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 : 000A36 ( PubMed/Corpus ); précédent : 000A35; suivant : 000A37Accessory 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 ; To Sing Fung ; Shouguo Fang ; Mei Huang ; My Tra Le ; Ding Xiang LiuSource :
- Virology [ 1096-0341 ] ; 2018.
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.
DOI: 10.1016/j.virol.2017.12.028
PubMed: 29294448
Links to Exploration step
pubmed:29294448Le document en format XML
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Electronic address: dxliu0001@163.com.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Virology</title><idno type="eISSN">1096-0341</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Humans</term><term>Interferon Regulatory Factor-3 (chemistry)</term><term>Interferon Regulatory Factor-3 (genetics)</term><term>Interferon Regulatory Factor-3 (metabolism)</term><term>Proteasome Endopeptidase Complex (genetics)</term><term>Proteasome Endopeptidase Complex (metabolism)</term><term>Protein Binding</term><term>Protein Domains</term><term>Proteolysis</term><term>SARS Virus (genetics)</term><term>SARS Virus (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="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="metabolism" xml:lang="en"><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</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></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29294448</PMID><DateCompleted><Year>2018</Year><Month>04</Month><Day>27</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>07</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1096-0341</ISSN><JournalIssue CitedMedium="Internet"><Volume>515</Volume><PubDate><Year>2018</Year><Month>02</Month></PubDate></JournalIssue><Title>Virology</Title><ISOAbbreviation>Virology</ISOAbbreviation></Journal><ArticleTitle>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.</ArticleTitle><Pagination><MedlinePgn>165-175</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0042-6822(17)30442-7</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.virol.2017.12.028</ELocationID><Abstract><AbstractText>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.</AbstractText><CopyrightInformation>Copyright © 2017 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wong</LastName><ForeName>Hui Hui</ForeName><Initials>HH</Initials><AffiliationInfo><Affiliation>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; Institute of Molecular and Cell Biology, 61 Biopolis Drive, Proteos, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fung</LastName><ForeName>To Sing</ForeName><Initials>TS</Initials><AffiliationInfo><Affiliation>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.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fang</LastName><ForeName>Shouguo</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, 637551, Singapore; Agricultural School, Yangtze University, 266 Jingmilu, Jingzhou City, Hubei Province 434025, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Mei</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, 637551, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Le</LastName><ForeName>My Tra</ForeName><Initials>MT</Initials><AffiliationInfo><Affiliation>Institute of Molecular and Cell Biology, 61 Biopolis Drive, Proteos, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Ding Xiang</ForeName><Initials>DX</Initials><AffiliationInfo><Affiliation>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; School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, 637551, Singapore. Electronic address: dxliu0001@163.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>12</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Virology</MedlineTA><NlmUniqueID>0110674</NlmUniqueID><ISSNLinking>0042-6822</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050838">Interferon Regulatory Factor-3</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D025801">Ubiquitin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054334">Viral Regulatory and Accessory 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MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D025801" MajorTopicYN="N">Ubiquitin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054334" MajorTopicYN="N">Viral Regulatory and Accessory Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">IFN antagonist</Keyword><Keyword MajorTopicYN="Y">IRF3</Keyword><Keyword MajorTopicYN="Y">ORF8</Keyword><Keyword MajorTopicYN="Y">SARS-CoV</Keyword><Keyword MajorTopicYN="Y">Ubiquitin-dependent degradation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate 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