The Severe Acute Respiratory Syndrome Coronavirus Nucleocapsid Inhibits Type I Interferon Production by Interfering with TRIM25-Mediated RIG-I Ubiquitination
Identifieur interne : 000D54 ( Main/Exploration ); précédent : 000D53; suivant : 000D55The Severe Acute Respiratory Syndrome Coronavirus Nucleocapsid Inhibits Type I Interferon Production by Interfering with TRIM25-Mediated RIG-I Ubiquitination
Auteurs : Yong Hu ; Wei Li ; Ting Gao ; Yan Cui ; Yanwen Jin ; Ping Li ; Qingjun Ma ; Xuan Liu ; Cheng CaoSource :
- Journal of Virology [ 0022-538X ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux, Facteurs de transcription (métabolisme), Humains, Interféron de type I (métabolisme), Liaison aux protéines, Lignée cellulaire, Protéines nucléocapside (métabolisme), Protéines à motif tripartite (métabolisme), Réplication virale, Tolérance immunitaire, Ubiquitin-protein ligases (métabolisme), Ubiquitinylation, Virus du SRAS (immunologie), Virus du SRAS (pathogénicité), Virus du SRAS (physiologie), Échappement immunitaire.
- MESH :
- immunologie : Virus du SRAS.
- métabolisme : Facteurs de transcription, Interféron de type I, Protéines nucléocapside, Protéines à motif tripartite, Ubiquitin-protein ligases.
- pathogénicité : Virus du SRAS.
- physiologie : Virus du SRAS.
- Animaux, Humains, Liaison aux protéines, Lignée cellulaire, Réplication virale, Tolérance immunitaire, Ubiquitinylation, Échappement immunitaire.
English descriptors
- KwdEn :
- Animals, Cell Line, Humans, Immune Evasion, Immune Tolerance, Interferon Type I (metabolism), Nucleocapsid Proteins (metabolism), Protein Binding, SARS Virus (immunology), SARS Virus (pathogenicity), SARS Virus (physiology), Transcription Factors (metabolism), Tripartite Motif Proteins (metabolism), Ubiquitin-Protein Ligases (metabolism), Ubiquitination, Virus Replication.
- MESH :
- chemical , metabolism : Interferon Type I, Nucleocapsid Proteins, Transcription Factors, Tripartite Motif Proteins, Ubiquitin-Protein Ligases.
- immunology : SARS Virus.
- pathogenicity : SARS Virus.
- physiology : SARS Virus.
- Animals, Cell Line, Humans, Immune Evasion, Immune Tolerance, Protein Binding, Ubiquitination, Virus Replication.
Abstract
Severe acute respiratory syndrome (SARS) is a respiratory disease, caused by a coronavirus (SARS-CoV), that is characterized by atypical pneumonia. The nucleocapsid protein (N protein) of SARS-CoV plays an important role in inhibition of type I interferon (IFN) production via an unknown mechanism. In this study, the SARS-CoV N protein was found to bind to the SPRY domain of the tripartite motif protein 25 (TRIM25) E3 ubiquitin ligase, thereby interfering with the association between TRIM25 and retinoic acid-inducible gene I (RIG-I) and inhibiting TRIM25-mediated RIG-I ubiquitination and activation. Type I IFN production induced by poly I·C or Sendai virus (SeV) was suppressed by the SARS-CoV N protein. SARS-CoV replication was increased by overexpression of the full-length N protein but not N amino acids 1 to 361, which could not interact with TRIM25. These findings provide an insightful interpretation of the SARS-CoV-mediated host innate immune suppression caused by the N protein.
Url:
DOI: 10.1128/JVI.02143-16
PubMed: 28148787
PubMed Central: 5375661
Affiliations:
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Le document en format XML
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xml:lang="en" level="a" type="main">The Severe Acute Respiratory Syndrome Coronavirus Nucleocapsid Inhibits Type I Interferon Production by Interfering with TRIM25-Mediated RIG-I Ubiquitination</title><author><name sortKey="Hu, Yong" sort="Hu, Yong" uniqKey="Hu Y" first="Yong" last="Hu">Yong Hu</name></author><author><name sortKey="Li, Wei" sort="Li, Wei" uniqKey="Li W" first="Wei" last="Li">Wei Li</name></author><author><name sortKey="Gao, Ting" sort="Gao, Ting" uniqKey="Gao T" first="Ting" last="Gao">Ting Gao</name></author><author><name sortKey="Cui, Yan" sort="Cui, Yan" uniqKey="Cui Y" first="Yan" last="Cui">Yan Cui</name></author><author><name sortKey="Jin, Yanwen" sort="Jin, Yanwen" uniqKey="Jin Y" first="Yanwen" last="Jin">Yanwen Jin</name></author><author><name sortKey="Li, Ping" sort="Li, Ping" uniqKey="Li P" first="Ping" last="Li">Ping Li</name></author><author><name sortKey="Ma, Qingjun" sort="Ma, Qingjun" uniqKey="Ma Q" first="Qingjun" last="Ma">Qingjun Ma</name></author><author><name sortKey="Liu, Xuan" sort="Liu, Xuan" uniqKey="Liu X" first="Xuan" last="Liu">Xuan Liu</name></author><author><name sortKey="Cao, Cheng" sort="Cao, Cheng" uniqKey="Cao C" first="Cheng" last="Cao">Cheng Cao</name></author></analytic><series><title level="j">Journal of Virology</title><idno type="ISSN">0022-538X</idno><idno