SrasV1, PascalFrancis, Corpus, bibRecord, 000341

The coronavirus spike protein induces endoplasmic reticulum stress and upregulation of intracellular chemokine mRNA concentrations

Identifieur interne : 000341 ( PascalFrancis/Corpus ); précédent : 000340; suivant : 000342

The coronavirus spike protein induces endoplasmic reticulum stress and upregulation of intracellular chemokine mRNA concentrations

Auteurs : Gijs A. Versteeg ; Paula S. Van De Nes ; Peter J. Bredenbeek ; Willy J. M. Spaan

Source :

Journal of virology [ 0022-538X ] ; 2007.

RBID : Pascal:07-0485996

Descripteurs français

Pascal (Inist)
- Coronavirus, Protéine, Réticulum endoplasmique, Stress, Intracellulaire, Chimiokine, RNA messager, Virologie.

English descriptors

KwdEn :
- Chemokine, Coronavirus, Endoplasmic reticulum, Intracellular, Messenger RNA, Protein, Stress, Virology.

Abstract

Murine hepatitis virus (MHV) and severe acute respiratory syndrome (SARS) coronavirus (CoV) are two of the best-studied representatives of the family Coronaviridae. During CoV infection, numerous cytokines and chemokines are induced in vitro and in vivo. Human interleukin 8 and its mouse functional counterpart, CXCL2, are early-expressed chemokines. Here we show that SARS-CoV and MHV induce endoplasmic reticulum (ER) stress and Cxcl2 mRNA transcription during infection in vitro. Expression of the viral spike protein significantly induced ER stress and Cxcl2 mRNA upregulation, while expression of the other structural genes did not. Additional experiments with UV-inactivated virus, cell-cell fusion-blocking antibodies, and an MHV mutant with a defect in spike protein maturation demonstrated that spike-host interactions in the ER are responsible for the induction of ER stress and subsequent Cxcl2 mRNA transcription. Despite significant increases in levels of Cxcl2 mRNA and functional nucleus-to-cytoplasm RNA transport, no CXCL2 protein was released into the medium from MHV-infected cells. Yet Sendai virus-infected cells showed substantial Cxcl2 mRNA induction and a simultaneous increase in levels of secreted CXCL2 protein. Our results demonstrate that expression of CoV spike proteins induces ER stress, which could subsequently trigger innate immune responses. However, at that point in infection, translation of host mRNA is already severely reduced in infected cells, preventing the synthesis of CXCL2 and ER stress proteins despite their increased mRNA concentrations.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11	`02`	`1`		`@1 VAN DE NES (Paula S.)`
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Format Inist (serveur)

NO :	PASCAL 07-0485996 INIST
ET :	The coronavirus spike protein induces endoplasmic reticulum stress and upregulation of intracellular chemokine mRNA concentrations
AU :	VERSTEEG (Gijs A.); VAN DE NES (Paula S.); BREDENBEEK (Peter J.); SPAAN (Willy J. M.)
AF :	Molecular Virology Laboratory, Department of Medical Microbiology, Center of Infectious Diseases, Leiden University Medical Center, P.O. Box 9600/2300 RC Leiden/Pays-Bas (1 aut., 2 aut., 3 aut., 4 aut.)
DT :	Publication en série; Niveau analytique
SO :	Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2007; Vol. 81; No. 20; Pp. 10981-10990; Bibl. 52 ref.
LA :	Anglais
EA :	Murine hepatitis virus (MHV) and severe acute respiratory syndrome (SARS) coronavirus (CoV) are two of the best-studied representatives of the family Coronaviridae. During CoV infection, numerous cytokines and chemokines are induced in vitro and in vivo. Human interleukin 8 and its mouse functional counterpart, CXCL2, are early-expressed chemokines. Here we show that SARS-CoV and MHV induce endoplasmic reticulum (ER) stress and Cxcl2 mRNA transcription during infection in vitro. Expression of the viral spike protein significantly induced ER stress and Cxcl2 mRNA upregulation, while expression of the other structural genes did not. Additional experiments with UV-inactivated virus, cell-cell fusion-blocking antibodies, and an MHV mutant with a defect in spike protein maturation demonstrated that spike-host interactions in the ER are responsible for the induction of ER stress and subsequent Cxcl2 mRNA transcription. Despite significant increases in levels of Cxcl2 mRNA and functional nucleus-to-cytoplasm RNA transport, no CXCL2 protein was released into the medium from MHV-infected cells. Yet Sendai virus-infected cells showed substantial Cxcl2 mRNA induction and a simultaneous increase in levels of secreted CXCL2 protein. Our results demonstrate that expression of CoV spike proteins induces ER stress, which could subsequently trigger innate immune responses. However, at that point in infection, translation of host mRNA is already severely reduced in infected cells, preventing the synthesis of CXCL2 and ER stress proteins despite their increased mRNA concentrations.
CC :	002A05C10
FD :	Coronavirus; Protéine; Réticulum endoplasmique; Stress; Intracellulaire; Chimiokine; RNA messager; Virologie
FG :	Coronaviridae; Nidovirales; Virus
ED :	Coronavirus; Protein; Endoplasmic reticulum; Stress; Intracellular; Chemokine; Messenger RNA; Virology
EG :	Coronaviridae; Nidovirales; Virus
SD :	Coronavirus; Proteína; Retículo endoplásmico; Estrés; Intracelular; Quimioquina; RNA mensajero; Virología
LO :	INIST-13592.354000143477600150
ID :	07-0485996

