Severe acute respiratory syndrome coronavirus envelope protein regulates cell stress response and apoptosis.
Identifieur interne : 001516 ( Main/Exploration ); précédent : 001515; suivant : 001517Severe acute respiratory syndrome coronavirus envelope protein regulates cell stress response and apoptosis.
Auteurs : Marta L. Dediego [Espagne] ; Jose L. Nieto-Torres ; Jose M. Jiménez-Guarde O ; Jose A. Regla-Nava ; Enrique Alvarez ; Juan Carlos Oliveros ; Jincun Zhao ; Craig Fett ; Stanley Perlman ; Luis EnjuanesSource :
- PLoS pathogens [ 1553-7374 ] ; 2011.
Descripteurs français
- KwdFr :
- Apoptose (physiologie), Délétion de gène, Humains, Interactions hôte-pathogène, Lignée cellulaire tumorale, Protéines de l'enveloppe virale (génétique), Protéines de l'enveloppe virale (métabolisme), Régulation de l'expression des gènes viraux, Réplication virale, Stress physiologique (), Stress physiologique (génétique), Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (métabolisme), Syndrome respiratoire aigu sévère (virologie), Virulence (génétique), Virus du SRAS (génétique), Virus du SRAS (pathogénicité).
- MESH :
- anatomopathologie : Syndrome respiratoire aigu sévère.
- génétique : Protéines de l'enveloppe virale, Stress physiologique, Virulence, Virus du SRAS.
- métabolisme : Protéines de l'enveloppe virale, Syndrome respiratoire aigu sévère.
- pathogénicité : Virus du SRAS.
- physiologie : Apoptose.
- virologie : Syndrome respiratoire aigu sévère.
- Délétion de gène, Humains, Interactions hôte-pathogène, Lignée cellulaire tumorale, Régulation de l'expression des gènes viraux, Réplication virale, Stress physiologique.
English descriptors
- KwdEn :
- Apoptosis (physiology), Cell Line, Tumor, Gene Deletion, Gene Expression Regulation, Viral, Host-Pathogen Interactions, Humans, SARS Virus (genetics), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology), Stress, Physiological (drug effects), Stress, Physiological (genetics), Viral Envelope Proteins (genetics), Viral Envelope Proteins (metabolism), Virulence (genetics), Virus Replication.
- MESH :
- chemical , genetics : Viral Envelope Proteins.
- drug effects : Stress, Physiological.
- genetics : SARS Virus, Stress, Physiological, Virulence.
- metabolism : Severe Acute Respiratory Syndrome, Viral Envelope Proteins.
- pathogenicity : SARS Virus.
- pathology : Severe Acute Respiratory Syndrome.
- physiology : Apoptosis.
- virology : Severe Acute Respiratory Syndrome.
- Cell Line, Tumor, Gene Deletion, Gene Expression Regulation, Viral, Host-Pathogen Interactions, Humans, Virus Replication.
Abstract
Severe acute respiratory syndrome virus (SARS-CoV) that lacks the envelope (E) gene (rSARS-CoV-ΔE) is attenuated in vivo. To identify factors that contribute to rSARS-CoV-ΔE attenuation, gene expression in cells infected by SARS-CoV with or without E gene was compared. Twenty-five stress response genes were preferentially upregulated during infection in the absence of the E gene. In addition, genes involved in signal transduction, transcription, cell metabolism, immunoregulation, inflammation, apoptosis and cell cycle and differentiation were differentially regulated in cells infected with rSARS-CoV with or without the E gene. Administration of E protein in trans reduced the stress response in cells infected with rSARS-CoV-ΔE or with respiratory syncytial virus, or treated with drugs, such as tunicamycin and thapsigargin that elicit cell stress by different mechanisms. In addition, SARS-CoV E protein down-regulated the signaling pathway inositol-requiring enzyme 1 (IRE-1) of the unfolded protein response, but not the PKR-like ER kinase (PERK) or activating transcription factor 6 (ATF-6) pathways, and reduced cell apoptosis. Overall, the activation of the IRE-1 pathway was not able to restore cell homeostasis, and apoptosis was induced probably as a measure to protect the host by limiting virus production and dissemination. The expression of proinflammatory cytokines was reduced in rSARS-CoV-ΔE-infected cells compared to rSARS-CoV-infected cells, suggesting that the increase in stress responses and the reduction of inflammation in the absence of the E gene contributed to the attenuation of rSARS-CoV-ΔE.
