accessoires (métabolisme), Protéolyse, Syndrome respiratoire aigu sévère (génétique), Syndrome respiratoire aigu sévère (métabolisme), Syndrome respiratoire aigu sévère (virologie), Transduction du signal, Ubiquitine (métabolisme), Virus du SRAS (génétique), Virus du SRAS (métabolisme).
- MESH :
- génétique : Facteur-3 de régulation d'interféron, Proteasome endopeptidase complex, Protéines virales régulatrices ou accessoires, Syndrome respiratoire aigu sévère, Virus du SRAS.
- métabolisme : Facteur-3 de régulation d'interféron, Proteasome endopeptidase complex, Protéines virales régulatrices ou accessoires, Syndrome respiratoire aigu sévère, Ubiquitine, Virus du SRAS.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Domaines protéiques, Facteur-3 de régulation d'interféron, Humains, Liaison aux protéines, Lignée cellulaire, Protéolyse, Transduction du signal.
English descriptors
- KwdEn :
- Animals, Cell Line, Humans, Interferon Regulatory Factor-3 (chemistry), Interferon Regulatory Factor-3 (genetics), Interferon Regulatory Factor-3 (metabolism), Proteasome Endopeptidase Complex (genetics), Proteasome Endopeptidase Complex (metabolism), Protein Binding, Protein Domains, Proteolysis, SARS Virus (genetics), SARS Virus (metabolism), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (virology), Signal Transduction, Ubiquitin (metabolism), Viral Regulatory and Accessory Proteins (genetics), Viral Regulatory and Accessory Proteins (metabolism).
- MESH :
- chemical , chemistry : Interferon Regulatory Factor-3.
- chemical , genetics : Interferon Regulatory Factor-3, Proteasome Endopeptidase Complex, Viral Regulatory and Accessory Proteins.
- chemical , metabolism : Interferon Regulatory Factor-3, Proteasome Endopeptidase Complex, Ubiquitin, Viral Regulatory and Accessory Proteins.
- genetics : SARS Virus, Severe Acute Respiratory Syndrome.
- metabolism : SARS Virus, Severe Acute Respiratory Syndrome.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Cell Line, Humans, Protein Binding, Protein Domains, Proteolysis, Signal Transduction.
Abstract
Severe acute respiratory syndrome coronavirus (SARS-CoV) is an inefficient inducer of interferon (IFN) response. It expresses various proteins that effectively circumvent IFN production at different levels via distinct mechanisms. Through the construction of recombinant IBV expressing proteins 8a, 8b and 8ab encoded by SARS-CoV ORF8, we demonstrate that expression of 8b and 8ab enables the corresponding recombinant viruses to partially overcome the inhibitory actions of IFN activation to achieve higher replication efficiencies in cells. We also found that proteins 8b and 8ab could physically interact with IRF3. Overexpression of 8b and 8ab resulted in the reduction of poly (I:C)-induced IRF3 dimerization and inhibition of the IFN-β signaling pathway. This counteracting effect was partially mediated by protein 8b/8ab-induced degradation of IRF3 in a ubiquitin-proteasome-dependent manner. Taken together, we propose that SARS-CoV may exploit the unique functions of proteins 8b and 8ab as novel mechanisms to overcome the effect of IFN response during virus infection.
