SrasV1, PascalFrancis, Corpus, bibRecord, 000499

Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections

Identifieur interne : 000499 ( PascalFrancis/Corpus ); précédent : 000498; suivant : 000500

Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections

Auteurs : Tamaki Okabayashi ; Hiroaki Kariwa ; Shin-Ichi Yokota ; Shigeo Iki ; Tomokazu Indoh ; Noriko Yokosawa ; Ikuo Takashima ; Hiroyuki Tsutsumi ; Nobuhiro Fujii

Source :

Journal of medical virology [ 0146-6615 ] ; 2006.

RBID : Pascal:06-0257225

Descripteurs français

Pascal (Inist)
- Virus syndrome respiratoire aigu sévère, Cytokine, Interleukine 6, Virose, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Cytokine, Interleukin 6, Severe acute respiratory syndrome, Severe acute respiratory syndrome virus, Viral disease.

Abstract

The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS-CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS-CoV infection. Therefore, SARS-CoV replication was suppressed by pretreatment with IFN. SARS-CoV and RSV induced high levels of IL-6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling-3 (SOCS3) by SARS-CoV was significantly lower than that by RSV in spite of the significant production of IL-6. Toll-like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS-CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with "severe" inflammation in SARS. J. Med. Virol.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

A01	`01`	`1`		`@0 0146-6615`
A02	`01`			`@0 JMVIDB`
A03		`1`		`@0 J. med. virol.`
A05				`@2 78`
A06				`@2 4`
A08	`01`	`1`	`ENG`	`@1 Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections`
A11	`01`	`1`		`@1 OKABAYASHI (Tamaki)`
A11	`02`	`1`		`@1 KARIWA (Hiroaki)`
A11	`03`	`1`		`@1 YOKOTA (Shin-Ichi)`
A11	`04`	`1`		`@1 IKI (Shigeo)`
A11	`05`	`1`		`@1 INDOH (Tomokazu)`
A11	`06`	`1`		`@1 YOKOSAWA (Noriko)`
A11	`07`	`1`		`@1 TAKASHIMA (Ikuo)`
A11	`08`	`1`		`@1 TSUTSUMI (Hiroyuki)`
A11	`09`	`1`		`@1 FUJII (Nobuhiro)`
A14	`01`			`@1 Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku @2 Sapporo, Hokkaido @3 JPN @Z 1 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 6 aut. @Z 9 aut.`
A14	`02`			`@1 Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University @2 Hokkaido @3 JPN @Z 2 aut. @Z 7 aut.`
A14	`03`			`@1 Department of Pediatrics, Sapporo Medical University School of Medicine @2 Hokkaido @3 JPN @Z 8 aut.`
A20				`@1 417-424`
A21				`@1 2006`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 17422 @5 354000153370750010`
A44				`@0 0000 @1 © 2006 INIST-CNRS. All rights reserved.`
A45				`@0 1 p.1/4`
A47	`01`	`1`		`@0 06-0257225`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Journal of medical virology`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS-CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS-CoV infection. Therefore, SARS-CoV replication was suppressed by pretreatment with IFN. SARS-CoV and RSV induced high levels of IL-6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling-3 (SOCS3) by SARS-CoV was significantly lower than that by RSV in spite of the significant production of IL-6. Toll-like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS-CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with "severe" inflammation in SARS. J. Med. Virol.
C02	`01`	`X`		`@0 002A05C10`
C02	`02`	`X`		`@0 002B05C02J`
C03	`01`	`X`	`FRE`	`@0 Virus syndrome respiratoire aigu sévère @2 NW @5 01`
C03	`01`	`X`	`ENG`	`@0 Severe acute respiratory syndrome virus @2 NW @5 01`
C03	`01`	`X`	`SPA`	`@0 Severe acute respiratory syndrome virus @2 NW @5 01`
