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Comparative host gene transcription by microarray analysis early after infection of the Huh7 cell line by severe acute respiratory syndrome coronavirus and human coronavirus 229E

Identifieur interne : 000685 ( PascalFrancis/Corpus ); précédent : 000684; suivant : 000686

Comparative host gene transcription by microarray analysis early after infection of the Huh7 cell line by severe acute respiratory syndrome coronavirus and human coronavirus 229E

Auteurs : Bone S. F. Tang ; Kwok-Hung Chan ; Vincent C. C. Cheng ; Patrick C. Y. Woo ; Susanna K. P. Lau ; Clarence C. K. Lam ; Tsun-Leung Chan ; Alan K. L. Wu ; Ivan F. N. Hung ; Suet-Yi Leung ; Kwok-Yung Yuen

Source :

RBID : Pascal:05-0231505

Descripteurs français

English descriptors

Abstract

The pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) at the cellular level is unclear. No human cell line was previously known to be susceptible to both SARS-CoV and other human coronaviruses. Huh7 cells were found to be susceptible to both SARS-CoV, associated with SARS, and human coronavirus 229E (HCoV-229E), usually associated with the common cold. Highly lytic and productive rates of infections within 48 h of inoculation were reproducible with both viruses. The early transcriptional profiles of host cell response to both types of infection at 2 and 4 h postinoculation were determined by using the Affymetrix HG-U133A microarray (about 22,000 genes). Much more perturbation of cellular gene transcription was observed after infection by SARS-CoV than after infection by HCoV-229E. Besides the upregulation of genes associated with apoptosis, which was exactly opposite to the previously reported effect of SARS-CoV in a colonic carcinoma cell line, genes related to inflammation, stress response, and procoagulation were also upregulated. These findings were confirmed by semiquantitative reverse transcription-PCR, reverse transcription-quantitative PCR for mRNA of genes, and immunoassays for some encoded proteins. These transcriptomal changes are compatible with the histological changes of pulmonary vasculitis and microvascular thrombosis in addition to the diffuse alveolar damage involving the pneumocytes.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

