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.

Inhibition of replication and infection of severe acute respiratory syndrome-associated coronavirus with plasmid-mediated interference RNA

Identifieur interne : 000642 ( PascalFrancis/Corpus ); précédent : 000641; suivant : 000643

Inhibition of replication and infection of severe acute respiratory syndrome-associated coronavirus with plasmid-mediated interference RNA

Auteurs : BING NI ; XINFU SHI ; YANG LI ; WENDA GAO ; XILIANG WANG ; YUZHANG WU

Source :

RBID : Pascal:05-0328774

Descripteurs français

English descriptors

Abstract

Severe acute respiratory syndrome (SARS) is a newly emerged infectious disease caused by a novel coronavirus (SARS-CoV), which spread to over 30 countries in early 2003. Until recently, no specific vaccines and effective drugs have been available to protect patients from infection by this virus. To exploit a new strategy to fight this disease, we investigated the effect of interference RNA (RNAi) on the virus infection and replication with 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazolium bromide (MTT), plaque-forming, Western-blot and real-time PCR assays. Results showed that the plasmid-derived siRNAs targeting the non-structural protein 1 (NSP1) sequence of the SARS-CoV genome could specifically inhibit the expression of the NSP1 sequence and effectively suppress the replication and propagation of SARS-CoV in cultured Vero E6 cell lines. The expression of the Spike and Nucleoprotein genes of SARS-CoV at mRNA and protein levels in small interfering (si)RNA-expressing cells was significantly less than that in controls when analysed with PCR and Western-blot assays, 3 days post SARS-CoV infection. Our study provides strong evidence that the NSP1 sequence in the SARS-CoV genome is a valid target for RNAi and the effect of the siRNAs probably mainly resulted from effects on global reduction of subgenome synthesis and subsequent protein expression of SARS-CoV.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

pA  
A01 01  1    @0 1359-6535
A03   1    @0 Antivir. ther. : (Lond.)
A05       @2 10
A06       @2 4
A08 01  1  ENG  @1 Inhibition of replication and infection of severe acute respiratory syndrome-associated coronavirus with plasmid-mediated interference RNA
A11 01  1    @1 BING NI
A11 02  1    @1 XINFU SHI
A11 03  1    @1 YANG LI
A11 04  1    @1 WENDA GAO
A11 05  1    @1 XILIANG WANG
A11 06  1    @1 YUZHANG WU
A14 01      @1 Institute of Immunology PLA, Third Military Medical University @2 Chongqing @3 CHN @Z 1 aut. @Z 3 aut. @Z 6 aut.
A14 02      @1 Department of Immunology, Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences (AMMS) @2 Beijing @3 CHN @Z 2 aut. @Z 5 aut.
A14 03      @1 Beth Israel Deaconess Medical Center, Harvard Medical School @2 Boston, MA @3 USA @Z 4 aut.
A20       @1 527-533
A21       @1 2005
A23 01      @0 ENG
A43 01      @1 INIST @2 27047 @5 354000124671150070
A44       @0 0000 @1 © 2005 INIST-CNRS. All rights reserved.
A45       @0 26 ref.
A47 01  1    @0 05-0328774
A60       @1 P
A61       @0 A
A64 01  1    @0 Antiviral therapy : (London)
A66 01      @0 GBR
C01 01    ENG  @0 Severe acute respiratory syndrome (SARS) is a newly emerged infectious disease caused by a novel coronavirus (SARS-CoV), which spread to over 30 countries in early 2003. Until recently, no specific vaccines and effective drugs have been available to protect patients from infection by this virus. To exploit a new strategy to fight this disease, we investigated the effect of interference RNA (RNAi) on the virus infection and replication with 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazolium bromide (MTT), plaque-forming, Western-blot and real-time PCR assays. Results showed that the plasmid-derived siRNAs targeting the non-structural protein 1 (NSP1) sequence of the SARS-CoV genome could specifically inhibit the expression of the NSP1 sequence and effectively suppress the replication and propagation of SARS-CoV in cultured Vero E6 cell lines. The expression of the Spike and Nucleoprotein genes of SARS-CoV at mRNA and protein levels in small interfering (si)RNA-expressing cells was significantly less than that in controls when analysed with PCR and Western-blot assays, 3 days post SARS-CoV infection. Our study provides strong evidence that the NSP1 sequence in the SARS-CoV genome is a valid target for RNAi and the effect of the siRNAs probably mainly resulted from effects on global reduction of subgenome synthesis and subsequent protein expression of SARS-CoV.
C02 01  X    @0 002B02S05
C03 01  X  FRE  @0 Réplication @5 01
C03 01  X  ENG  @0 Replication @5 01
C03 01  X  SPA  @0 Replicación @5 01
C03 02  X  FRE  @0 Infection @5 02
C03 02  X  ENG  @0 Infection @5 02
C03 02  X  SPA  @0 Infección @5 02
C03 03  X  FRE  @0 Syndrome respiratoire aigu sévère @2 NM @5 03
C03 03  X  ENG  @0 Severe acute respiratory syndrome @2 NM @5 03
C03 03  X  SPA  @0 Síndrome respiratorio agudo severo @2 NM @5 03
C03 04  X  FRE  @0 Coronavirus @2 NW @5 04
C03 04  X  ENG  @0 Coronavirus @2 NW @5 04
C03 04  X  SPA  @0 Coronavirus @2 NW @5 04
C03 05  X  FRE  @0 Plasmide @5 05
C03 05  X  ENG  @0 Plasmid @5 05
C03 05  X  SPA  @0 Plasmido @5 05
C03 06  X  FRE  @0 Interférence ARN @4 CD @5 96
C03 06  X  ENG  @0 RNA interference @4 CD @5 96
C07 01  X  FRE  @0 Virose
C07 01  X  ENG  @0 Viral disease
C07 01  X  SPA  @0 Virosis
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 37
C07 05  X  ENG  @0 Respiratory disease @5 37
C07 05  X  SPA  @0 Aparato respiratorio patología @5 37
C07 06  X  FRE  @0 Poumon pathologie @5 38
C07 06  X  ENG  @0 Lung disease @5 38
C07 06  X  SPA  @0 Pulmón patología @5 38
N21       @1 234
N44 01      @1 OTO
N82       @1 OTO