C03	`02`	`X`	`FRE`	`@0 Cytokine @5 05`
C03	`02`	`X`	`ENG`	`@0 Cytokine @5 05`
C03	`02`	`X`	`SPA`	`@0 Citoquina @5 05`
C03	`03`	`X`	`FRE`	`@0 Interleukine 6 @5 06`
C03	`03`	`X`	`ENG`	`@0 Interleukin 6 @5 06`
C03	`03`	`X`	`SPA`	`@0 Interleuquina 6 @5 06`
C03	`04`	`X`	`FRE`	`@0 Virose @5 14`
C03	`04`	`X`	`ENG`	`@0 Viral disease @5 14`
C03	`04`	`X`	`SPA`	`@0 Virosis @5 14`
C03	`05`	`X`	`FRE`	`@0 Syndrome respiratoire aigu sévère @2 NM @5 15`
C03	`05`	`X`	`ENG`	`@0 Severe acute respiratory syndrome @2 NM @5 15`
C03	`05`	`X`	`SPA`	`@0 Síndrome respiratorio agudo severo @2 NM @5 15`
C07	`01`	`X`	`FRE`	`@0 Coronavirus @2 NW`
C07	`01`	`X`	`ENG`	`@0 Coronavirus @2 NW`
C07	`01`	`X`	`SPA`	`@0 Coronavirus @2 NW`
C07	`02`	`X`	`FRE`	`@0 Coronaviridae @2 NW`
C07	`02`	`X`	`ENG`	`@0 Coronaviridae @2 NW`
C07	`02`	`X`	`SPA`	`@0 Coronaviridae @2 NW`
C07	`03`	`X`	`FRE`	`@0 Nidovirales @2 NW`
C07	`03`	`X`	`ENG`	`@0 Nidovirales @2 NW`
C07	`03`	`X`	`SPA`	`@0 Nidovirales @2 NW`
C07	`04`	`X`	`FRE`	`@0 Virus @2 NW`
C07	`04`	`X`	`ENG`	`@0 Virus @2 NW`
C07	`04`	`X`	`SPA`	`@0 Virus @2 NW`
C07	`05`	`X`	`FRE`	`@0 Appareil respiratoire pathologie @5 13`
C07	`05`	`X`	`ENG`	`@0 Respiratory disease @5 13`
C07	`05`	`X`	`SPA`	`@0 Aparato respiratorio patología @5 13`
C07	`06`	`X`	`FRE`	`@0 Infection`
C07	`06`	`X`	`ENG`	`@0 Infection`
C07	`06`	`X`	`SPA`	`@0 Infección`
C07	`07`	`X`	`FRE`	`@0 Poumon pathologie @5 16`
C07	`07`	`X`	`ENG`	`@0 Lung disease @5 16`
C07	`07`	`X`	`SPA`	`@0 Pulmón patología @5 16`
N21				`@1 163`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 06-0257225 INIST
ET :	Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections
AU :	OKABAYASHI (Tamaki); KARIWA (Hiroaki); YOKOTA (Shin-Ichi); IKI (Shigeo); INDOH (Tomokazu); YOKOSAWA (Noriko); TAKASHIMA (Ikuo); TSUTSUMI (Hiroyuki); FUJII (Nobuhiro)
AF :	Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku/Sapporo, Hokkaido/Japon (1 aut., 3 aut., 4 aut., 5 aut., 6 aut., 9 aut.); Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University/Hokkaido/Japon (2 aut., 7 aut.); Department of Pediatrics, Sapporo Medical University School of Medicine/Hokkaido/Japon (8 aut.)
DT :	Publication en série; Niveau analytique
SO :	Journal of medical virology; ISSN 0146-6615; Coden JMVIDB; Etats-Unis; Da. 2006; Vol. 78; No. 4; Pp. 417-424; Bibl. 1 p.1/4
LA :	Anglais
EA :	The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS-CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS-CoV infection. Therefore, SARS-CoV replication was suppressed by pretreatment with IFN. SARS-CoV and RSV induced high levels of IL-6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling-3 (SOCS3) by SARS-CoV was significantly lower than that by RSV in spite of the significant production of IL-6. Toll-like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS-CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with "severe" inflammation in SARS. J. Med. Virol.
CC :	002A05C10; 002B05C02J
FD :	Virus syndrome respiratoire aigu sévère; Cytokine; Interleukine 6; Virose; Syndrome respiratoire aigu sévère
FG :	Coronavirus; Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Infection; Poumon pathologie
ED :	Severe acute respiratory syndrome virus; Cytokine; Interleukin 6; Viral disease; Severe acute respiratory syndrome
EG :	Coronavirus; Coronaviridae; Nidovirales; Virus; Respiratory disease; Infection; Lung disease
SD :	Severe acute respiratory syndrome virus; Citoquina; Interleuquina 6; Virosis; Síndrome respiratorio agudo severo
LO :	INIST-17422.354000153370750010
ID :	06-0257225

