Nsp1 proteins of group I and SARS coronaviruses share structural and functional similarities
Identifieur interne : 002523 ( Main/Merge ); précédent : 002522; suivant : 002524Nsp1 proteins of group I and SARS coronaviruses share structural and functional similarities
Auteurs : Yongjin Wang [République populaire de Chine] ; Huiling Shi [République populaire de Chine] ; Pascal Rigolet [France] ; Nannan Wu [République populaire de Chine] ; Lichen Zhu [République populaire de Chine] ; Xu-Guang Xi [France] ; Astrid Vabret [France] ; Xiaoming Wang [République populaire de Chine] ; Tianhou Wang [République populaire de Chine]Source :
- Infection, Genetics and Evolution [ 1567-1348 ] ; 2010.
Descripteurs français
- KwdFr :
- Coronavirus (), Coronavirus (enzymologie), Coronavirus (génétique), Données de séquences moléculaires, Humains, Immunité innée, Lignée cellulaire, Modèles moléculaires, Prolifération cellulaire, RNA replicase (génétique), RNA replicase (métabolisme), Régulation de l'expression des gènes codant pour des enzymes, Régulation de l'expression des gènes viraux (physiologie), Séquence d'acides aminés.
- MESH :
- enzymologie : Coronavirus.
- génétique : Coronavirus, RNA replicase.
- métabolisme : RNA replicase.
- physiologie : Régulation de l'expression des gènes viraux.
- Coronavirus, Données de séquences moléculaires, Humains, Immunité innée, Lignée cellulaire, Modèles moléculaires, Prolifération cellulaire, Régulation de l'expression des gènes codant pour des enzymes, Séquence d'acides aminés.
English descriptors
- KwdEn :
- Amino Acid Sequence, Cell Line, Cell Proliferation, Coronavirus (classification), Coronavirus (enzymology), Coronavirus (genetics), Gene Expression Regulation, Enzymologic, Gene Expression Regulation, Viral (physiology), Humans, Immunity, Innate, Models, Molecular, Molecular Sequence Data, RNA Replicase (genetics), RNA Replicase (metabolism).
- MESH :
- chemical , genetics : RNA Replicase.
- classification : Coronavirus.
- enzymology : Coronavirus.
- genetics : Coronavirus.
- chemical , metabolism : RNA Replicase.
- physiology : Gene Expression Regulation, Viral.
- Amino Acid Sequence, Cell Line, Cell Proliferation, Gene Expression Regulation, Enzymologic, Humans, Immunity, Innate, Models, Molecular, Molecular Sequence Data.
Abstract
The nsp1 protein of the highly pathogenic SARS coronavirus suppresses host protein synthesis, including genes involved in the innate immune system. A bioinformatic analysis revealed that the nsp1 proteins of group I and SARS coronaviruses have similar structures. Nsp1 proteins of group I coronaviruses interacted with host ribosomal 40S subunit and did not inhibit IRF-3 activation. However, synthesis of host immune and non-immune proteins was inhibited by nsp1 proteins at both transcriptional and translational levels, similar to SARS coronavirus nsp1. These results indicate that different coronaviruses might employ the same nsp1 mechanism to antagonize host innate immunity and cell proliferation. However, nsp1 may not be the key determinant of viral pathogenicity, or the factor used by the SARS coronavirus to evade host innate immunity.
