Interaction of severe acute respiratory syndrome-associated coronavirus with dendritic cells.
Identifieur interne : 001529 ( Ncbi/Checkpoint ); précédent : 001528; suivant : 001530Interaction of severe acute respiratory syndrome-associated coronavirus with dendritic cells.
Auteurs : Martin Spiegel [Allemagne] ; Kerstin Schneider ; Friedemann Weber ; Manfred Weidmann ; Frank T. HufertSource :
- The Journal of general virology [ 0022-1317 ] ; 2006.
Descripteurs français
- KwdFr :
- ADN viral (génétique), Antigènes de surface (métabolisme), Apoptose, Cellules dendritiques (cytologie), Cellules dendritiques (immunologie), Cellules dendritiques (virologie), Différenciation cellulaire, Humains, Immunité innée, Interféron alpha (biosynthèse), Phénotype, Réplication virale, Séquence nucléotidique, Techniques in vitro, Virus du SRAS (génétique), Virus du SRAS (pathogénicité), Virus du SRAS (physiologie).
- MESH :
- biosynthèse : Interféron alpha.
- cytologie : Cellules dendritiques.
- génétique : ADN viral, Virus du SRAS.
- immunologie : Cellules dendritiques.
- métabolisme : Antigènes de surface.
- pathogénicité : Virus du SRAS.
- physiologie : Virus du SRAS.
- virologie : Cellules dendritiques.
- Apoptose, Différenciation cellulaire, Humains, Immunité innée, Phénotype, Réplication virale, Séquence nucléotidique, Techniques in vitro.
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
Affiliations:
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pubmed:16760397Le document en format XML
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<affiliation wicri:level="3"><nlm:affiliation>Institute for Virology, University of Goettingen, Kreuzbergring 57, 37075 Goettingen, Germany.</nlm:affiliation>
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<term>Apoptosis</term>
<term>Base Sequence</term>
<term>Cell Differentiation</term>
<term>DNA, Viral (genetics)</term>
<term>Dendritic Cells (cytology)</term>
<term>Dendritic Cells (immunology)</term>
<term>Dendritic Cells (virology)</term>
<term>Humans</term>
<term>Immunity, Innate</term>
<term>In Vitro Techniques</term>
<term>Interferon-alpha (biosynthesis)</term>
<term>Phenotype</term>
<term>SARS Virus (genetics)</term>
<term>SARS Virus (pathogenicity)</term>
<term>SARS Virus (physiology)</term>
<term>Virus Replication</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>ADN viral (génétique)</term>
<term>Antigènes de surface (métabolisme)</term>
<term>Apoptose</term>
<term>Cellules dendritiques (cytologie)</term>
<term>Cellules dendritiques (immunologie)</term>
<term>Cellules dendritiques (virologie)</term>
<term>Différenciation cellulaire</term>
<term>Humains</term>
<term>Immunité innée</term>
<term>Interféron alpha (biosynthèse)</term>
<term>Phénotype</term>
<term>Réplication virale</term>
<term>Séquence nucléotidique</term>
<term>Techniques in vitro</term>
<term>Virus du SRAS (génétique)</term>
<term>Virus du SRAS (pathogénicité)</term>
<term>Virus du SRAS (physiologie)</term>
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<term>Virus du SRAS</term>
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<term>Base Sequence</term>
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<term>In Vitro Techniques</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>
</front>
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<name sortKey="Weber, Friedemann" sort="Weber, Friedemann" uniqKey="Weber F" first="Friedemann" last="Weber">Friedemann Weber</name>
<name sortKey="Weidmann, Manfred" sort="Weidmann, Manfred" uniqKey="Weidmann M" first="Manfred" last="Weidmann">Manfred Weidmann</name>
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