Links to Exploration step

Pascal:06-0257225

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections</title>
<author><name sortKey="Okabayashi, Tamaki" sort="Okabayashi, Tamaki" uniqKey="Okabayashi T" first="Tamaki" last="Okabayashi">Tamaki Okabayashi</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku</s1>
<s2>Sapporo, Hokkaido</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Kariwa, Hiroaki" sort="Kariwa, Hiroaki" uniqKey="Kariwa H" first="Hiroaki" last="Kariwa">Hiroaki Kariwa</name>
<affiliation><inist:fA14 i1="02"><s1>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University</s1>
<s2>Hokkaido</s2>
<s3>JPN</s3>
<sZ>2 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Yokota, Shin Ichi" sort="Yokota, Shin Ichi" uniqKey="Yokota S" first="Shin-Ichi" last="Yokota">Shin-Ichi Yokota</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku</s1>
<s2>Sapporo, Hokkaido</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Iki, Shigeo" sort="Iki, Shigeo" uniqKey="Iki S" first="Shigeo" last="Iki">Shigeo Iki</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku</s1>
<s2>Sapporo, Hokkaido</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Indoh, Tomokazu" sort="Indoh, Tomokazu" uniqKey="Indoh T" first="Tomokazu" last="Indoh">Tomokazu Indoh</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku</s1>
<s2>Sapporo, Hokkaido</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Yokosawa, Noriko" sort="Yokosawa, Noriko" uniqKey="Yokosawa N" first="Noriko" last="Yokosawa">Noriko Yokosawa</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku</s1>
<s2>Sapporo, Hokkaido</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Takashima, Ikuo" sort="Takashima, Ikuo" uniqKey="Takashima I" first="Ikuo" last="Takashima">Ikuo Takashima</name>
<affiliation><inist:fA14 i1="02"><s1>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University</s1>
<s2>Hokkaido</s2>
<s3>JPN</s3>
<sZ>2 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Tsutsumi, Hiroyuki" sort="Tsutsumi, Hiroyuki" uniqKey="Tsutsumi H" first="Hiroyuki" last="Tsutsumi">Hiroyuki Tsutsumi</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Pediatrics, Sapporo Medical University School of Medicine</s1>
<s2>Hokkaido</s2>
<s3>JPN</s3>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Fujii, Nobuhiro" sort="Fujii, Nobuhiro" uniqKey="Fujii N" first="Nobuhiro" last="Fujii">Nobuhiro Fujii</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku</s1>
<s2>Sapporo, Hokkaido</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">06-0257225</idno>
<date when="2006">2006</date>
<idno type="stanalyst">PASCAL 06-0257225 INIST</idno>
<idno type="RBID">Pascal:06-0257225</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">000499</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections</title>
<author><name sortKey="Okabayashi, Tamaki" sort="Okabayashi, Tamaki" uniqKey="Okabayashi T" first="Tamaki" last="Okabayashi">Tamaki Okabayashi</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku</s1>
<s2>Sapporo, Hokkaido</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Kariwa, Hiroaki" sort="Kariwa, Hiroaki" uniqKey="Kariwa H" first="Hiroaki" last="Kariwa">Hiroaki Kariwa</name>
<affiliation><inist:fA14 i1="02"><s1>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University</s1>
<s2>Hokkaido</s2>
<s3>JPN</s3>
<sZ>2 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Yokota, Shin Ichi" sort="Yokota, Shin Ichi" uniqKey="Yokota S" first="Shin-Ichi" last="Yokota">Shin-Ichi Yokota</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku</s1>
<s2>Sapporo, Hokkaido</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Iki, Shigeo" sort="Iki, Shigeo" uniqKey="Iki S" first="Shigeo" last="Iki">Shigeo Iki</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku</s1>
<s2>Sapporo, Hokkaido</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Indoh, Tomokazu" sort="Indoh, Tomokazu" uniqKey="Indoh T" first="Tomokazu" last="Indoh">Tomokazu Indoh</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku</s1>
<s2>Sapporo, Hokkaido</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Yokosawa, Noriko" sort="Yokosawa, Noriko" uniqKey="Yokosawa N" first="Noriko" last="Yokosawa">Noriko Yokosawa</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku</s1>
<s2>Sapporo, Hokkaido</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Takashima, Ikuo" sort="Takashima, Ikuo" uniqKey="Takashima I" first="Ikuo" last="Takashima">Ikuo Takashima</name>
<affiliation><inist:fA14 i1="02"><s1>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University</s1>
<s2>Hokkaido</s2>
<s3>JPN</s3>