Format Inist (serveur)

NO : PASCAL 05-0328774 INIST
ET : Inhibition of replication and infection of severe acute respiratory syndrome-associated coronavirus with plasmid-mediated interference RNA
AU : BING NI; XINFU SHI; YANG LI; WENDA GAO; XILIANG WANG; YUZHANG WU
AF : Institute of Immunology PLA, Third Military Medical University/Chongqing/Chine (1 aut., 3 aut., 6 aut.); Department of Immunology, Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences (AMMS)/Beijing/Chine (2 aut., 5 aut.); Beth Israel Deaconess Medical Center, Harvard Medical School/Boston, MA/Etats-Unis (4 aut.)
DT : Publication en série; Niveau analytique
SO : Antiviral therapy : (London); ISSN 1359-6535; Royaume-Uni; Da. 2005; Vol. 10; No. 4; Pp. 527-533; Bibl. 26 ref.
LA : Anglais
EA : Severe acute respiratory syndrome (SARS) is a newly emerged infectious disease caused by a novel coronavirus (SARS-CoV), which spread to over 30 countries in early 2003. Until recently, no specific vaccines and effective drugs have been available to protect patients from infection by this virus. To exploit a new strategy to fight this disease, we investigated the effect of interference RNA (RNAi) on the virus infection and replication with 3-(4,5-dimethyl-2-thiazolyl)-2,5-dipheny ltetrazolium bromide (MTT), plaque-forming, Western-blot and real-time PCR assays. Results showed that the plasmid-derived siRNAs targeting the non-structural protein 1 (NSP1) sequence of the SARS-CoV genome could specifically inhibit the expression of the NSP1 sequence and effectively suppress the replication and propagation of SARS-CoV in cultured Vero E6 cell lines. The expression of the Spike and Nucleoprotein genes of SARS-CoV at mRNA and protein levels in small interfering (si)RNA-expressing cells was significantly less than that in controls when analysed with PCR and Western-blot assays, 3 days post SARS-CoV infection. Our study provides strong evidence that the NSP1 sequence in the SARS-CoV genome is a valid target for RNAi and the effect of the siRNAs probably mainly resulted from effects on global reduction of subgenome synthesis and subsequent protein expression of SARS-CoV.
CC : 002B02S05
FD : Réplication; Infection; Syndrome respiratoire aigu sévère; Coronavirus; Plasmide; Interférence ARN
FG : Virose; Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Poumon pathologie
ED : Replication; Infection; Severe acute respiratory syndrome; Coronavirus; Plasmid; RNA interference
EG : Viral disease; Coronaviridae; Nidovirales; Virus; Respiratory disease; Lung disease
SD : Replicación; Infección; Síndrome respiratorio agudo severo; Coronavirus; Plasmido
LO : INIST-27047.354000124671150070
ID : 05-0328774

Links to Exploration step

Pascal:05-0328774

Le document en format XML

<record>
<TEI>
<teiHeader>
<fileDesc>
<titleStmt>
<title xml:lang="en" level="a">Inhibition of replication and infection of severe acute respiratory syndrome-associated coronavirus with plasmid-mediated interference RNA</title>
<author>
<name sortKey="Bing Ni" sort="Bing Ni" uniqKey="Bing Ni" last="Bing Ni">BING NI</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institute of Immunology PLA, Third Military Medical University</s1>
<s2>Chongqing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Xinfu Shi" sort="Xinfu Shi" uniqKey="Xinfu Shi" last="Xinfu Shi">XINFU SHI</name>
<affiliation>
<inist:fA14 i1="02">
<s1>Department of Immunology, Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences (AMMS)</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Yang Li" sort="Yang Li" uniqKey="Yang Li" last="Yang Li">YANG LI</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institute of Immunology PLA, Third Military Medical University</s1>
<s2>Chongqing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Wenda Gao" sort="Wenda Gao" uniqKey="Wenda Gao" last="Wenda Gao">WENDA GAO</name>
<affiliation>
<inist:fA14 i1="03">
<s1>Beth Israel Deaconess Medical Center, Harvard Medical School</s1>
<s2>Boston, MA</s2>
<s3>USA</s3>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Xiliang Wang" sort="Xiliang Wang" uniqKey="Xiliang Wang" last="Xiliang Wang">XILIANG WANG</name>
<affiliation>
<inist:fA14 i1="02">
<s1>Department of Immunology, Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences (AMMS)</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Yuzhang Wu" sort="Yuzhang Wu" uniqKey="Yuzhang Wu" last="Yuzhang Wu">YUZHANG WU</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institute of Immunology PLA, Third Military Medical University</s1>
<s2>Chongqing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</titleStmt>
<publicationStmt>
<idno type="wicri:source">INIST</idno>
<idno type="inist">05-0328774</idno>
<date when="2005">2005</date>
<idno type="stanalyst">PASCAL 05-0328774 INIST</idno>
<idno type="RBID">Pascal:05-0328774</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">000642</idno>
</publicationStmt>
<sourceDesc>
<biblStruct>
<analytic>
<title xml:lang="en" level="a">Inhibition of replication and infection of severe acute respiratory syndrome-associated coronavirus with plasmid-mediated interference RNA</title>
<author>
<name sortKey="Bing Ni" sort="Bing Ni" uniqKey="Bing Ni" last="Bing Ni">BING NI</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institute of Immunology PLA, Third Military Medical University</s1>
<s2>Chongqing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Xinfu Shi" sort="Xinfu Shi" uniqKey="Xinfu Shi" last="Xinfu Shi">XINFU SHI</name>
<affiliation>
<inist:fA14 i1="02">
<s1>Department of Immunology, Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences (AMMS)</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Yang Li" sort="Yang Li" uniqKey="Yang Li" last="Yang Li">YANG LI</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institute of Immunology PLA, Third Military Medical University</s1>
<s2>Chongqing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Wenda Gao" sort="Wenda Gao" uniqKey="Wenda Gao" last="Wenda Gao">WENDA GAO</name>
<affiliation>
<inist:fA14 i1="03">
<s1>Beth Israel Deaconess Medical Center, Harvard Medical School</s1>
<s2>Boston, MA</s2>
<s3>USA</s3>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Xiliang Wang" sort="Xiliang Wang" uniqKey="Xiliang Wang" last="Xiliang Wang">XILIANG WANG</name>
<affiliation>
<inist:fA14 i1="02">
<s1>Department of Immunology, Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences (AMMS)</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Yuzhang Wu" sort="Yuzhang Wu" uniqKey="Yuzhang Wu" last="Yuzhang Wu">YUZHANG WU</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institute of Immunology PLA, Third Military Medical University</s1>
<s2>Chongqing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series>
<title level="j" type="main">Antiviral therapy : (London)</title>
<title level="j" type="abbreviated">Antivir. ther. : (Lond.)</title>
<idno type="ISSN">1359-6535</idno>
<imprint>
<date when="2005">2005</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt>
<title level="j" type="main">Antiviral therapy : (London)</title>
<title level="j" type="abbreviated">Antivir. ther. : (Lond.)</title>
<idno type="ISSN">1359-6535</idno>
</seriesStmt>
</fileDesc>
<profileDesc>
<textClass>
<keywords scheme="KwdEn" xml:lang="en">
<term>Coronavirus</term>
<term>Infection</term>
<term>Plasmid</term>
<term>RNA interference</term>
<term>Replication</term>
<term>Severe acute respiratory syndrome</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Réplication</term>
<term>Infection</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Coronavirus</term>
