Interaction of severe acute respiratory syndrome-associated coronavirus with dendritic cells.
Identifieur interne : 002209 ( PubMed/Corpus ); précédent : 002208; suivant : 002210Interaction of severe acute respiratory syndrome-associated coronavirus with dendritic cells.
Auteurs : Martin Spiegel ; Kerstin Schneider ; Friedemann Weber ; Manfred Weidmann ; Frank T. HufertSource :
- The Journal of general virology [ 0022-1317 ] ; 2006.
English descriptors
- KwdEn :
- Antigens, Surface (metabolism), Apoptosis, Base Sequence, Cell Differentiation, DNA, Viral (genetics), Dendritic Cells (cytology), Dendritic Cells (immunology), Dendritic Cells (virology), Humans, Immunity, Innate, In Vitro Techniques, Interferon-alpha (biosynthesis), Phenotype, SARS Virus (genetics), SARS Virus (pathogenicity), SARS Virus (physiology), Virus Replication.
- MESH :
- chemical , biosynthesis : Interferon-alpha.
- chemical , genetics : DNA, Viral.
- chemical , metabolism : Antigens, Surface.
- cytology : Dendritic Cells.
- genetics : SARS Virus.
- immunology : Dendritic Cells.
- pathogenicity : SARS Virus.
- physiology : SARS Virus.
- virology : Dendritic Cells.
- Apoptosis, Base Sequence, Cell Differentiation, Humans, Immunity, Innate, In Vitro Techniques, Phenotype, Virus Replication.
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-alpha) 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-alpha expression. Therefore, it is concluded that SARS-CoV has the ability to circumvent both the innate and the adaptive immune systems.
DOI: 10.1099/vir.0.81624-0
PubMed: 16760397
Links to Exploration step
pubmed:16760397Le document en format XML
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<author><name sortKey="Schneider, Kerstin" sort="Schneider, Kerstin" uniqKey="Schneider K" first="Kerstin" last="Schneider">Kerstin Schneider</name>
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<author><name sortKey="Weber, Friedemann" sort="Weber, Friedemann" uniqKey="Weber F" first="Friedemann" last="Weber">Friedemann Weber</name>
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<author><name sortKey="Weidmann, Manfred" sort="Weidmann, Manfred" uniqKey="Weidmann M" first="Manfred" last="Weidmann">Manfred Weidmann</name>
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<author><name sortKey="Hufert, Frank T" sort="Hufert, Frank T" uniqKey="Hufert F" first="Frank T" last="Hufert">Frank T. Hufert</name>
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<term>Dendritic Cells (cytology)</term>
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<term>Dendritic Cells (virology)</term>
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<term>Immunity, Innate</term>
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<term>Interferon-alpha (biosynthesis)</term>
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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-alpha) 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-alpha 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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<Abstract><AbstractText>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-alpha) 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-alpha expression. Therefore, it is concluded that SARS-CoV has the ability to circumvent both the innate and the adaptive immune systems.</AbstractText>
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