pA  
A01 01  1    @0 0022-538X
A03   1    @0 J. virol.
A05       @2 79
A06       @2 10
A08 01  1  ENG  @1 Comparative host gene transcription by microarray analysis early after infection of the Huh7 cell line by severe acute respiratory syndrome coronavirus and human coronavirus 229E
A11 01  1    @1 TANG (Bone S. F.)
A11 02  1    @1 CHAN (Kwok-Hung)
A11 03  1    @1 CHENG (Vincent C. C.)
A11 04  1    @1 WOO (Patrick C. Y.)
A11 05  1    @1 LAU (Susanna K. P.)
A11 06  1    @1 LAM (Clarence C. K.)
A11 07  1    @1 CHAN (Tsun-Leung)
A11 08  1    @1 WU (Alan K. L.)
A11 09  1    @1 HUNG (Ivan F. N.)
A11 10  1    @1 LEUNG (Suet-Yi)
A11 11  1    @1 YUEN (Kwok-Yung)
A14 01      @1 Department of Microbiology, Centre of Infection and Immunology, State Key Laboratory of Emerging Infectious Diseases, The University of Hong Kong @3 HKG @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 8 aut. @Z 9 aut. @Z 11 aut.
A14 02      @1 Division of Haematology, Department of Pathology, The University of Hong Kong @3 HKG @Z 6 aut.
A14 03      @1 Division of Anatomical Pathology, Department of Pathology, The University of Hong Kong @3 HKG @Z 7 aut. @Z 10 aut.
A20       @1 6180-6193
A21       @1 2005
A23 01      @0 ENG
A43 01      @1 INIST @2 13592 @5 354000129572140300
A44       @0 0000 @1 © 2005 INIST-CNRS. All rights reserved.
A45       @0 56 ref.
A47 01  1    @0 05-0231505
A60       @1 P
A61       @0 A
A64 01  1    @0 Journal of virology
A66 01      @0 USA
C01 01    ENG  @0 The pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) at the cellular level is unclear. No human cell line was previously known to be susceptible to both SARS-CoV and other human coronaviruses. Huh7 cells were found to be susceptible to both SARS-CoV, associated with SARS, and human coronavirus 229E (HCoV-229E), usually associated with the common cold. Highly lytic and productive rates of infections within 48 h of inoculation were reproducible with both viruses. The early transcriptional profiles of host cell response to both types of infection at 2 and 4 h postinoculation were determined by using the Affymetrix HG-U133A microarray (about 22,000 genes). Much more perturbation of cellular gene transcription was observed after infection by SARS-CoV than after infection by HCoV-229E. Besides the upregulation of genes associated with apoptosis, which was exactly opposite to the previously reported effect of SARS-CoV in a colonic carcinoma cell line, genes related to inflammation, stress response, and procoagulation were also upregulated. These findings were confirmed by semiquantitative reverse transcription-PCR, reverse transcription-quantitative PCR for mRNA of genes, and immunoassays for some encoded proteins. These transcriptomal changes are compatible with the histological changes of pulmonary vasculitis and microvascular thrombosis in addition to the diffuse alveolar damage involving the pneumocytes.
C02 01  X    @0 002A05C10
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C03 01  X  SPA  @0 Coronavirus @2 NW @5 01
C03 02  X  FRE  @0 Homme @5 02
C03 02  X  ENG  @0 Human @5 02
C03 02  X  SPA  @0 Hombre @5 02
C03 03  X  FRE  @0 Gène @5 05
C03 03  X  ENG  @0 Gene @5 05
C03 03  X  SPA  @0 Gen @5 05
C03 04  X  FRE  @0 Transcription @5 06
C03 04  X  ENG  @0 Transcription @5 06
C03 04  X  SPA  @0 Transcripción @5 06
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C03 06  X  FRE  @0 Microbiologie @5 08
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C03 06  X  SPA  @0 Microbiología @5 08
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C03 08  X  FRE  @0 Syndrome respiratoire aigu sévère @2 NM @5 14
C03 08  X  ENG  @0 Severe acute respiratory syndrome @2 NM @5 14
C03 08  X  SPA  @0 Síndrome respiratorio agudo severo @2 NM @5 14
C07 01  X  FRE  @0 Coronaviridae @2 NW
C07 01  X  ENG  @0 Coronaviridae @2 NW
C07 01  X  SPA  @0 Coronaviridae @2 NW
C07 02  X  FRE  @0 Nidovirales @2 NW
C07 02  X  ENG  @0 Nidovirales @2 NW
C07 02  X  SPA  @0 Nidovirales @2 NW
C07 03  X  FRE  @0 Virus @2 NW
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C07 04  X  FRE  @0 Appareil respiratoire pathologie @5 13
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N21       @1 157
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Format Inist (serveur)

NO : PASCAL 05-0231505 INIST
ET : Comparative host gene transcription by microarray analysis early after infection of the Huh7 cell line by severe acute respiratory syndrome coronavirus and human coronavirus 229E
AU : TANG (Bone S. F.); CHAN (Kwok-Hung); CHENG (Vincent C. C.); WOO (Patrick C. Y.); LAU (Susanna K. P.); LAM (Clarence C. K.); CHAN (Tsun-Leung); WU (Alan K. L.); HUNG (Ivan F. N.); LEUNG (Suet-Yi); YUEN (Kwok-Yung)
AF : Department of Microbiology, Centre of Infection and Immunology, State Key Laboratory of Emerging Infectious Diseases, The University of Hong Kong/Hong-Kong (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 8 aut., 9 aut., 11 aut.); Division of Haematology, Department of Pathology, The University of Hong Kong/Hong-Kong (6 aut.); Division of Anatomical Pathology, Department of Pathology, The University of Hong Kong/Hong-Kong (7 aut., 10 aut.)
DT : Publication en série; Niveau analytique
SO : Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2005; Vol. 79; No. 10; Pp. 6180-6193; Bibl. 56 ref.
LA : Anglais
EA : The pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) at the cellular level is unclear. No human cell line was previously known to be susceptible to both SARS-CoV and other human coronaviruses. Huh7 cells were found to be susceptible to both SARS-CoV, associated with SARS, and human coronavirus 229E (HCoV-229E), usually associated with the common cold. Highly lytic and productive rates of infections within 48 h of inoculation were reproducible with both viruses. The early transcriptional profiles of host cell response to both types of infection at 2 and 4 h postinoculation were determined by using the Affymetrix HG-U133A microarray (about 22,000 genes). Much more perturbation of cellular gene transcription was observed after infection by SARS-CoV than after infection by HCoV-229E. Besides the upregulation of genes associated with apoptosis, which was exactly opposite to the previously reported effect of SARS-CoV in a colonic carcinoma cell line, genes related to inflammation, stress response, and procoagulation were also upregulated. These findings were confirmed by semiquantitative reverse transcription-PCR, reverse transcription-quantitative PCR for mRNA of genes, and immunoassays for some encoded proteins. These transcriptomal changes are compatible with the histological changes of pulmonary vasculitis and microvascular thrombosis in addition to the diffuse alveolar damage involving the pneumocytes.
CC : 002A05C10
FD : Coronavirus; Homme; Gène; Transcription; Lignée cellulaire; Microbiologie; Virologie; Syndrome respiratoire aigu sévère
FG : Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie
ED : Coronavirus; Human; Gene; Transcription; Cell line; Microbiology; Virology; Severe acute respiratory syndrome
EG : Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease
SD : Coronavirus; Hombre; Gen; Transcripción; Línea celular; Microbiología; Virología; Síndrome respiratorio agudo severo
LO : INIST-13592.354000129572140300
ID : 05-0231505

