SrasV1, PascalFrancis, Curation, bibRecord, 000808

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

Identifieur interne : 000808 ( PascalFrancis/Curation ); précédent : 000807; suivant : 000809

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

Pascal (Inist)
- Virus syndrome respiratoire aigu sévère, Interféron, Cytokine, In vitro, Immunité naturelle, Microbiologie.

English descriptors

KwdEn :
- Cytokine, In vitro, Interferon, Microbiology, Natural immunity, Severe acute respiratory syndrome virus.

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.

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A11	`03`	`1`		`@1 HABJAN (Matthias)`
A11	`04`	`1`		`@1 MARTINEZ-SOBRIDO (Luis)`
A11	`05`	`1`		`@1 GARCIA-SASTRE (Adolfo)`
A11	`06`	`1`		`@1 ZHENGHONG YUAN`
A11	`07`	`1`		`@1 WEBER (Friedemann)`
A14	`01`			`@1 Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg @2 79008 Freiburg @3 DEU @Z 1 aut. @Z 3 aut. @Z 7 aut.`
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A14	`03`			`@1 School of Medicine and Dentistry, University of Rochester @2 Rochester, NY 14642 @3 USA @Z 4 aut.`
A14	`04`			`@1 Department of Microbiology, Department of Medicine (Division of Infectious Diseases) and Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine @2 New York, NY 10029 @3 USA @Z 5 aut.`
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C01	`01`		`ENG`	@0 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.
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C03	`06`	`X`	`FRE`	`@0 Microbiologie @5 09`
C03	`06`	`X`	`ENG`	`@0 Microbiology @5 09`
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C07	`01`	`X`	`ENG`	`@0 Coronavirus @2 NW`
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C07	`02`	`X`	`FRE`	`@0 Coronaviridae @2 NW`
C07	`02`	`X`	`ENG`	`@0 Coronaviridae @2 NW`
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C07	`03`	`X`	`FRE`	`@0 Nidovirales @2 NW`
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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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<fC01 i1="01" l="ENG"><s0>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.</s0>
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   |wiki=    Sante
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   |texte=   Interferon priming enables cells to partially overturn the SARS coronavirus-induced block in innate immune activation
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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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