<sZ>2 aut.</sZ>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Tsutsumi, Hiroyuki" sort="Tsutsumi, Hiroyuki" uniqKey="Tsutsumi H" first="Hiroyuki" last="Tsutsumi">Hiroyuki Tsutsumi</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Pediatrics, Sapporo Medical University School of Medicine</s1>
<s2>Hokkaido</s2>
<s3>JPN</s3>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Fujii, Nobuhiro" sort="Fujii, Nobuhiro" uniqKey="Fujii N" first="Nobuhiro" last="Fujii">Nobuhiro Fujii</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku</s1>
<s2>Sapporo, Hokkaido</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Journal of medical virology</title>
<title level="j" type="abbreviated">J. med. virol.</title>
<idno type="ISSN">0146-6615</idno>
<imprint><date when="2006">2006</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Journal of medical virology</title>
<title level="j" type="abbreviated">J. med. virol.</title>
<idno type="ISSN">0146-6615</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cytokine</term>
<term>Interleukin 6</term>
<term>Severe acute respiratory syndrome</term>
<term>Severe acute respiratory syndrome virus</term>
<term>Viral disease</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Virus syndrome respiratoire aigu sévère</term>
<term>Cytokine</term>
<term>Interleukine 6</term>
<term>Virose</term>
<term>Syndrome respiratoire aigu sévère</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS-CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS-CoV infection. Therefore, SARS-CoV replication was suppressed by pretreatment with IFN. SARS-CoV and RSV induced high levels of IL-6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling-3 (SOCS3) by SARS-CoV was significantly lower than that by RSV in spite of the significant production of IL-6. Toll-like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS-CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with "severe" inflammation in SARS. J. Med. Virol.</div>
</front>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0146-6615</s0>
</fA01>
<fA02 i1="01"><s0>JMVIDB</s0>
</fA02>
<fA03 i2="1"><s0>J. med. virol.</s0>
</fA03>
<fA05><s2>78</s2>
</fA05>
<fA06><s2>4</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>OKABAYASHI (Tamaki)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>KARIWA (Hiroaki)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>YOKOTA (Shin-Ichi)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>IKI (Shigeo)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>INDOH (Tomokazu)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>YOKOSAWA (Noriko)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>TAKASHIMA (Ikuo)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>TSUTSUMI (Hiroyuki)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>FUJII (Nobuhiro)</s1>
</fA11>
<fA14 i1="01"><s1>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku</s1>
<s2>Sapporo, Hokkaido</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University</s1>
<s2>Hokkaido</s2>
<s3>JPN</s3>
<sZ>2 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Pediatrics, Sapporo Medical University School of Medicine</s1>
<s2>Hokkaido</s2>
<s3>JPN</s3>
<sZ>8 aut.</sZ>
</fA14>
<fA20><s1>417-424</s1>
</fA20>
<fA21><s1>2006</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>17422</s2>
<s5>354000153370750010</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2006 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>1 p.1/4</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>06-0257225</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Journal of medical virology</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS-CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS-CoV infection. Therefore, SARS-CoV replication was suppressed by pretreatment with IFN. SARS-CoV and RSV induced high levels of IL-6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling-3 (SOCS3) by SARS-CoV was significantly lower than that by RSV in spite of the significant production of IL-6. Toll-like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS-CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with "severe" inflammation in SARS. J. Med. Virol.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A05C10</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B05C02J</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Virus syndrome respiratoire aigu sévère</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Severe acute respiratory syndrome virus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Severe acute respiratory syndrome virus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Cytokine</s0>
<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Cytokine</s0>