DOI: 10.1371/journal.ppat.1002315
PubMed: 22028656
Affiliations:
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Dediego</name><affiliation wicri:level="4"><nlm:affiliation>Department of Molecular and Cell Biology, Centro Nacional de Biotecnología (CNB-CSIC), Campus Universidad Autónoma de Madrid, Madrid, Spain.</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Department of Molecular and Cell Biology, Centro Nacional de Biotecnología (CNB-CSIC), Campus Universidad Autónoma de Madrid, Madrid</wicri:regionArea><placeName><settlement type="city">Madrid</settlement><region nuts="2" type="region">Communauté de Madrid</region></placeName><orgName type="university">Université autonome de Madrid</orgName></affiliation></author><author><name sortKey="Nieto Torres, Jose L" sort="Nieto Torres, Jose L" uniqKey="Nieto Torres J" first="Jose L" last="Nieto-Torres">Jose L. Nieto-Torres</name></author><author><name sortKey="Jimenez Guarde O, Jose M" sort="Jimenez Guarde O, Jose M" uniqKey="Jimenez Guarde O J" first="Jose M" last="Jiménez-Guarde O">Jose M. Jiménez-Guarde O</name></author><author><name sortKey="Regla Nava, Jose A" sort="Regla Nava, Jose A" uniqKey="Regla Nava J" first="Jose A" last="Regla-Nava">Jose A. 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hôte-pathogène</term><term>Lignée cellulaire tumorale</term><term>Protéines de l'enveloppe virale (génétique)</term><term>Protéines de l'enveloppe virale (métabolisme)</term><term>Régulation de l'expression des gènes viraux</term><term>Réplication virale</term><term>Stress physiologique ()</term><term>Stress physiologique (génétique)</term><term>Syndrome respiratoire aigu sévère (anatomopathologie)</term><term>Syndrome respiratoire aigu sévère (métabolisme)</term><term>Syndrome respiratoire aigu sévère (virologie)</term><term>Virulence (génétique)</term><term>Virus du SRAS (génétique)</term><term>Virus du SRAS (pathogénicité)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Viral Envelope Proteins</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Stress, Physiological</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>SARS Virus</term><term>Stress, Physiological</term><term>Virulence</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéines de l'enveloppe virale</term><term>Stress physiologique</term><term>Virulence</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term><term>Viral Envelope Proteins</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protéines de l'enveloppe virale</term><term>Syndrome respiratoire aigu sévère</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="pathology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Apoptose</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Apoptosis</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Gene Deletion</term><term>Gene Expression Regulation, Viral</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Délétion de gène</term><term>Humains</term><term>Interactions hôte-pathogène</term><term>Lignée cellulaire tumorale</term><term>Régulation de l'expression des gènes viraux</term><term>Réplication virale</term><term>Stress physiologique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome virus (SARS-CoV) that lacks the envelope (E) gene (rSARS-CoV-ΔE) is attenuated in vivo. To identify factors that contribute to rSARS-CoV-ΔE attenuation, gene expression in cells infected by SARS-CoV with or without E gene was compared. Twenty-five stress response genes were preferentially upregulated during infection in the absence of the E gene. In addition, genes involved in signal transduction, transcription, cell metabolism, immunoregulation, inflammation, apoptosis and cell cycle and differentiation were differentially regulated in cells infected with rSARS-CoV with or without the E gene. Administration of E protein in trans reduced the stress response in cells infected with rSARS-CoV-ΔE or with respiratory syncytial virus, or treated with drugs, such as tunicamycin and thapsigargin that elicit cell stress by different mechanisms. In addition, SARS-CoV E protein down-regulated the signaling pathway inositol-requiring enzyme 1 (IRE-1) of the unfolded protein response, but not the PKR-like ER kinase (PERK) or activating transcription factor 6 (ATF-6) pathways, and reduced cell apoptosis. Overall, the activation of the IRE-1 pathway was not able to restore cell homeostasis, and apoptosis was induced probably as a measure to protect the host by limiting virus production and dissemination. The expression of proinflammatory cytokines was reduced in rSARS-CoV-ΔE-infected cells compared to rSARS-CoV-infected cells, suggesting that the increase in stress responses and the reduction of inflammation in the absence of the E gene contributed to the attenuation of rSARS-CoV-ΔE.</div></front></TEI><affiliations><list><country><li>Espagne</li></country><region><li>Communauté de Madrid</li></region><settlement><li>Madrid</li></settlement><orgName><li>Université autonome de Madrid</li></orgName></list><tree><noCountry><name sortKey="Alvarez, Enrique" sort="Alvarez, Enrique" uniqKey="Alvarez E" first="Enrique" last="Alvarez">Enrique Alvarez</name><name sortKey="Enjuanes, Luis" sort="Enjuanes, Luis" uniqKey="Enjuanes L" first="Luis" last="Enjuanes">Luis Enjuanes</name><name sortKey="Fett, Craig" sort="Fett, Craig" uniqKey="Fett C" first="Craig" last="Fett">Craig Fett</name><name sortKey="Jimenez Guarde O, Jose M" sort="Jimenez Guarde O, Jose M" uniqKey="Jimenez Guarde O J" first="Jose M" last="Jiménez-Guarde O">Jose M. Jiménez-Guarde O</name><name sortKey="Nieto Torres, Jose L" sort="Nieto Torres, Jose L" uniqKey="Nieto Torres J" first="Jose L" last="Nieto-Torres">Jose L. Nieto-Torres</name><name sortKey="Oliveros, Juan Carlos" sort="Oliveros, Juan Carlos" uniqKey="Oliveros J" first="Juan Carlos" last="Oliveros">Juan Carlos Oliveros</name><name sortKey="Perlman, Stanley" sort="Perlman, Stanley" uniqKey="Perlman S" first="Stanley" last="Perlman">Stanley Perlman</name><name sortKey="Regla Nava, Jose A" sort="Regla Nava, Jose A" uniqKey="Regla Nava J" first="Jose A" last="Regla-Nava">Jose A. Regla-Nava</name><name sortKey="Zhao, Jincun" sort="Zhao, Jincun" uniqKey="Zhao J" first="Jincun" last="Zhao">Jincun Zhao</name></noCountry><country name="Espagne"><region name="Communauté de Madrid"><name sortKey="Dediego, Marta L" sort="Dediego, Marta L" uniqKey="Dediego M" first="Marta L" last="Dediego">Marta L. 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