SrasV1, Main, Exploration, bibRecord, 002F28

Interferon priming enables cells to partially overturn the SARS coronavirus-induced block in innate immune activation

Identifieur interne : 002F28 ( Main/Exploration ); précédent : 002F27; suivant : 002F29

Interferon 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 Martinez-Sobrido [États-Unis] ; Adolfo Garcia-Sastre [États-Unis] ; ZHENGHONG YUAN [République populaire de Chine] ; Friedemann Weber [Allemagne]

Source :

Journal of general virology [ 0022-1317 ] ; 2009.

RBID : Pascal:09-0458424

Descripteurs français

KwdFr :
- Animaux, Cytokines (métabolisme), Facteur-3 de régulation d'interféron (métabolisme), Facteur-7 de régulation d'interféron (métabolisme), Humains, Interféron alpha (immunologie), Lignée cellulaire, Noyau de la cellule (), Transport de protéines, Virus du SRAS (immunologie).
MESH :
- immunologie : Interféron alpha, Virus du SRAS.
- métabolisme : Cytokines, Facteur-3 de régulation d'interféron, Facteur-7 de régulation d'interféron.
Pascal (Inist)
- Animaux, Humains, Lignée cellulaire, Noyau de la cellule, Transport de protéines, Virus syndrome respiratoire aigu sévère, Interféron, Cytokine, In vitro, Immunité naturelle, Microbiologie.

English descriptors

KwdEn :
- Animals, Cell Line, Cell Nucleus (chemistry), Chlorocebus aethiops, Cytokine, Cytokines (metabolism), Humans, In vitro, Interferon, Interferon Regulatory Factor-3 (metabolism), Interferon Regulatory Factor-7 (metabolism), Interferon-alpha (immunology), Microbiology, Natural immunity, Protein Transport, SARS Virus (immunology), Severe acute respiratory syndrome virus.
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-α/β) 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-α (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.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2888313

Affiliations:

Le 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-α/β) 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-α (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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Interferon priming enables cells to partially overturn the SARS coronavirus-induced block in innate immune activation

Interferon priming enables cells to partially overturn the SARS coronavirus-induced block in innate immune activation

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Abstract

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