Message in a bottle: lessons learned from antagonism of STING signalling during RNA virus infection
Identifieur interne : 001619 ( Main/Exploration ); précédent : 001618; suivant : 001620Message in a bottle: lessons learned from antagonism of STING signalling during RNA virus infection
Auteurs : Kevin Maringer [États-Unis, Royaume-Uni] ; Ana Fernandez-Sesma [États-Unis]Source :
- Cytokine & Growth Factor Reviews [ 1359-6101 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux, Coronavirus humain NL63 (génétique), Coronavirus humain NL63 (immunologie), Dengue (génétique), Dengue (immunologie), Humains, Nucleotidyltransferases (génétique), Nucleotidyltransferases (immunologie), Protéines membranaires (génétique), Protéines membranaires (immunologie), Protéines virales (génétique), Protéines virales (immunologie), Souris, Syndrome respiratoire aigu sévère (génétique), Syndrome respiratoire aigu sévère (immunologie), Transduction du signal (génétique), Transduction du signal (immunologie), Virus de la dengue (génétique), Virus de la dengue (immunologie), Virus du SRAS (génétique), Virus du SRAS (immunologie).
- MESH :
- génétique : Coronavirus humain NL63, Dengue, Nucleotidyltransferases, Protéines membranaires, Protéines virales, Syndrome respiratoire aigu sévère, Transduction du signal, Virus de la dengue, Virus du SRAS.
- immunologie : Coronavirus humain NL63, Dengue, Nucleotidyltransferases, Protéines membranaires, Protéines virales, Syndrome respiratoire aigu sévère, Transduction du signal, Virus de la dengue, Virus du SRAS.
- Animaux, Humains, Souris.
English descriptors
- KwdEn :
- Animals, Coronavirus NL63, Human (genetics), Coronavirus NL63, Human (immunology), Dengue (genetics), Dengue (immunology), Dengue Virus (genetics), Dengue Virus (immunology), Humans, Membrane Proteins (genetics), Membrane Proteins (immunology), Mice, Nucleotidyltransferases (genetics), Nucleotidyltransferases (immunology), SARS Virus (genetics), SARS Virus (immunology), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (immunology), Signal Transduction (genetics), Signal Transduction (immunology), Viral Proteins (genetics), Viral Proteins (immunology).
- MESH :
- chemical , genetics : Membrane Proteins, Nucleotidyltransferases, Viral Proteins.
- genetics : Coronavirus NL63, Human, Dengue, Dengue Virus, SARS Virus, Severe Acute Respiratory Syndrome, Signal Transduction.
- immunology : Coronavirus NL63, Human, Dengue, Dengue Virus, Membrane Proteins, Nucleotidyltransferases, SARS Virus, Severe Acute Respiratory Syndrome, Signal Transduction, Viral Proteins.
- Animals, Humans, Mice.
Abstract
STING has emerged in recent years as an important signalling adaptor in the activation of type I interferon responses during infection with DNA viruses and bacteria. An increasing body of evidence suggests that STING also modulates responses to RNA viruses, though the mechanisms remain less clear. In this review, we give a brief overview of the ways in which STING facilitates sensing of RNA viruses. These include modulation of RIG-I-dependent responses through STING's interaction with MAVS, and more speculative mechanisms involving the DNA sensor cGAS and sensing of membrane remodelling events. We then provide an in-depth literature review to summarise the known mechanisms by which RNA viruses of the families
Url:
DOI: 10.1016/j.cytogfr.2014.08.004
PubMed: 25212897
PubMed Central: 4330990
Affiliations:
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Le document en format XML
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School of Medicine at Mount Sinai, New York, NY 10029</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation><affiliation wicri:level="1"><nlm:aff id="aff0010">School of Cellular and Molecular Medicine, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, United Kingdom</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>School of Cellular and Molecular Medicine, School of Medical Sciences, University of Bristol, Bristol BS8 1TD</wicri:regionArea><wicri:noRegion>Bristol BS8 1TD</wicri:noRegion></affiliation></author><author><name sortKey="Fernandez Sesma, Ana" sort="Fernandez Sesma, Ana" uniqKey="Fernandez Sesma A" first="Ana" last="Fernandez-Sesma">Ana Fernandez-Sesma</name><affiliation wicri:level="2"><nlm:aff id="aff0005">Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author></analytic><series><title level="j">Cytokine & Growth Factor Reviews</title><idno type="ISSN">1359-6101</idno><idno type="eISSN">1879-0305</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Coronavirus NL63, Human (genetics)</term><term>Coronavirus NL63, Human (immunology)</term><term>Dengue (genetics)</term><term>Dengue (immunology)</term><term>Dengue Virus (genetics)</term><term>Dengue Virus (immunology)</term><term>Humans</term><term>Membrane Proteins (genetics)</term><term>Membrane Proteins (immunology)</term><term>Mice</term><term>Nucleotidyltransferases (genetics)</term><term>Nucleotidyltransferases (immunology)</term><term>SARS Virus (genetics)</term><term>SARS Virus (immunology)</term><term>Severe Acute Respiratory Syndrome (genetics)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Signal Transduction (genetics)</term><term>Signal Transduction (immunology)</term><term>Viral Proteins (genetics)</term><term>Viral Proteins (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Coronavirus humain NL63 (génétique)</term><term>Coronavirus humain NL63 (immunologie)</term><term>Dengue (génétique)</term><term>Dengue (immunologie)</term><term>Humains</term><term>Nucleotidyltransferases (génétique)</term><term>Nucleotidyltransferases (immunologie)</term><term>Protéines membranaires (génétique)</term><term>Protéines membranaires (immunologie)</term><term>Protéines virales (génétique)</term><term>Protéines virales (immunologie)</term><term>Souris</term><term>Syndrome respiratoire aigu sévère (génétique)</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Transduction du signal (génétique)</term><term>Transduction du signal (immunologie)</term><term>Virus de la dengue (génétique)</term><term>Virus de la dengue (immunologie)</term><term>Virus du SRAS (génétique)</term><term>Virus du SRAS (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Membrane Proteins</term><term>Nucleotidyltransferases</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Coronavirus NL63, Human</term><term>Dengue</term><term>Dengue Virus</term><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Coronavirus humain NL63</term><term>Dengue</term><term>Nucleotidyltransferases</term><term>Protéines membranaires</term><term>Protéines virales</term><term>Syndrome respiratoire aigu sévère</term><term>Transduction du signal</term><term>Virus de la dengue</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Coronavirus humain NL63</term><term>Dengue</term><term>Nucleotidyltransferases</term><term>Protéines membranaires</term><term>Protéines virales</term><term>Syndrome respiratoire aigu sévère</term><term>Transduction du signal</term><term>Virus de la dengue</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Coronavirus NL63, Human</term><term>Dengue</term><term>Dengue Virus</term><term>Membrane Proteins</term><term>Nucleotidyltransferases</term><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term><term>Signal Transduction</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Mice</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>STING has emerged in recent years as an important signalling adaptor in the activation of type I interferon responses during infection with DNA viruses and bacteria. An increasing body of evidence suggests that STING also modulates responses to RNA viruses, though the mechanisms remain less clear. In this review, we give a brief overview of the ways in which STING facilitates sensing of RNA viruses. These include modulation of RIG-I-dependent responses through STING's interaction with MAVS, and more speculative mechanisms involving the DNA sensor cGAS and sensing of membrane remodelling events. We then provide an in-depth literature review to summarise the known mechanisms by which RNA viruses of the families <italic>Flaviviridae</italic> and <italic>Coronaviridae</italic> evade sensing through STING. Our own work has shown that the NS2B/3 protease complex of the flavivirus dengue virus binds and cleaves STING, and that an inability to degrade murine STING may contribute to host restriction in this virus. We contrast this to the mechanism employed by the distantly related hepacivirus hepatitis C virus, in which STING is bound and inactivated by the NS4B protein. Finally, we discuss STING antagonism in the coronaviruses SARS coronavirus and human coronavirus NL63, which disrupt K63-linked polyubiquitination and dimerisation of STING (both of which are required for STING-mediated activation of IRF-3) <italic>via</italic> their papain-like proteases. We draw parallels with less-well characterised mechanisms of STING antagonism in related viruses, and place our current knowledge in the context of species tropism restrictions that potentially affect the emergence of new human pathogens.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Yoneyama, M" uniqKey="Yoneyama M">M. Yoneyama</name></author><author><name sortKey="Fujita, T" uniqKey="Fujita T">T. 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Chen</name></author><author><name sortKey="Guo, B" uniqKey="Guo B">B. Guo</name></author><author><name sortKey="Cheng, G" uniqKey="Cheng G">G. Cheng</name></author><author><name sortKey="Tang, H" uniqKey="Tang H">H. Tang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wang, G" uniqKey="Wang G">G. Wang</name></author><author><name sortKey="Chen, G" uniqKey="Chen G">G. Chen</name></author><author><name sortKey="Zheng, D" uniqKey="Zheng D">D. Zheng</name></author><author><name sortKey="Cheng, G" uniqKey="Cheng G">G. Cheng</name></author><author><name sortKey="Tang, H" uniqKey="Tang H">H. Tang</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Royaume-Uni</li><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Maringer, Kevin" sort="Maringer, Kevin" uniqKey="Maringer K" first="Kevin" last="Maringer">Kevin Maringer</name></region><name sortKey="Fernandez Sesma, Ana" sort="Fernandez Sesma, Ana" uniqKey="Fernandez Sesma A" first="Ana" last="Fernandez-Sesma">Ana Fernandez-Sesma</name></country><country name="Royaume-Uni"><noRegion><name sortKey="Maringer, Kevin" sort="Maringer, Kevin" uniqKey="Maringer K" first="Kevin" last="Maringer">Kevin Maringer</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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