<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Citoquina</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Interleukine 6</s0>
<s5>06</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Interleukin 6</s0>
<s5>06</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Interleuquina 6</s0>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Virose</s0>
<s5>14</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Viral disease</s0>
<s5>14</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Virosis</s0>
<s5>14</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Syndrome respiratoire aigu sévère</s0>
<s2>NM</s2>
<s5>15</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Severe acute respiratory syndrome</s0>
<s2>NM</s2>
<s5>15</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Síndrome respiratorio agudo severo</s0>
<s2>NM</s2>
<s5>15</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Coronavirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Coronavirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Coronavirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Appareil respiratoire pathologie</s0>
<s5>13</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Respiratory disease</s0>
<s5>13</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0>
<s5>13</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Poumon pathologie</s0>
<s5>16</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Lung disease</s0>
<s5>16</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Pulmón patología</s0>
<s5>16</s5>
</fC07>
<fN21><s1>163</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 06-0257225 INIST</NO>
<ET>Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections</ET>
<AU>OKABAYASHI (Tamaki); KARIWA (Hiroaki); YOKOTA (Shin-Ichi); IKI (Shigeo); INDOH (Tomokazu); YOKOSAWA (Noriko); TAKASHIMA (Ikuo); TSUTSUMI (Hiroyuki); FUJII (Nobuhiro)</AU>
<AF>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku/Sapporo, Hokkaido/Japon (1 aut., 3 aut., 4 aut., 5 aut., 6 aut., 9 aut.); Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University/Hokkaido/Japon (2 aut., 7 aut.); Department of Pediatrics, Sapporo Medical University School of Medicine/Hokkaido/Japon (8 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of medical virology; ISSN 0146-6615; Coden JMVIDB; Etats-Unis; Da. 2006; Vol. 78; No. 4; Pp. 417-424; Bibl. 1 p.1/4</SO>
<LA>Anglais</LA>
<EA>The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS-CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS-CoV infection. Therefore, SARS-CoV replication was suppressed by pretreatment with IFN. SARS-CoV and RSV induced high levels of IL-6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling-3 (SOCS3) by SARS-CoV was significantly lower than that by RSV in spite of the significant production of IL-6. Toll-like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS-CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with "severe" inflammation in SARS. J. Med. Virol.</EA>
<CC>002A05C10; 002B05C02J</CC>
<FD>Virus syndrome respiratoire aigu sévère; Cytokine; Interleukine 6; Virose; Syndrome respiratoire aigu sévère</FD>
<FG>Coronavirus; Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Infection; Poumon pathologie</FG>
<ED>Severe acute respiratory syndrome virus; Cytokine; Interleukin 6; Viral disease; Severe acute respiratory syndrome</ED>
<EG>Coronavirus; Coronaviridae; Nidovirales; Virus; Respiratory disease; Infection; Lung disease</EG>
<SD>Severe acute respiratory syndrome virus; Citoquina; Interleuquina 6; Virosis; Síndrome respiratorio agudo severo</SD>
<LO>INIST-17422.354000153370750010</LO>
<ID>06-0257225</ID>
</server>
</inist>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Sante/explor/SrasV1/Data/PascalFrancis/Corpus

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000499 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Corpus/biblio.hfd -nk 000499 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Sante
   |area=    SrasV1
   |flux=    PascalFrancis
   |étape=   Corpus
   |type=    RBID
   |clé=     Pascal:06-0257225
   |texte=   Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections
}}

This area was generated with Dilib version V0.6.33.
Data generation: Tue Apr 28 14:49:16 2020. Site generation: Sat Mar 27 22:06:49 2021

	Serveur d'exploration SRAS
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration SRAS

Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections

Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections

Source :

Descripteurs français

English descriptors

Abstract

Notice en format standard (ISO 2709)

Format Inist (serveur)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri