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Interaction of severe acute respiratory syndrome- associated coronavirus with dendritic cells

Identifieur interne : 000480 ( PascalFrancis/Corpus ); précédent : 000479; suivant : 000481

Interaction of severe acute respiratory syndrome- associated coronavirus with dendritic cells

Auteurs : Martin Spiegel ; Kerstin Schneider ; Friedemann Weber ; Manfred Weidmann ; Frank T. Hufert

Source :

RBID : Pascal:06-0345668

Descripteurs français

English descriptors

Abstract

Severe acute respiratory syndrome (SARS) of humans is caused by a novel coronavirus of zoonotic origin termed SARS-associated coronavirus (SARS-CoV). The virus induces severe injury of lung tissue, as well as lymphopenia and destruction of the architecture of lymphatic tissue by as-yet-unknown mechanisms. In this study, the interaction of SARS-CoV with dendritic cells (DCs), the key regulators of immune responses, was analysed. Monocyte-derived DCs were infected with SARS-CoV and analysed for viability, surface-marker expression and alpha interferon (IFN-α) induction. SARS-CoV infection was monitored by quantitative RT-PCR, immunofluorescence analysis and recovery experiments. SARS-CoV infected both immature and mature DCs, although replication efficiency was low. Immature DCs were activated by SARS-CoV infection and by UV-inactivated SARS-CoV. Infected DCs were still viable on day 6 post-infection, but major histocompatibility complex class I upregulation was missing, indicating that DC function was impaired. Additionally, SARS-CoV infection induced a delayed activation of IFN-a expression. Therefore, it is concluded that SARS-CoV has the ability to circumvent both the innate and the adaptive immune systems.

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Pour connaître la documentation sur le format Inist Standard.

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A02 01      @0 JGVIAY
A03   1    @0 J. gen. virol.
A05       @2 87
A06       @3 p.7
A08 01  1  ENG  @1 Interaction of severe acute respiratory syndrome- associated coronavirus with dendritic cells
A11 01  1    @1 SPIEGEL (Martin)
A11 02  1    @1 SCHNEIDER (Kerstin)
A11 03  1    @1 WEBER (Friedemann)
A11 04  1    @1 WEIDMANN (Manfred)
A11 05  1    @1 HUFERT (Frank T.)
A14 01      @1 Institute for Virology, University of Goettingen, Kreuzbergring 57 @2 37075 Goettingen @3 DEU @Z 1 aut. @Z 4 aut. @Z 5 aut.
A14 02      @1 Department of Virology, Institute for Medical Microbiology and Hygiene, University of Freiburg, Hermann-Herder-Strasse 11 @2 79104 Freiburg @3 DEU @Z 2 aut. @Z 3 aut.
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A45       @0 1 p.1/4
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C01 01    ENG  @0 Severe acute respiratory syndrome (SARS) of humans is caused by a novel coronavirus of zoonotic origin termed SARS-associated coronavirus (SARS-CoV). The virus induces severe injury of lung tissue, as well as lymphopenia and destruction of the architecture of lymphatic tissue by as-yet-unknown mechanisms. In this study, the interaction of SARS-CoV with dendritic cells (DCs), the key regulators of immune responses, was analysed. Monocyte-derived DCs were infected with SARS-CoV and analysed for viability, surface-marker expression and alpha interferon (IFN-α) induction. SARS-CoV infection was monitored by quantitative RT-PCR, immunofluorescence analysis and recovery experiments. SARS-CoV infected both immature and mature DCs, although replication efficiency was low. Immature DCs were activated by SARS-CoV infection and by UV-inactivated SARS-CoV. Infected DCs were still viable on day 6 post-infection, but major histocompatibility complex class I upregulation was missing, indicating that DC function was impaired. Additionally, SARS-CoV infection induced a delayed activation of IFN-a expression. Therefore, it is concluded that SARS-CoV has the ability to circumvent both the innate and the adaptive immune systems.
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C07 01  X  FRE  @0 Coronaviridae @2 NW
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C07 01  X  SPA  @0 Coronaviridae @2 NW
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C07 05  X  FRE  @0 Virose
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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       @1 227
N44 01      @1 OTO
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Format Inist (serveur)

NO : PASCAL 06-0345668 INIST
ET : Interaction of severe acute respiratory syndrome- associated coronavirus with dendritic cells
AU : SPIEGEL (Martin); SCHNEIDER (Kerstin); WEBER (Friedemann); WEIDMANN (Manfred); HUFERT (Frank T.)
AF : Institute for Virology, University of Goettingen, Kreuzbergring 57/37075 Goettingen/Allemagne (1 aut., 4 aut., 5 aut.); Department of Virology, Institute for Medical Microbiology and Hygiene, University of Freiburg, Hermann-Herder-Strasse 11/79104 Freiburg/Allemagne (2 aut., 3 aut.)
DT : Publication en série; Niveau analytique
SO : Journal of general virology; ISSN 0022-1317; Coden JGVIAY; Royaume-Uni; Da. 2006; Vol. 87; No. p.7; Pp. 1953-1960; Bibl. 1 p.1/4
LA : Anglais
EA : Severe acute respiratory syndrome (SARS) of humans is caused by a novel coronavirus of zoonotic origin termed SARS-associated coronavirus (SARS-CoV). The virus induces severe injury of lung tissue, as well as lymphopenia and destruction of the architecture of lymphatic tissue by as-yet-unknown mechanisms. In this study, the interaction of SARS-CoV with dendritic cells (DCs), the key regulators of immune responses, was analysed. Monocyte-derived DCs were infected with SARS-CoV and analysed for viability, surface-marker expression and alpha interferon (IFN-α) induction. SARS-CoV infection was monitored by quantitative RT-PCR, immunofluorescence analysis and recovery experiments. SARS-CoV infected both immature and mature DCs, although replication efficiency was low. Immature DCs were activated by SARS-CoV infection and by UV-inactivated SARS-CoV. Infected DCs were still viable on day 6 post-infection, but major histocompatibility complex class I upregulation was missing, indicating that DC function was impaired. Additionally, SARS-CoV infection induced a delayed activation of IFN-a expression. Therefore, it is concluded that SARS-CoV has the ability to circumvent both the innate and the adaptive immune systems.
CC : 002A05C10
FD : Coronavirus; Cellule dendritique; Microbiologie; Virologie; Syndrome respiratoire aigu sévère
FG : Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie
ED : Coronavirus; Dendritic cell; Microbiology; Virology; Severe acute respiratory syndrome
EG : Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease
SD : Coronavirus; Célula dendrítica; Microbiología; Virología; Síndrome respiratorio agudo severo
LO : INIST-13533.354000142400560170
ID : 06-0345668

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Le document en format XML

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<NO>PASCAL 06-0345668 INIST</NO>
<ET>Interaction of severe acute respiratory syndrome- associated coronavirus with dendritic cells</ET>
<AU>SPIEGEL (Martin); SCHNEIDER (Kerstin); WEBER (Friedemann); WEIDMANN (Manfred); HUFERT (Frank T.)</AU>
<AF>Institute for Virology, University of Goettingen, Kreuzbergring 57/37075 Goettingen/Allemagne (1 aut., 4 aut., 5 aut.); Department of Virology, Institute for Medical Microbiology and Hygiene, University of Freiburg, Hermann-Herder-Strasse 11/79104 Freiburg/Allemagne (2 aut., 3 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of general virology; ISSN 0022-1317; Coden JGVIAY; Royaume-Uni; Da. 2006; Vol. 87; No. p.7; Pp. 1953-1960; Bibl. 1 p.1/4</SO>
<LA>Anglais</LA>
<EA>Severe acute respiratory syndrome (SARS) of humans is caused by a novel coronavirus of zoonotic origin termed SARS-associated coronavirus (SARS-CoV). The virus induces severe injury of lung tissue, as well as lymphopenia and destruction of the architecture of lymphatic tissue by as-yet-unknown mechanisms. In this study, the interaction of SARS-CoV with dendritic cells (DCs), the key regulators of immune responses, was analysed. Monocyte-derived DCs were infected with SARS-CoV and analysed for viability, surface-marker expression and alpha interferon (IFN-α) induction. SARS-CoV infection was monitored by quantitative RT-PCR, immunofluorescence analysis and recovery experiments. SARS-CoV infected both immature and mature DCs, although replication efficiency was low. Immature DCs were activated by SARS-CoV infection and by UV-inactivated SARS-CoV. Infected DCs were still viable on day 6 post-infection, but major histocompatibility complex class I upregulation was missing, indicating that DC function was impaired. Additionally, SARS-CoV infection induced a delayed activation of IFN-a expression. Therefore, it is concluded that SARS-CoV has the ability to circumvent both the innate and the adaptive immune systems.</EA>
<CC>002A05C10</CC>
<FD>Coronavirus; Cellule dendritique; Microbiologie; Virologie; Syndrome respiratoire aigu sévère</FD>
<FG>Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie</FG>
<ED>Coronavirus; Dendritic cell; Microbiology; Virology; Severe acute respiratory syndrome</ED>
<EG>Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease</EG>
<SD>Coronavirus; Célula dendrítica; Microbiología; Virología; Síndrome respiratorio agudo severo</SD>
<LO>INIST-13533.354000142400560170</LO>
<ID>06-0345668</ID>
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