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Pascal:05-0231505

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<div type="abstract" xml:lang="en">The pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) at the cellular level is unclear. No human cell line was previously known to be susceptible to both SARS-CoV and other human coronaviruses. Huh7 cells were found to be susceptible to both SARS-CoV, associated with SARS, and human coronavirus 229E (HCoV-229E), usually associated with the common cold. Highly lytic and productive rates of infections within 48 h of inoculation were reproducible with both viruses. The early transcriptional profiles of host cell response to both types of infection at 2 and 4 h postinoculation were determined by using the Affymetrix HG-U133A microarray (about 22,000 genes). Much more perturbation of cellular gene transcription was observed after infection by SARS-CoV than after infection by HCoV-229E. Besides the upregulation of genes associated with apoptosis, which was exactly opposite to the previously reported effect of SARS-CoV in a colonic carcinoma cell line, genes related to inflammation, stress response, and procoagulation were also upregulated. These findings were confirmed by semiquantitative reverse transcription-PCR, reverse transcription-quantitative PCR for mRNA of genes, and immunoassays for some encoded proteins. These transcriptomal changes are compatible with the histological changes of pulmonary vasculitis and microvascular thrombosis in addition to the diffuse alveolar damage involving the pneumocytes.</div>
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<AU>TANG (Bone S. F.); CHAN (Kwok-Hung); CHENG (Vincent C. C.); WOO (Patrick C. Y.); LAU (Susanna K. P.); LAM (Clarence C. K.); CHAN (Tsun-Leung); WU (Alan K. L.); HUNG (Ivan F. N.); LEUNG (Suet-Yi); YUEN (Kwok-Yung)</AU>
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<EA>The pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) at the cellular level is unclear. No human cell line was previously known to be susceptible to both SARS-CoV and other human coronaviruses. Huh7 cells were found to be susceptible to both SARS-CoV, associated with SARS, and human coronavirus 229E (HCoV-229E), usually associated with the common cold. Highly lytic and productive rates of infections within 48 h of inoculation were reproducible with both viruses. The early transcriptional profiles of host cell response to both types of infection at 2 and 4 h postinoculation were determined by using the Affymetrix HG-U133A microarray (about 22,000 genes). Much more perturbation of cellular gene transcription was observed after infection by SARS-CoV than after infection by HCoV-229E. Besides the upregulation of genes associated with apoptosis, which was exactly opposite to the previously reported effect of SARS-CoV in a colonic carcinoma cell line, genes related to inflammation, stress response, and procoagulation were also upregulated. These findings were confirmed by semiquantitative reverse transcription-PCR, reverse transcription-quantitative PCR for mRNA of genes, and immunoassays for some encoded proteins. These transcriptomal changes are compatible with the histological changes of pulmonary vasculitis and microvascular thrombosis in addition to the diffuse alveolar damage involving the pneumocytes.</EA>
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