SrasV1, Main, Exploration, bibRecord, 004E06

Inhibition of beta interferon induction by severe acute respiratory syndrome coronavirus suggests a two-step model for activation of interferon regulatory factor 3

Identifieur interne : 004E06 ( Main/Exploration ); précédent : 004E05; suivant : 004E07

Inhibition of beta interferon induction by severe acute respiratory syndrome coronavirus suggests a two-step model for activation of interferon regulatory factor 3

Auteurs : Martin Spiegel [Allemagne] ; Andreas Pichlmair [Allemagne] ; Luis Martinez-Sobrido [États-Unis] ; Jerome Cros [États-Unis] ; Adolfo Garcia-Sastre [États-Unis] ; Otto Haller [Allemagne] ; Friedemann Weber [Allemagne]

Source :

Journal of virology [ 0022-538X ] ; 2005.

RBID : Pascal:05-0132671

Descripteurs français

KwdFr :
- Animaux, Cellules Vero, Facteur-3 de régulation d'interféron, Facteurs de transcription (métabolisme), Interféron bêta (métabolisme), Phosphorylation, Protéines de liaison à l'ADN (métabolisme), Virus du SRAS (physiologie).
MESH :
- métabolisme : Facteurs de transcription, Interféron bêta, Protéines de liaison à l'ADN.
- physiologie : Virus du SRAS.
Pascal (Inist)
- Animaux, Cellules Vero, Coronavirus, Facteur-3 de régulation d'interféron, Interféron bêta, Modèle, Microbiologie, Phosphorylation, Virologie, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Animals, Beta interferon, Chlorocebus aethiops, Coronavirus, DNA-Binding Proteins (metabolism), Interferon Regulatory Factor-3, Interferon-beta (metabolism), Microbiology, Models, Phosphorylation, SARS Virus (physiology), Severe acute respiratory syndrome, Transcription Factors (metabolism), Vero Cells, Virology.
MESH :
- chemical , metabolism : DNA-Binding Proteins, Interferon-beta, Transcription Factors.
- physiology : SARS Virus.
- Animals, Chlorocebus aethiops, Interferon Regulatory Factor-3, Phosphorylation, Vero Cells.

Abstract

Severe acute respiratory syndrome (SARS) is caused by a novel coronavirus termed SARS-CoV. We and others have previously shown that the replication of SARS-CoV can be suppressed by exogenously added interferon (IFN), a cytokine which is normally synthesized by cells as a reaction to virus infection. Here, we demonstrate that SARS-CoV escapes IFN-mediated growth inhibition by preventing the induction of IFN-β. In SARS-CoV-infected cells, no endogenous IFN-β transcripts and no IFN-β promoter activity were detected. Nevertheless, the transcription factor interferon regulatory factor 3 (IRF-3), which is essential for IFN-β promoter activity, was transported from the cytoplasm to the nucleus early after infection with SARS-CoV. However, at a later time point in infection, IRF-3 was again localized in the cytoplasm. By contrast, IRF-3 remained in the nucleus of cells infected with the IFN-inducing control virus Bunyamwera delNSs. Other signs of IRF-3 activation such as hyperphosphorylation, homodimer formation, and recruitment of the coactivator CREB-binding protein (CBP) were found late after infection with the control virus but not with SARS-CoV. Our data suggest that nuclear transport of IRF-3 is an immediate-early reaction to virus infection and may precede its hyperphosphorylation, homodimer formation, and binding to CBP. In order to escape activation of the IFN system, SARS-CoV appears to block a step after the early nuclear transport of IRF-3.

Affiliations:

Le document en format XML

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<term>Beta interferon</term>
<term>Chlorocebus aethiops</term>
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<term>DNA-Binding Proteins (metabolism)</term>
<term>Interferon Regulatory Factor-3</term>
<term>Interferon-beta (metabolism)</term>
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<front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) is caused by a novel coronavirus termed SARS-CoV. We and others have previously shown that the replication of SARS-CoV can be suppressed by exogenously added interferon (IFN), a cytokine which is normally synthesized by cells as a reaction to virus infection. Here, we demonstrate that SARS-CoV escapes IFN-mediated growth inhibition by preventing the induction of IFN-β. In SARS-CoV-infected cells, no endogenous IFN-β transcripts and no IFN-β promoter activity were detected. Nevertheless, the transcription factor interferon regulatory factor 3 (IRF-3), which is essential for IFN-β promoter activity, was transported from the cytoplasm to the nucleus early after infection with SARS-CoV. However, at a later time point in infection, IRF-3 was again localized in the cytoplasm. By contrast, IRF-3 remained in the nucleus of cells infected with the IFN-inducing control virus Bunyamwera delNSs. Other signs of IRF-3 activation such as hyperphosphorylation, homodimer formation, and recruitment of the coactivator CREB-binding protein (CBP) were found late after infection with the control virus but not with SARS-CoV. Our data suggest that nuclear transport of IRF-3 is an immediate-early reaction to virus infection and may precede its hyperphosphorylation, homodimer formation, and binding to CBP. In order to escape activation of the IFN system, SARS-CoV appears to block a step after the early nuclear transport of IRF-3.</div>
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<name sortKey="Garcia Sastre, Adolfo" sort="Garcia Sastre, Adolfo" uniqKey="Garcia Sastre A" first="Adolfo" last="Garcia-Sastre">Adolfo Garcia-Sastre</name>
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Inhibition of beta interferon induction by severe acute respiratory syndrome coronavirus suggests a two-step model for activation of interferon regulatory factor 3

Inhibition of beta interferon induction by severe acute respiratory syndrome coronavirus suggests a two-step model for activation of interferon regulatory factor 3

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Descripteurs français

English descriptors

Abstract

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