Url:
DOI: 10.1016/j.meegid.2010.05.014
PubMed: 20609418
PubMed Central: 7106014
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PMC:7106014Le document en format XML
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<term>Coronavirus (enzymology)</term>
<term>Coronavirus (genetics)</term>
<term>Gene Expression Regulation, Enzymologic</term>
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<term>Immunity, Innate</term>
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<term>Immunité innée</term>
<term>Lignée cellulaire</term>
<term>Modèles moléculaires</term>
<term>Prolifération cellulaire</term>
<term>RNA replicase (génétique)</term>
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<term>Séquence d'acides aminés</term>
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<front><div type="abstract" xml:lang="en"><p>The nsp1 protein of the highly pathogenic SARS coronavirus suppresses host protein synthesis, including genes involved in the innate immune system. A bioinformatic analysis revealed that the nsp1 proteins of group I and SARS coronaviruses have similar structures. Nsp1 proteins of group I coronaviruses interacted with host ribosomal 40S subunit and did not inhibit IRF-3 activation. However, synthesis of host immune and non-immune proteins was inhibited by nsp1 proteins at both transcriptional and translational levels, similar to SARS coronavirus nsp1. These results indicate that different coronaviruses might employ the same nsp1 mechanism to antagonize host innate immunity and cell proliferation. However, nsp1 may not be the key determinant of viral pathogenicity, or the factor used by the SARS coronavirus to evade host innate immunity.</p>
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<wicri:regionArea>Laboratory of Wildlife Epidemic Diseases, East China Normal University, Shanghai 200062</wicri:regionArea>
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</affiliation>
</author>
<author><name sortKey="Rigolet, Pascal" sort="Rigolet, Pascal" uniqKey="Rigolet P" first="Pascal" last="Rigolet">Pascal Rigolet</name>
<affiliation wicri:level="3"><nlm:aff id="aff2">CNRS, UMR 3348, Institut Curie-Section de Recherche, Centre Universitaire, Batiment 110, F-91405 Orsay, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>CNRS, UMR 3348, Institut Curie-Section de Recherche, Centre Universitaire, Batiment 110, F-91405 Orsay</wicri:regionArea>
<placeName><region type="region" nuts="2">Île-de-France</region>
<settlement type="city">Orsay</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Wu, Nannan" sort="Wu, Nannan" uniqKey="Wu N" first="Nannan" last="Wu">Nannan Wu</name>
<affiliation wicri:level="1"><nlm:aff id="aff1">Laboratory of Wildlife Epidemic Diseases, East China Normal University, Shanghai 200062, China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Laboratory of Wildlife Epidemic Diseases, East China Normal University, Shanghai 200062</wicri:regionArea>
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</affiliation>
</author>
<author><name sortKey="Zhu, Lichen" sort="Zhu, Lichen" uniqKey="Zhu L" first="Lichen" last="Zhu">Lichen Zhu</name>
<affiliation wicri:level="1"><nlm:aff id="aff1">Laboratory of Wildlife Epidemic Diseases, East China Normal University, Shanghai 200062, China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Laboratory of Wildlife Epidemic Diseases, East China Normal University, Shanghai 200062</wicri:regionArea>
<wicri:noRegion>Shanghai 200062</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Xi, Xu Guang" sort="Xi, Xu Guang" uniqKey="Xi X" first="Xu-Guang" last="Xi">Xu-Guang Xi</name>
<affiliation wicri:level="3"><nlm:aff id="aff2">CNRS, UMR 3348, Institut Curie-Section de Recherche, Centre Universitaire, Batiment 110, F-91405 Orsay, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>CNRS, UMR 3348, Institut Curie-Section de Recherche, Centre Universitaire, Batiment 110, F-91405 Orsay</wicri:regionArea>
<placeName><region type="region" nuts="2">Île-de-France</region>
<settlement type="city">Orsay</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Vabret, Astrid" sort="Vabret, Astrid" uniqKey="Vabret A" first="Astrid" last="Vabret">Astrid Vabret</name>
<affiliation wicri:level="3"><nlm:aff id="aff3">Laboratory of Virology, University Hospital of Caen, Avenue Georges Clemenceau, 14033 Caen cedex, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>Laboratory of Virology, University Hospital of Caen, Avenue Georges Clemenceau, 14033 Caen cedex</wicri:regionArea>
<placeName><region type="region" nuts="2">Région Normandie</region>
<region type="old region" nuts="2">Basse-Normandie</region>
<settlement type="city">Caen</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Wang, Xiaoming" sort="Wang, Xiaoming" uniqKey="Wang X" first="Xiaoming" last="Wang">Xiaoming Wang</name>
<affiliation wicri:level="1"><nlm:aff id="aff1">Laboratory of Wildlife Epidemic Diseases, East China Normal University, Shanghai 200062, China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Laboratory of Wildlife Epidemic Diseases, East China Normal University, Shanghai 200062</wicri:regionArea>
<wicri:noRegion>Shanghai 200062</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Wang, Tianhou" sort="Wang, Tianhou" uniqKey="Wang T" first="Tianhou" last="Wang">Tianhou Wang</name>
<affiliation wicri:level="1"><nlm:aff id="aff1">Laboratory of Wildlife Epidemic Diseases, East China Normal University, Shanghai 200062, China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Laboratory of Wildlife Epidemic Diseases, East China Normal University, Shanghai 200062</wicri:regionArea>
<wicri:noRegion>Shanghai 200062</wicri:noRegion>
</affiliation>
</author>
</analytic>
<series><title level="j">Infection, Genetics and Evolution</title>
<idno type="ISSN">1567-1348</idno>
<idno type="eISSN">1567-7257</idno>
<imprint><date when="2010">2010</date>
</imprint>
</series>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amino Acid Sequence</term>
<term>Cell Line</term>
<term>Cell Proliferation</term>
<term>Coronavirus (classification)</term>
<term>Coronavirus (enzymology)</term>
<term>Coronavirus (genetics)</term>
<term>Gene Expression Regulation, Enzymologic</term>
<term>Gene Expression Regulation, Viral (physiology)</term>
<term>Humans</term>
<term>Immunity, Innate</term>
<term>Models, Molecular</term>
<term>Molecular Sequence Data</term>
<term>RNA Replicase (genetics)</term>
<term>RNA Replicase (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Coronavirus ()</term>
<term>Coronavirus (enzymologie)</term>
<term>Coronavirus (génétique)</term>
<term>Données de séquences moléculaires</term>
<term>Humains</term>
<term>Immunité innée</term>
<term>Lignée cellulaire</term>
<term>Modèles moléculaires</term>
<term>Prolifération cellulaire</term>
<term>RNA replicase (génétique)</term>
<term>RNA replicase (métabolisme)</term>
<term>Régulation de l'expression des gènes codant pour des enzymes</term>
<term>Régulation de l'expression des gènes viraux (physiologie)</term>
<term>Séquence d'acides aminés</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>RNA Replicase</term>
</keywords>
<keywords scheme="MESH" qualifier="classification" xml:lang="en"><term>Coronavirus</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Coronavirus</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Coronavirus</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Coronavirus</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Coronavirus</term>
<term>RNA replicase</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>RNA Replicase</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>RNA replicase</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Régulation de l'expression des gènes viraux</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Gene Expression Regulation, Viral</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Amino Acid Sequence</term>
<term>Cell Line</term>
<term>Cell Proliferation</term>
<term>Gene Expression Regulation, Enzymologic</term>
<term>Humans</term>
<term>Immunity, Innate</term>
<term>Models, Molecular</term>
<term>Molecular Sequence Data</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Coronavirus</term>
<term>Données de séquences moléculaires</term>
<term>Humains</term>
<term>Immunité innée</term>
<term>Lignée cellulaire</term>
<term>Modèles moléculaires</term>
<term>Prolifération cellulaire</term>
<term>Régulation de l'expression des gènes codant pour des enzymes</term>
<term>Séquence d'acides aminés</term>
</keywords>
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<front><div type="abstract" xml:lang="en"><p>The nsp1 protein of the highly pathogenic SARS coronavirus suppresses host protein synthesis, including genes involved in the innate immune system. A bioinformatic analysis revealed that the nsp1 proteins of group I and SARS coronaviruses have similar structures. Nsp1 proteins of group I coronaviruses interacted with host ribosomal 40S subunit and did not inhibit IRF-3 activation. However, synthesis of host immune and non-immune proteins was inhibited by nsp1 proteins at both transcriptional and translational levels, similar to SARS coronavirus nsp1. These results indicate that different coronaviruses might employ the same nsp1 mechanism to antagonize host innate immunity and cell proliferation. However, nsp1 may not be the key determinant of viral pathogenicity, or the factor used by the SARS coronavirus to evade host innate immunity.</p>
</div>
</front>
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</listBibl>
</div1>
</back>
</TEI>
</PMC>
</double>
</record>
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