Interferon priming enables cells to partially overturn the SARS coronavirus-induced block in innate immune activation.
Identifieur interne : 001851 ( PubMed/Checkpoint ); précédent : 001850; suivant : 001852Interferon priming enables cells to partially overturn the SARS coronavirus-induced block in innate immune activation.
Auteurs : Thomas Kuri [Allemagne] ; Xiaonan Zhang [République populaire de Chine] ; Matthias Habjan [Allemagne] ; Luis Martínez-Sobrido [États-Unis] ; Adolfo García-Sastre [États-Unis] ; Zhenghong Yuan [République populaire de Chine] ; Friedemann Weber [Allemagne]Source :
- The Journal of general virology [ 1465-2099 ] ; 2009.
Descripteurs français
- KwdFr :
- MESH :
- immunologie : Interféron alpha, Virus du SRAS.
- métabolisme : Cytokines, Facteur-3 de régulation d'interféron, Facteur-7 de régulation d'interféron.
- Animaux, Humains, Lignée cellulaire, Noyau de la cellule, Transport de protéines.
English descriptors
- KwdEn :
- MESH :
- chemical , immunology : Interferon-alpha.
- chemical , metabolism : Cytokines, Interferon Regulatory Factor-3, Interferon Regulatory Factor-7.
- chemistry : Cell Nucleus.
- immunology : SARS Virus.
- Animals, Cell Line, Chlorocebus aethiops, Humans, Protein Transport.
Abstract
SARS coronavirus (SARS-CoV) is known to efficiently suppress the induction of antiviral type I interferons (IFN-alpha/beta) in non-lymphatic cells through inhibition of the transcription factor IRF-3. Plasmacytoid dendritic cells, in contrast, respond to infection with production of high levels of IFNs. Here, we show that pretreatment of non-lymphatic cells with small amounts of IFN-alpha (IFN priming) partially overturns the block in IFN induction imposed by SARS-CoV. IFN priming combined with SARS-CoV infection substantially induced genes for IFN induction, IFN signalling, antiviral effector proteins, ubiquitination and ISGylation, antigen presentation and other cytokines and chemokines, whereas each individual treatment had no major effect. Curiously, however, despite this typical IFN response, neither IRF-3 nor IRF-7 was transported to the nucleus as a sign of activation. Taken together, our results suggest that (i) IFN, as it is produced by plasmacytoid dendritic cells, could enable tissue cells to launch a host response to SARS-CoV, (ii) IRF-3 and IRF-7 may be active at subdetectable levels, and (iii) SARS-CoV does not activate IRF-7.
DOI: 10.1099/vir.0.013599-0
PubMed: 19625461
Affiliations:
- Allemagne, République populaire de Chine, États-Unis
- Bade-Wurtemberg, District de Fribourg-en-Brisgau, État de New York
- Fribourg-en-Brisgau
Links toward previous steps (curation, corpus...)
Links to Exploration step
pubmed:19625461Le document en format XML
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<front><div type="abstract" xml:lang="en">SARS coronavirus (SARS-CoV) is known to efficiently suppress the induction of antiviral type I interferons (IFN-alpha/beta) in non-lymphatic cells through inhibition of the transcription factor IRF-3. Plasmacytoid dendritic cells, in contrast, respond to infection with production of high levels of IFNs. Here, we show that pretreatment of non-lymphatic cells with small amounts of IFN-alpha (IFN priming) partially overturns the block in IFN induction imposed by SARS-CoV. IFN priming combined with SARS-CoV infection substantially induced genes for IFN induction, IFN signalling, antiviral effector proteins, ubiquitination and ISGylation, antigen presentation and other cytokines and chemokines, whereas each individual treatment had no major effect. Curiously, however, despite this typical IFN response, neither IRF-3 nor IRF-7 was transported to the nucleus as a sign of activation. Taken together, our results suggest that (i) IFN, as it is produced by plasmacytoid dendritic cells, could enable tissue cells to launch a host response to SARS-CoV, (ii) IRF-3 and IRF-7 may be active at subdetectable levels, and (iii) SARS-CoV does not activate IRF-7.</div>
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<Abstract><AbstractText>SARS coronavirus (SARS-CoV) is known to efficiently suppress the induction of antiviral type I interferons (IFN-alpha/beta) in non-lymphatic cells through inhibition of the transcription factor IRF-3. Plasmacytoid dendritic cells, in contrast, respond to infection with production of high levels of IFNs. Here, we show that pretreatment of non-lymphatic cells with small amounts of IFN-alpha (IFN priming) partially overturns the block in IFN induction imposed by SARS-CoV. IFN priming combined with SARS-CoV infection substantially induced genes for IFN induction, IFN signalling, antiviral effector proteins, ubiquitination and ISGylation, antigen presentation and other cytokines and chemokines, whereas each individual treatment had no major effect. Curiously, however, despite this typical IFN response, neither IRF-3 nor IRF-7 was transported to the nucleus as a sign of activation. Taken together, our results suggest that (i) IFN, as it is produced by plasmacytoid dendritic cells, could enable tissue cells to launch a host response to SARS-CoV, (ii) IRF-3 and IRF-7 may be active at subdetectable levels, and (iii) SARS-CoV does not activate IRF-7.</AbstractText>
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