Url:
DOI: 10.1016/j.virol.2017.12.028
PubMed: 29294448
PubMed Central: 7112132
Affiliations:
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Le document en format XML
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proteins 8b and 8ab of severe acute respiratory syndrome coronavirus suppress the interferon signaling pathway by mediating ubiquitin-dependent rapid degradation of interferon regulatory factor 3</title><author><name sortKey="Wong, Hui Hui" sort="Wong, Hui Hui" uniqKey="Wong H" first="Hui Hui" last="Wong">Hui Hui Wong</name><affiliation wicri:level="1"><nlm:aff id="aff0005">South China Agricultural University, Guangdong Province Key Laboratory Microbial Signals & Disease Co, and Integrative Microbiology Research Centre, Guangzhou 510642, Guangdong, People's Republic of China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>South China Agricultural University, Guangdong Province Key Laboratory Microbial Signals & Disease Co, and Integrative Microbiology Research Centre, Guangzhou 510642, Guangdong</wicri:regionArea><wicri:noRegion>Guangdong</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff0010">Institute of Molecular and Cell Biology, 61 Biopolis Drive, Proteos, Singapore</nlm:aff><country xml:lang="fr">Singapour</country><wicri:regionArea>Institute of Molecular and Cell Biology, 61 Biopolis Drive, Proteos</wicri:regionArea><wicri:noRegion>Proteos</wicri:noRegion></affiliation></author><author><name sortKey="Fung, To Sing" sort="Fung, To Sing" uniqKey="Fung T" first="To Sing" last="Fung">To Sing Fung</name><affiliation wicri:level="1"><nlm:aff id="aff0005">South China Agricultural University, Guangdong Province Key Laboratory Microbial Signals & Disease Co, and Integrative Microbiology Research Centre, Guangzhou 510642, Guangdong, People's Republic of China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>South China Agricultural University, Guangdong Province Key Laboratory Microbial Signals & Disease Co, and Integrative Microbiology Research Centre, Guangzhou 510642, Guangdong</wicri:regionArea><wicri:noRegion>Guangdong</wicri:noRegion></affiliation></author><author><name sortKey="Fang, Shouguo" sort="Fang, Shouguo" uniqKey="Fang S" first="Shouguo" last="Fang">Shouguo Fang</name><affiliation wicri:level="1"><nlm:aff id="aff0015">School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, 637551, Singapore</nlm:aff><country xml:lang="fr">Singapour</country><wicri:regionArea>School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, 637551</wicri:regionArea><wicri:noRegion>637551</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff0020">Agricultural School, Yangtze University, 266 Jingmilu, Jingzhou City, Hubei Province 434025, China.</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Agricultural School, Yangtze University, 266 Jingmilu, Jingzhou City, Hubei Province 434025</wicri:regionArea><wicri:noRegion>Hubei Province 434025</wicri:noRegion></affiliation></author><author><name sortKey="Huang, Mei" sort="Huang, Mei" uniqKey="Huang M" first="Mei" last="Huang">Mei Huang</name><affiliation wicri:level="1"><nlm:aff id="aff0015">School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, 637551, Singapore</nlm:aff><country xml:lang="fr">Singapour</country><wicri:regionArea>School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, 637551</wicri:regionArea><wicri:noRegion>637551</wicri:noRegion></affiliation></author><author><name sortKey="Le, My Tra" sort="Le, My Tra" uniqKey="Le M" first="My Tra" last="Le">My Tra Le</name><affiliation wicri:level="1"><nlm:aff id="aff0010">Institute of Molecular and Cell Biology, 61 Biopolis Drive, Proteos, Singapore</nlm:aff><country xml:lang="fr">Singapour</country><wicri:regionArea>Institute of Molecular and Cell Biology, 61 Biopolis Drive, Proteos</wicri:regionArea><wicri:noRegion>Proteos</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Ding Xiang" sort="Liu, Ding Xiang" uniqKey="Liu D" first="Ding Xiang" last="Liu">Ding Xiang Liu</name><affiliation wicri:level="1"><nlm:aff id="aff0005">South China Agricultural University, Guangdong Province Key Laboratory Microbial Signals & Disease Co, and Integrative Microbiology Research Centre, Guangzhou 510642, Guangdong, People's Republic of China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>South China Agricultural University, Guangdong Province Key Laboratory Microbial Signals & Disease Co, and Integrative Microbiology Research Centre, Guangzhou 510642, Guangdong</wicri:regionArea><wicri:noRegion>Guangdong</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff0015">School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, 637551, Singapore</nlm:aff><country 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(metabolism)</term><term>Severe Acute Respiratory Syndrome (genetics)</term><term>Severe Acute Respiratory Syndrome (metabolism)</term><term>Severe Acute Respiratory Syndrome (virology)</term><term>Signal Transduction</term><term>Ubiquitin (metabolism)</term><term>Viral Regulatory and Accessory Proteins (genetics)</term><term>Viral Regulatory and Accessory Proteins (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Domaines protéiques</term><term>Facteur-3 de régulation d'interféron ()</term><term>Facteur-3 de régulation d'interféron (génétique)</term><term>Facteur-3 de