Interaction of severe acute respiratory syndrome- associated coronavirus with dendritic cells
Identifieur interne : 000480 ( PascalFrancis/Corpus ); précédent : 000479; suivant : 000481Interaction of severe acute respiratory syndrome- associated coronavirus with dendritic cells
Auteurs : Martin Spiegel ; Kerstin Schneider ; Friedemann Weber ; Manfred Weidmann ; Frank T. HufertSource :
- Journal of general virology [ 0022-1317 ] ; 2006.
Descripteurs français
- Pascal (Inist)
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.
Notice en format standard (ISO 2709)
Pour connaître la documentation sur le format Inist Standard.
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Format Inist (serveur)
NO : | PASCAL 06-0345668 INIST |
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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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Pascal:06-0345668Le document en format XML
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<front><div type="abstract" xml:lang="en">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.</div>
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<server><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>
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<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>
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