<term>Plasmide</term>
<term>Interférence ARN</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) is a newly emerged infectious disease caused by a novel coronavirus (SARS-CoV), which spread to over 30 countries in early 2003. Until recently, no specific vaccines and effective drugs have been available to protect patients from infection by this virus. To exploit a new strategy to fight this disease, we investigated the effect of interference RNA (RNAi) on the virus infection and replication with 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazolium bromide (MTT), plaque-forming, Western-blot and real-time PCR assays. Results showed that the plasmid-derived siRNAs targeting the non-structural protein 1 (NSP1) sequence of the SARS-CoV genome could specifically inhibit the expression of the NSP1 sequence and effectively suppress the replication and propagation of SARS-CoV in cultured Vero E6 cell lines. The expression of the Spike and Nucleoprotein genes of SARS-CoV at mRNA and protein levels in small interfering (si)RNA-expressing cells was significantly less than that in controls when analysed with PCR and Western-blot assays, 3 days post SARS-CoV infection. Our study provides strong evidence that the NSP1 sequence in the SARS-CoV genome is a valid target for RNAi and the effect of the siRNAs probably mainly resulted from effects on global reduction of subgenome synthesis and subsequent protein expression of SARS-CoV.</div>
</front>
</TEI>
<inist>
<standard h6="B">
<pA>
<fA01 i1="01" i2="1">
<s0>1359-6535</s0>
</fA01>
<fA03 i2="1">
<s0>Antivir. ther. : (Lond.)</s0>
</fA03>
<fA05>
<s2>10</s2>
</fA05>
<fA06>
<s2>4</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG">
<s1>Inhibition of replication and infection of severe acute respiratory syndrome-associated coronavirus with plasmid-mediated interference RNA</s1>
</fA08>
<fA11 i1="01" i2="1">
<s1>BING NI</s1>
</fA11>
<fA11 i1="02" i2="1">
<s1>XINFU SHI</s1>
</fA11>
<fA11 i1="03" i2="1">
<s1>YANG LI</s1>
</fA11>
<fA11 i1="04" i2="1">
<s1>WENDA GAO</s1>
</fA11>
<fA11 i1="05" i2="1">
<s1>XILIANG WANG</s1>
</fA11>
<fA11 i1="06" i2="1">
<s1>YUZHANG WU</s1>
</fA11>
<fA14 i1="01">
<s1>Institute of Immunology PLA, Third Military Medical University</s1>
<s2>Chongqing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="02">
<s1>Department of Immunology, Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences (AMMS)</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="03">
<s1>Beth Israel Deaconess Medical Center, Harvard Medical School</s1>
<s2>Boston, MA</s2>
<s3>USA</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA20>
<s1>527-533</s1>
</fA20>
<fA21>
<s1>2005</s1>
</fA21>
<fA23 i1="01">
<s0>ENG</s0>
</fA23>
<fA43 i1="01">
<s1>INIST</s1>
<s2>27047</s2>
<s5>354000124671150070</s5>
</fA43>
<fA44>
<s0>0000</s0>
<s1>© 2005 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>26 ref.</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>05-0328774</s0>
</fA47>
<fA60>
<s1>P</s1>
</fA60>
<fA61>
<s0>A</s0>
</fA61>
<fA64 i1="01" i2="1">
<s0>Antiviral therapy : (London)</s0>
</fA64>
<fA66 i1="01">
<s0>GBR</s0>
</fA66>
<fC01 i1="01" l="ENG">
<s0>Severe acute respiratory syndrome (SARS) is a newly emerged infectious disease caused by a novel coronavirus (SARS-CoV), which spread to over 30 countries in early 2003. Until recently, no specific vaccines and effective drugs have been available to protect patients from infection by this virus. To exploit a new strategy to fight this disease, we investigated the effect of interference RNA (RNAi) on the virus infection and replication with 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazolium bromide (MTT), plaque-forming, Western-blot and real-time PCR assays. Results showed that the plasmid-derived siRNAs targeting the non-structural protein 1 (NSP1) sequence of the SARS-CoV genome could specifically inhibit the expression of the NSP1 sequence and effectively suppress the replication and propagation of SARS-CoV in cultured Vero E6 cell lines. The expression of the Spike and Nucleoprotein genes of SARS-CoV at mRNA and protein levels in small interfering (si)RNA-expressing cells was significantly less than that in controls when analysed with PCR and Western-blot assays, 3 days post SARS-CoV infection. Our study provides strong evidence that the NSP1 sequence in the SARS-CoV genome is a valid target for RNAi and the effect of the siRNAs probably mainly resulted from effects on global reduction of subgenome synthesis and subsequent protein expression of SARS-CoV.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002B02S05</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Réplication</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Replication</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Replicación</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Infection</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Infection</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Infección</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Syndrome respiratoire aigu sévère</s0>
