SrasV1, PubMed, Curation, bibRecord, 000F44

SARS-coronavirus open reading frame-9b suppresses innate immunity by targeting mitochondria and the MAVS/TRAF3/TRAF6 signalosome.

Identifieur interne : 000F44 ( PubMed/Curation ); précédent : 000F43; suivant : 000F45

SARS-coronavirus open reading frame-9b suppresses innate immunity by targeting mitochondria and the MAVS/TRAF3/TRAF6 signalosome.

Auteurs : Chong-Shan Shi [États-Unis] ; Hai-Yan Qi [États-Unis] ; Cedric Boularan [États-Unis] ; Ning-Na Huang [États-Unis] ; Mones Abu-Asab [États-Unis] ; James H. Shelhamer [États-Unis] ; John H. Kehrl [États-Unis]

Source :

Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2014.

RBID : pubmed:25135833

Descripteurs français

English descriptors

KwdEn :
- Adaptor Proteins, Signal Transducing (metabolism), Autophagy (genetics), Autophagy-Related Protein 5, Cell Line, GTP Phosphohydrolases (genetics), GTP Phosphohydrolases (metabolism), Green Fluorescent Proteins, HEK293 Cells, Humans, Immune Evasion, Immunity, Innate (genetics), Microtubule-Associated Proteins (biosynthesis), Microtubule-Associated Proteins (genetics), Microtubule-Associated Proteins (metabolism), Mitochondria (genetics), Mitochondria (immunology), Mitochondria (virology), Mitochondrial Proteins (genetics), Mitochondrial Proteins (metabolism), Open Reading Frames (genetics), Open Reading Frames (immunology), RNA Interference, RNA, Small Interfering, RNA-Binding Proteins (biosynthesis), RNA-Binding Proteins (genetics), Repressor Proteins (biosynthesis), Repressor Proteins (genetics), SARS Virus (genetics), SARS Virus (immunology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (virology), TNF Receptor-Associated Factor 3 (metabolism), TNF Receptor-Associated Factor 6 (metabolism), Ubiquitin-Protein Ligases (biosynthesis), Ubiquitin-Protein Ligases (genetics), Ubiquitination, Viral Proteins (genetics), Viral Proteins (immunology).
MESH :
- chemical , biosynthesis : Microtubule-Associated Proteins, RNA-Binding Proteins, Repressor Proteins, Ubiquitin-Protein Ligases.
- chemical , genetics : GTP Phosphohydrolases, Microtubule-Associated Proteins, Mitochondrial Proteins, RNA-Binding Proteins, Repressor Proteins, Ubiquitin-Protein Ligases, Viral Proteins.
- chemical , immunology : Viral Proteins.
- chemical , metabolism : Adaptor Proteins, Signal Transducing, GTP Phosphohydrolases, Microtubule-Associated Proteins, Mitochondrial Proteins, TNF Receptor-Associated Factor 3, TNF Receptor-Associated Factor 6.
- genetics : Autophagy, Immunity, Innate, Mitochondria, Open Reading Frames, SARS Virus.
- immunology : Mitochondria, Open Reading Frames, SARS Virus, Severe Acute Respiratory Syndrome.
- virology : Mitochondria, Severe Acute Respiratory Syndrome.
- chemical : Autophagy-Related Protein 5, Cell Line, Green Fluorescent Proteins, HEK293 Cells, Humans, Immune Evasion, RNA Interference, RNA, Small Interfering, Ubiquitination.

Abstract

Coronaviruses (CoV) have recently emerged as potentially serious pathogens that can cause significant human morbidity and death. The severe acute respiratory syndrome (SARS)-CoV was identified as the etiologic agent of the 2002-2003 international SARS outbreak. Yet, how SARS evades innate immune responses to cause human disease remains poorly understood. In this study, we show that a protein encoded by SARS-CoV designated as open reading frame-9b (ORF-9b) localizes to mitochondria and causes mitochondrial elongation by triggering ubiquitination and proteasomal degradation of dynamin-like protein 1, a host protein involved in mitochondrial fission. Also, acting on mitochondria, ORF-9b targets the mitochondrial-associated adaptor molecule MAVS signalosome by usurping PCBP2 and the HECT domain E3 ligase AIP4 to trigger the degradation of MAVS, TRAF3, and TRAF 6. This severely limits host cell IFN responses. Reducing either PCBP2 or AIP4 expression substantially reversed the ORF-9b-mediated reduction of MAVS and the suppression of antiviral transcriptional responses. Finally, transient ORF-9b expression led to a strong induction of autophagy in cells. The induction of autophagy depended upon ATG5, a critical autophagy regulator, but the inhibition of MAVS signaling did not. These results indicate that SARS-CoV ORF-9b manipulates host cell mitochondria and mitochondrial function to help evade host innate immunity. This study has uncovered an important clue to the pathogenesis of SARS-CoV infection and illustrates the havoc that a small ORF can cause in cells.