régulation d'interféron (métabolisme)</term><term>Humains</term><term>Liaison aux protéines</term><term>Lignée cellulaire</term><term>Proteasome endopeptidase complex (génétique)</term><term>Proteasome endopeptidase complex (métabolisme)</term><term>Protéines virales régulatrices ou accessoires (génétique)</term><term>Protéines virales régulatrices ou accessoires (métabolisme)</term><term>Protéolyse</term><term>Syndrome respiratoire aigu sévère (génétique)</term><term>Syndrome respiratoire aigu sévère (métabolisme)</term><term>Syndrome respiratoire aigu sévère (virologie)</term><term>Transduction du signal</term><term>Ubiquitine (métabolisme)</term><term>Virus du SRAS (génétique)</term><term>Virus du SRAS (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Interferon Regulatory Factor-3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interferon Regulatory Factor-3</term><term>Proteasome Endopeptidase Complex</term><term>Viral Regulatory and Accessory Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Interferon Regulatory Factor-3</term><term>Proteasome Endopeptidase Complex</term><term>Ubiquitin</term><term>Viral Regulatory and Accessory Proteins</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur-3 de régulation d'interféron</term><term>Proteasome endopeptidase complex</term><term>Protéines virales régulatrices ou accessoires</term><term>Syndrome respiratoire aigu sévère</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur-3 de régulation d'interféron</term><term>Proteasome endopeptidase complex</term><term>Protéines virales régulatrices ou accessoires</term><term>Syndrome respiratoire aigu sévère</term><term>Ubiquitine</term><term>Virus du SRAS</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>Animals</term><term>Cell Line</term><term>Humans</term><term>Protein Binding</term><term>Protein Domains</term><term>Proteolysis</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Domaines protéiques</term><term>Facteur-3 de régulation d'interféron</term><term>Humains</term><term>Liaison aux protéines</term><term>Lignée cellulaire</term><term>Protéolyse</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Severe acute respiratory syndrome coronavirus (SARS-CoV) is an inefficient inducer of interferon (IFN) response. It expresses various proteins that effectively circumvent IFN production at different levels via distinct mechanisms. Through the construction of recombinant IBV expressing proteins 8a, 8b and 8ab encoded by SARS-CoV ORF8, we demonstrate that expression of 8b and 8ab enables the corresponding recombinant viruses to partially overcome the inhibitory actions of IFN activation to achieve higher replication efficiencies in cells. We also found that proteins 8b and 8ab could physically interact with IRF3. Overexpression of 8b and 8ab resulted in the reduction of poly (I:C)-induced IRF3 dimerization and inhibition of the IFN-β signaling pathway. This counteracting effect was partially mediated by protein 8b/8ab-induced degradation of IRF3 in a ubiquitin-proteasome-dependent manner. Taken together, we propose that SARS-CoV may exploit the unique functions of proteins 8b and 8ab as novel mechanisms to overcome the effect of IFN response during virus infection.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Anderson, R A" uniqKey="Anderson R">R.A. Anderson</name></author><author><name sortKey="Liu, D X" uniqKey="Liu D">D.X. Liu</name></author><author><name sortKey="Gompels, U A" uniqKey="Gompels U">U.A. Gompels</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bibeau Poirier, A" uniqKey="Bibeau Poirier A">A. Bibeau-Poirier</name></author><author><name sortKey="Gravel, S P" uniqKey="Gravel S">S.-P. Gravel</name></author><author><name sortKey="Clement, J F" uniqKey="Clement J">J.-F. Clément</name></author><author><name sortKey="Rolland, S" uniqKey="Rolland S">S. Rolland</name></author><author><name sortKey="Rodier, G" uniqKey="Rodier G">G. 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Liu</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>République populaire de Chine</li><li>Singapour</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Wong, Hui Hui" sort="Wong, Hui Hui" uniqKey="Wong H" first="Hui Hui" last="Wong">Hui Hui Wong</name></noRegion><name sortKey="Fang, Shouguo" sort="Fang, Shouguo" uniqKey="Fang S" first="Shouguo" last="Fang">Shouguo Fang</name><name sortKey="Fung, To Sing" sort="Fung, To Sing" uniqKey="Fung T" first="To Sing" last="Fung">To Sing Fung</name><name sortKey="Liu, Ding Xiang" sort="Liu, Ding Xiang" uniqKey="Liu D" first="Ding Xiang" last="Liu">Ding Xiang Liu</name></country><country name="Singapour"><noRegion><name sortKey="Wong, Hui Hui" sort="Wong, Hui Hui" uniqKey="Wong H" first="Hui Hui" last="Wong">Hui Hui Wong</name></noRegion><name sortKey="Fang, Shouguo" sort="Fang, Shouguo" uniqKey="Fang S" first="Shouguo" last="Fang">Shouguo Fang</name><name sortKey="Huang, Mei" sort="Huang, Mei" uniqKey="Huang M" first="Mei" last="Huang">Mei Huang</name><name sortKey="Le, My Tra" sort="Le, My Tra" uniqKey="Le M" first="My Tra" last="Le">My Tra Le</name><name sortKey="Liu, Ding Xiang" sort="Liu, Ding Xiang" uniqKey="Liu D" first="Ding Xiang" last="Liu">Ding Xiang Liu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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