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 : 000643Inhibition 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 WUSource :
- Antiviral therapy : (London) [ 1359-6535 ] ; 2005.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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.
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Pour connaître la documentation sur le format Inist Standard.
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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 |
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Pascal:05-0328774Le document en format XML
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<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>
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<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>
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<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>
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