DOI: 10.4049/jimmunol.1303196
PubMed: 25135833

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<term>Autophagy-Related Protein 5</term>
<term>Cell Line</term>
<term>GTP Phosphohydrolases (genetics)</term>
<term>GTP Phosphohydrolases (metabolism)</term>
<term>Green Fluorescent Proteins</term>
<term>HEK293 Cells</term>
<term>Humans</term>
<term>Immune Evasion</term>
<term>Immunity, Innate (genetics)</term>
<term>Microtubule-Associated Proteins (biosynthesis)</term>
<term>Microtubule-Associated Proteins (genetics)</term>
<term>Microtubule-Associated Proteins (metabolism)</term>
<term>Mitochondria (genetics)</term>
<term>Mitochondria (immunology)</term>
<term>Mitochondria (virology)</term>
<term>Mitochondrial Proteins (genetics)</term>
<term>Mitochondrial Proteins (metabolism)</term>
<term>Open Reading Frames (genetics)</term>
<term>Open Reading Frames (immunology)</term>
<term>RNA Interference</term>
<term>RNA, Small Interfering</term>
<term>RNA-Binding Proteins (biosynthesis)</term>
<term>RNA-Binding Proteins (genetics)</term>
<term>Repressor Proteins (biosynthesis)</term>
<term>Repressor Proteins (genetics)</term>
<term>SARS Virus (genetics)</term>
<term>SARS Virus (immunology)</term>
<term>Severe Acute Respiratory Syndrome (immunology)</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
<term>TNF Receptor-Associated Factor 3 (metabolism)</term>
<term>TNF Receptor-Associated Factor 6 (metabolism)</term>
<term>Ubiquitin-Protein Ligases (biosynthesis)</term>
<term>Ubiquitin-Protein Ligases (genetics)</term>
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<term>Viral Proteins (genetics)</term>
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<term>Cadres ouverts de lecture (génétique)</term>
<term>Cadres ouverts de lecture (immunologie)</term>
<term>Cellules HEK293</term>
<term>Facteur-3 associé aux récepteurs de TNF (métabolisme)</term>
<term>Facteur-6 associé aux récepteurs de TNF (métabolisme)</term>
<term>Humains</term>
<term>Immunité innée (génétique)</term>
<term>Interférence par ARN</term>
<term>Lignée cellulaire</term>
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<term>Mitochondries (immunologie)</term>
<term>Mitochondries (virologie)</term>
<term>Petit ARN interférent</term>
<term>Protéine-5 associée à l'autophagie</term>
<term>Protéines adaptatrices de la transduction du signal (métabolisme)</term>
<term>Protéines associées aux microtubules (biosynthèse)</term>
<term>Protéines associées aux microtubules (génétique)</term>
<term>Protéines associées aux microtubules (métabolisme)</term>
<term>Protéines de liaison à l'ARN (biosynthèse)</term>
<term>Protéines de liaison à l'ARN (génétique)</term>
<term>Protéines de répression (biosynthèse)</term>
<term>Protéines de répression (génétique)</term>
<term>Protéines mitochondriales (génétique)</term>
<term>Protéines mitochondriales (métabolisme)</term>
<term>Protéines virales (génétique)</term>
<term>Protéines virales (immunologie)</term>
<term>Protéines à fluorescence verte</term>
<term>Syndrome respiratoire aigu sévère (immunologie)</term>
<term>Syndrome respiratoire aigu sévère (virologie)</term>
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<term>Ubiquitin-protein ligases (génétique)</term>
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<term>Virus du SRAS (génétique)</term>
<term>Virus du SRAS (immunologie)</term>
<term>dGTPases (génétique)</term>
<term>dGTPases (métabolisme)</term>
<term>Échappement immunitaire</term>
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<term>Repressor Proteins</term>
<term>Ubiquitin-Protein Ligases</term>
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<term>Mitochondrial Proteins</term>
<term>RNA-Binding Proteins</term>
<term>Repressor Proteins</term>
<term>Ubiquitin-Protein Ligases</term>
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<term>Mitochondrial Proteins</term>
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<term>TNF Receptor-Associated Factor 6</term>
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<term>Protéines de liaison à l'ARN</term>
<term>Protéines de répression</term>
<term>Ubiquitin-protein ligases</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Autophagy</term>
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<term>Mitochondria</term>
<term>Open Reading Frames</term>
<term>SARS Virus</term>
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<term>Cadres ouverts de lecture</term>
<term>Immunité innée</term>
<term>Mitochondries</term>
<term>Protéines associées aux microtubules</term>
<term>Protéines de liaison à l'ARN</term>
<term>Protéines de répression</term>
<term>Protéines mitochondriales</term>
<term>Protéines virales</term>
<term>Ubiquitin-protein ligases</term>
<term>Virus du SRAS</term>
<term>dGTPases</term>
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<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cadres ouverts de lecture</term>
<term>Mitochondries</term>
<term>Protéines virales</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Virus du SRAS</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Mitochondria</term>
<term>Open Reading Frames</term>
<term>SARS Virus</term>
<term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur-3 associé aux récepteurs de TNF</term>
<term>Facteur-6 associé aux récepteurs de TNF</term>