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Pascal:07-0485996

Le document en format XML

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<front><div type="abstract" xml:lang="en">Murine hepatitis virus (MHV) and severe acute respiratory syndrome (SARS) coronavirus (CoV) are two of the best-studied representatives of the family Coronaviridae. During CoV infection, numerous cytokines and chemokines are induced in vitro and in vivo. Human interleukin 8 and its mouse functional counterpart, CXCL2, are early-expressed chemokines. Here we show that SARS-CoV and MHV induce endoplasmic reticulum (ER) stress and Cxcl2 mRNA transcription during infection in vitro. Expression of the viral spike protein significantly induced ER stress and Cxcl2 mRNA upregulation, while expression of the other structural genes did not. Additional experiments with UV-inactivated virus, cell-cell fusion-blocking antibodies, and an MHV mutant with a defect in spike protein maturation demonstrated that spike-host interactions in the ER are responsible for the induction of ER stress and subsequent Cxcl2 mRNA transcription. Despite significant increases in levels of Cxcl2 mRNA and functional nucleus-to-cytoplasm RNA transport, no CXCL2 protein was released into the medium from MHV-infected cells. Yet Sendai virus-infected cells showed substantial Cxcl2 mRNA induction and a simultaneous increase in levels of secreted CXCL2 protein. Our results demonstrate that expression of CoV spike proteins induces ER stress, which could subsequently trigger innate immune responses. However, at that point in infection, translation of host mRNA is already severely reduced in infected cells, preventing the synthesis of CXCL2 and ER stress proteins despite their increased mRNA concentrations.</div>
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<server><NO>PASCAL 07-0485996 INIST</NO>
<ET>The coronavirus spike protein induces endoplasmic reticulum stress and upregulation of intracellular chemokine mRNA concentrations</ET>
<AU>VERSTEEG (Gijs A.); VAN DE NES (Paula S.); BREDENBEEK (Peter J.); SPAAN (Willy J. M.)</AU>
<AF>Molecular Virology Laboratory, Department of Medical Microbiology, Center of Infectious Diseases, Leiden University Medical Center, P.O. Box 9600/2300 RC Leiden/Pays-Bas (1 aut., 2 aut., 3 aut., 4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2007; Vol. 81; No. 20; Pp. 10981-10990; Bibl. 52 ref.</SO>
<LA>Anglais</LA>
<EA>Murine hepatitis virus (MHV) and severe acute respiratory syndrome (SARS) coronavirus (CoV) are two of the best-studied representatives of the family Coronaviridae. During CoV infection, numerous cytokines and chemokines are induced in vitro and in vivo. Human interleukin 8 and its mouse functional counterpart, CXCL2, are early-expressed chemokines. Here we show that SARS-CoV and MHV induce endoplasmic reticulum (ER) stress and Cxcl2 mRNA transcription during infection in vitro. Expression of the viral spike protein significantly induced ER stress and Cxcl2 mRNA upregulation, while expression of the other structural genes did not. Additional experiments with UV-inactivated virus, cell-cell fusion-blocking antibodies, and an MHV mutant with a defect in spike protein maturation demonstrated that spike-host interactions in the ER are responsible for the induction of ER stress and subsequent Cxcl2 mRNA transcription. Despite significant increases in levels of Cxcl2 mRNA and functional nucleus-to-cytoplasm RNA transport, no CXCL2 protein was released into the medium from MHV-infected cells. Yet Sendai virus-infected cells showed substantial Cxcl2 mRNA induction and a simultaneous increase in levels of secreted CXCL2 protein. Our results demonstrate that expression of CoV spike proteins induces ER stress, which could subsequently trigger innate immune responses. However, at that point in infection, translation of host mRNA is already severely reduced in infected cells, preventing the synthesis of CXCL2 and ER stress proteins despite their increased mRNA concentrations.</EA>
<CC>002A05C10</CC>
<FD>Coronavirus; Protéine; Réticulum endoplasmique; Stress; Intracellulaire; Chimiokine; RNA messager; Virologie</FD>
<FG>Coronaviridae; Nidovirales; Virus</FG>
<ED>Coronavirus; Protein; Endoplasmic reticulum; Stress; Intracellular; Chemokine; Messenger RNA; Virology</ED>
<EG>Coronaviridae; Nidovirales; Virus</EG>
<SD>Coronavirus; Proteína; Retículo endoplásmico; Estrés; Intracelular; Quimioquina; RNA mensajero; Virología</SD>
<LO>INIST-13592.354000143477600150</LO>
<ID>07-0485996</ID>
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The coronavirus spike protein induces endoplasmic reticulum stress and upregulation of intracellular chemokine mRNA concentrations

The coronavirus spike protein induces endoplasmic reticulum stress and upregulation of intracellular chemokine mRNA concentrations

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