type="eISSN">1098-5514</idno><imprint><date when="2017">2017</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>Immune Evasion</term><term>Immune Tolerance</term><term>Interferon Type I (metabolism)</term><term>Nucleocapsid Proteins (metabolism)</term><term>Protein Binding</term><term>SARS Virus (immunology)</term><term>SARS Virus (pathogenicity)</term><term>SARS Virus (physiology)</term><term>Transcription Factors (metabolism)</term><term>Tripartite Motif Proteins (metabolism)</term><term>Ubiquitin-Protein Ligases (metabolism)</term><term>Ubiquitination</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Facteurs de transcription (métabolisme)</term><term>Humains</term><term>Interféron de type I (métabolisme)</term><term>Liaison aux protéines</term><term>Lignée cellulaire</term><term>Protéines nucléocapside (métabolisme)</term><term>Protéines à motif tripartite (métabolisme)</term><term>Réplication virale</term><term>Tolérance immunitaire</term><term>Ubiquitin-protein ligases (métabolisme)</term><term>Ubiquitinylation</term><term>Virus du SRAS (immunologie)</term><term>Virus du SRAS (pathogénicité)</term><term>Virus du SRAS (physiologie)</term><term>Échappement immunitaire</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Interferon Type I</term><term>Nucleocapsid Proteins</term><term>Transcription Factors</term><term>Tripartite Motif Proteins</term><term>Ubiquitin-Protein Ligases</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteurs de transcription</term><term>Interféron de type I</term><term>Protéines nucléocapside</term><term>Protéines à motif tripartite</term><term>Ubiquitin-protein ligases</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Humans</term><term>Immune Evasion</term><term>Immune Tolerance</term><term>Protein Binding</term><term>Ubiquitination</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Liaison aux protéines</term><term>Lignée cellulaire</term><term>Réplication virale</term><term>Tolérance immunitaire</term><term>Ubiquitinylation</term><term>Échappement immunitaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>ABSTRACT</title><p>Severe acute respiratory syndrome (SARS) is a respiratory disease, caused by a coronavirus (SARS-CoV), that is characterized by atypical pneumonia. The nucleocapsid protein (N protein) of SARS-CoV plays an important role in inhibition of type I interferon (IFN) production via an unknown mechanism. In this study, the SARS-CoV N protein was found to bind to the SPRY domain of the tripartite motif protein 25 (TRIM25) E3 ubiquitin ligase, thereby interfering with the association between TRIM25 and retinoic acid-inducible gene I (RIG-I) and inhibiting TRIM25-mediated RIG-I ubiquitination and activation. Type I IFN production induced by poly I·C or Sendai virus (SeV) was suppressed by the SARS-CoV N protein. SARS-CoV replication was increased by overexpression of the full-length N protein but not N amino acids 1 to 361, which could not interact with TRIM25. These findings provide an insightful interpretation of the SARS-CoV-mediated host innate immune suppression caused by the N protein.</p><p><bold>IMPORTANCE</bold> The SARS-CoV N protein is essential for the viral life cycle and plays a key role in the virus-host interaction. We demonstrated that the interaction between the C terminus of the N protein and the SPRY domain of TRIM25 inhibited TRIM25-mediated RIG-I ubiquitination, which resulted in the inhibition of IFN production. We also found that the Middle East respiratory syndrome CoV (MERS-CoV) N protein interacted with TRIM25 and inhibited RIG-I signaling. The outcomes of these findings indicate the function of the coronavirus N protein in modulating the host's initial innate immune response.</p></div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Cao, Cheng" sort="Cao, Cheng" uniqKey="Cao C" first="Cheng" last="Cao">Cheng Cao</name><name sortKey="Cui, Yan" sort="Cui, Yan" uniqKey="Cui Y" first="Yan" last="Cui">Yan Cui</name><name sortKey="Gao, Ting" sort="Gao, Ting" uniqKey="Gao T" first="Ting" last="Gao">Ting Gao</name><name sortKey="Hu, Yong" sort="Hu, Yong" uniqKey="Hu Y" first="Yong" last="Hu">Yong Hu</name><name sortKey="Jin, Yanwen" sort="Jin, Yanwen" uniqKey="Jin Y" first="Yanwen" last="Jin">Yanwen Jin</name><name sortKey="Li, Ping" sort="Li, Ping" uniqKey="Li P" first="Ping" last="Li">Ping Li</name><name sortKey="Li, Wei" sort="Li, Wei" uniqKey="Li W" first="Wei" last="Li">Wei Li</name><name sortKey="Liu, Xuan" sort="Liu, Xuan" uniqKey="Liu X" first="Xuan" last="Liu">Xuan Liu</name><name sortKey="Ma, Qingjun" sort="Ma, Qingjun" uniqKey="Ma Q" first="Qingjun" last="Ma">Qingjun Ma</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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