<s2>NM</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Severe acute respiratory syndrome</s0>
<s2>NM</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Síndrome respiratorio agudo severo</s0>
<s2>NM</s2>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Coronavirus</s0>
<s2>NW</s2>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Coronavirus</s0>
<s2>NW</s2>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Coronavirus</s0>
<s2>NW</s2>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Plasmide</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Plasmid</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Plasmido</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Interférence ARN</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>RNA interference</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Virose</s0>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Viral disease</s0>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Virosis</s0>
</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>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Respiratory disease</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Aparato respiratorio patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Poumon pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Lung disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Pulmón patología</s0>
<s5>38</s5>
</fC07>
<fN21>
<s1>234</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
<server>
<NO>PASCAL 05-0328774 INIST</NO>
<ET>Inhibition of replication and infection of severe acute respiratory syndrome-associated coronavirus with plasmid-mediated interference RNA</ET>
<AU>BING NI; XINFU SHI; YANG LI; WENDA GAO; XILIANG WANG; YUZHANG WU</AU>
<AF>Institute of Immunology PLA, Third Military Medical University/Chongqing/Chine (1 aut., 3 aut., 6 aut.); Department of Immunology, Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences (AMMS)/Beijing/Chine (2 aut., 5 aut.); Beth Israel Deaconess Medical Center, Harvard Medical School/Boston, MA/Etats-Unis (4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Antiviral therapy : (London); ISSN 1359-6535; Royaume-Uni; Da. 2005; Vol. 10; No. 4; Pp. 527-533; Bibl. 26 ref.</SO>
<LA>Anglais</LA>
<EA>Severe acute respiratory syndrome (SARS) is a newly emerged infectious disease caused by a novel coronavirus (SARS-CoV), which spread to over 30 countries in early 2003. Until recently, no specific vaccines and effective drugs have been available to protect patients from infection by this virus. To exploit a new strategy to fight this disease, we investigated the effect of interference RNA (RNAi) on the virus infection and replication with 3-(4,5-dimethyl-2-thiazolyl)-2,5-dipheny ltetrazolium bromide (MTT), plaque-forming, Western-blot and real-time PCR assays. Results showed that the plasmid-derived siRNAs targeting the non-structural protein 1 (NSP1) sequence of the SARS-CoV genome could specifically inhibit the expression of the NSP1 sequence and effectively suppress the replication and propagation of SARS-CoV in cultured Vero E6 cell lines. The expression of the Spike and Nucleoprotein genes of SARS-CoV at mRNA and protein levels in small interfering (si)RNA-expressing cells was significantly less than that in controls when analysed with PCR and Western-blot assays, 3 days post SARS-CoV infection. Our study provides strong evidence that the NSP1 sequence in the SARS-CoV genome is a valid target for RNAi and the effect of the siRNAs probably mainly resulted from effects on global reduction of subgenome synthesis and subsequent protein expression of SARS-CoV.</EA>
<CC>002B02S05</CC>
<FD>Réplication; Infection; Syndrome respiratoire aigu sévère; Coronavirus; Plasmide; Interférence ARN</FD>
<FG>Virose; Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Poumon pathologie</FG>
<ED>Replication; Infection; Severe acute respiratory syndrome; Coronavirus; Plasmid; RNA interference</ED>
<EG>Viral disease; Coronaviridae; Nidovirales; Virus; Respiratory disease; Lung disease</EG>
<SD>Replicación; Infección; Síndrome respiratorio agudo severo; Coronavirus; Plasmido</SD>
<LO>INIST-27047.354000124671150070</LO>
<ID>05-0328774</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 000642 | SxmlIndent | more

Ou

HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Corpus/biblio.hfd -nk 000642 | 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:05-0328774
   |texte=   Inhibition of replication and infection of severe acute respiratory syndrome-associated coronavirus with plasmid-mediated interference RNA
}}

Wicri

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