<term>Protéines adaptatrices de la transduction du signal</term>
<term>Protéines associées aux microtubules</term>
<term>Protéines mitochondriales</term>
<term>dGTPases</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Mitochondries</term>
<term>Syndrome respiratoire aigu sévère</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Mitochondria</term>
<term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Autophagy-Related Protein 5</term>
<term>Cell Line</term>
<term>Green Fluorescent Proteins</term>
<term>HEK293 Cells</term>
<term>Humans</term>
<term>Immune Evasion</term>
<term>RNA Interference</term>
<term>RNA, Small Interfering</term>
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<term>Humains</term>
<term>Interférence par ARN</term>
<term>Lignée cellulaire</term>
<term>Petit ARN interférent</term>
<term>Protéine-5 associée à l'autophagie</term>
<term>Protéines à fluorescence verte</term>
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<front><div type="abstract" xml:lang="en">Coronaviruses (CoV) have recently emerged as potentially serious pathogens that can cause significant human morbidity and death. The severe acute respiratory syndrome (SARS)-CoV was identified as the etiologic agent of the 2002-2003 international SARS outbreak. Yet, how SARS evades innate immune responses to cause human disease remains poorly understood. In this study, we show that a protein encoded by SARS-CoV designated as open reading frame-9b (ORF-9b) localizes to mitochondria and causes mitochondrial elongation by triggering ubiquitination and proteasomal degradation of dynamin-like protein 1, a host protein involved in mitochondrial fission. Also, acting on mitochondria, ORF-9b targets the mitochondrial-associated adaptor molecule MAVS signalosome by usurping PCBP2 and the HECT domain E3 ligase AIP4 to trigger the degradation of MAVS, TRAF3, and TRAF 6. This severely limits host cell IFN responses. Reducing either PCBP2 or AIP4 expression substantially reversed the ORF-9b-mediated reduction of MAVS and the suppression of antiviral transcriptional responses. Finally, transient ORF-9b expression led to a strong induction of autophagy in cells. The induction of autophagy depended upon ATG5, a critical autophagy regulator, but the inhibition of MAVS signaling did not. These results indicate that SARS-CoV ORF-9b manipulates host cell mitochondria and mitochondrial function to help evade host innate immunity. This study has uncovered an important clue to the pathogenesis of SARS-CoV infection and illustrates the havoc that a small ORF can cause in cells. </div>
</front>
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<DateCompleted><Year>2014</Year>
<Month>11</Month>
<Day>25</Day>
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<DateRevised><Year>2019</Year>
<Month>10</Month>
<Day>08</Day>
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<JournalIssue CitedMedium="Internet"><Volume>193</Volume>
<Issue>6</Issue>
<PubDate><Year>2014</Year>
<Month>Sep</Month>
<Day>15</Day>
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<Title>Journal of immunology (Baltimore, Md. : 1950)</Title>
<ISOAbbreviation>J. Immunol.</ISOAbbreviation>
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<ArticleTitle>SARS-coronavirus open reading frame-9b suppresses innate immunity by targeting mitochondria and the MAVS/TRAF3/TRAF6 signalosome.</ArticleTitle>
<Pagination><MedlinePgn>3080-9</MedlinePgn>
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<Abstract><AbstractText>Coronaviruses (CoV) have recently emerged as potentially serious pathogens that can cause significant human morbidity and death. The severe acute respiratory syndrome (SARS)-CoV was identified as the etiologic agent of the 2002-2003 international SARS outbreak. Yet, how SARS evades innate immune responses to cause human disease remains poorly understood. In this study, we show that a protein encoded by SARS-CoV designated as open reading frame-9b (ORF-9b) localizes to mitochondria and causes mitochondrial elongation by triggering ubiquitination and proteasomal degradation of dynamin-like protein 1, a host protein involved in mitochondrial fission. Also, acting on mitochondria, ORF-9b targets the mitochondrial-associated adaptor molecule MAVS signalosome by usurping PCBP2 and the HECT domain E3 ligase AIP4 to trigger the degradation of MAVS, TRAF3, and TRAF 6. This severely limits host cell IFN responses. Reducing either PCBP2 or AIP4 expression substantially reversed the ORF-9b-mediated reduction of MAVS and the suppression of antiviral transcriptional responses. Finally, transient ORF-9b expression led to a strong induction of autophagy in cells. The induction of autophagy depended upon ATG5, a critical autophagy regulator, but the inhibition of MAVS signaling did not. These results indicate that SARS-CoV ORF-9b manipulates host cell mitochondria and mitochondrial function to help evade host innate immunity. This study has uncovered an important clue to the pathogenesis of SARS-CoV infection and illustrates the havoc that a small ORF can cause in cells. </AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Shi</LastName>
<ForeName>Chong-Shan</ForeName>
<Initials>CS</Initials>
<AffiliationInfo><Affiliation>B Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Qi</LastName>
<ForeName>Hai-Yan</ForeName>
<Initials>HY</Initials>
<AffiliationInfo><Affiliation>Critical Care Medicine Department, National Institutes of Health, Bethesda, MD 20892; and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Boularan</LastName>
<ForeName>Cedric</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>B Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Huang</LastName>
<ForeName>Ning-Na</ForeName>
<Initials>NN</Initials>
<AffiliationInfo><Affiliation>B Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Abu-Asab</LastName>
<ForeName>Mones</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Immunopathology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shelhamer</LastName>
<ForeName>James H</ForeName>
<Initials>JH</Initials>
<AffiliationInfo><Affiliation>Critical Care Medicine Department, National Institutes of Health, Bethesda, MD 20892; and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kehrl</LastName>
<ForeName>John H</ForeName>
<Initials>JH</Initials>
<AffiliationInfo><Affiliation>B Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; jkehrl@niaid.nih.gov.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>ZIA AI000739-14</GrantID>
<Agency>Intramural NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
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<PublicationType UI="D052060">Research Support, N.I.H., Intramural</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2014</Year>
<Month>08</Month>
<Day>18</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>J Immunol</MedlineTA>
<NlmUniqueID>2985117R</NlmUniqueID>
<ISSNLinking>0022-1767</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C502778">ATG5 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D048868">Adaptor Proteins, Signal Transducing</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071187">Autophagy-Related Protein 5</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D008869">Microtubule-Associated Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D024101">Mitochondrial Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C000593134">ORF-9b protein, SARS coronavirus</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C501903">PCBP2 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D034741">RNA, Small Interfering</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016601">RNA-Binding Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D012097">Repressor Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D048008">TNF Receptor-Associated Factor 3</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D048029">TNF Receptor-Associated Factor 6</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C090656">TRAF3 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C505371">VISA protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014764">Viral Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>147336-22-9</RegistryNumber>
<NameOfSubstance UI="D049452">Green Fluorescent Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.3.2.26</RegistryNumber>
<NameOfSubstance UI="C432966">ITCH protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.3.2.27</RegistryNumber>
<NameOfSubstance UI="D044767">Ubiquitin-Protein Ligases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.6.1.-</RegistryNumber>
<NameOfSubstance UI="D020558">GTP Phosphohydrolases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.6.5.5</RegistryNumber>
<NameOfSubstance UI="C110768">DNM1L protein, human</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>AIM</CitationSubset>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D048868" MajorTopicYN="N">Adaptor Proteins, Signal Transducing</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071187" MajorTopicYN="N">Autophagy-Related Protein 5</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020558" MajorTopicYN="N">GTP Phosphohydrolases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D049452" MajorTopicYN="N">Green Fluorescent Proteins</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D057809" MajorTopicYN="N">HEK293 Cells</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D057131" MajorTopicYN="N">Immune Evasion</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007113" MajorTopicYN="N">Immunity, Innate</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
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<MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName>
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<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
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<MeshHeading><DescriptorName UI="D016366" MajorTopicYN="N">Open Reading Frames</DescriptorName>
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<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
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<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
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SARS-coronavirus open reading frame-9b suppresses innate immunity by targeting mitochondria and the MAVS/TRAF3/TRAF6 signalosome.

SARS-coronavirus open reading frame-9b suppresses innate immunity by targeting mitochondria and the MAVS/TRAF3/TRAF6 signalosome.

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