Severe acute respiratory syndrome coronavirus open reading frame (ORF) 3b, ORF 6, and nucleocapsid proteins function as interferon antagonists⊇
Identifieur interne : 003B28 ( Main/Exploration ); précédent : 003B27; suivant : 003B29Severe acute respiratory syndrome coronavirus open reading frame (ORF) 3b, ORF 6, and nucleocapsid proteins function as interferon antagonists⊇
Auteurs : Sarah A. Kopecky-Bromberg [États-Unis] ; Luis Martinez-Sobrido [États-Unis] ; Matthew Frieman [États-Unis] ; Ralph A. Baric [États-Unis] ; Peter Palese [États-Unis]Source :
- Journal of virology [ 0022-538X ] ; 2007.
Descripteurs français
- KwdFr :
- Apoptose, Cadres ouverts de lecture (génétique), Cadres ouverts de lecture (physiologie), Facteur de transcription NF-kappa B (antagonistes et inhibiteurs), Facteur-3 de régulation d'interféron (antagonistes et inhibiteurs), Humains, Interféron bêta (antagonistes et inhibiteurs), Interféron bêta (biosynthèse), Lignée cellulaire, Microscopie confocale, Protéines nucléocapside (génétique), Protéines nucléocapside (métabolisme), Protéines virales (génétique), Protéines virales (métabolisme), Transfection, Virus du SRAS (génétique), Virus du SRAS (métabolisme), Virus du SRAS (pathogénicité).
- MESH :
- antagonistes et inhibiteurs : Facteur de transcription NF-kappa B, Facteur-3 de régulation d'interféron, Interféron bêta.
- biosynthèse : Interféron bêta.
- génétique : Cadres ouverts de lecture, Protéines nucléocapside, Protéines virales, Virus du SRAS.
- métabolisme : Protéines nucléocapside, Protéines virales, Virus du SRAS.
- pathogénicité : Virus du SRAS.
- physiologie : Cadres ouverts de lecture.
- Pascal (Inist)
English descriptors
- KwdEn :
- Apoptosis, Cell Line, Coronavirus, Humans, Interferon, Interferon Regulatory Factor-3 (antagonists & inhibitors), Interferon-beta (antagonists & inhibitors), Interferon-beta (biosynthesis), Microscopy, Confocal, NF-kappa B (antagonists & inhibitors), Nucleocapsid, Nucleocapsid Proteins (genetics), Nucleocapsid Proteins (metabolism), Open Reading Frames (genetics), Open Reading Frames (physiology), Open reading frame, Protein, SARS Virus (genetics), SARS Virus (metabolism), SARS Virus (pathogenicity), Severe acute respiratory syndrome, Transfection, Viral Proteins (genetics), Viral Proteins (metabolism), Virology.
- MESH :
- chemical , antagonists & inhibitors : Interferon Regulatory Factor-3, Interferon-beta, NF-kappa B.
- chemical , biosynthesis : Interferon-beta.
- chemical , genetics : Nucleocapsid Proteins, Viral Proteins.
- chemical , metabolism : Nucleocapsid Proteins, Viral Proteins.
- genetics : Open Reading Frames, SARS Virus.
- metabolism : SARS Virus.
- pathogenicity : SARS Virus.
- physiology : Open Reading Frames.
- Apoptosis, Cell Line, Humans, Microscopy, Confocal, Transfection.
Abstract
The severe acute respiratory syndrome coronavirus (SARS-CoV) is highly pathogenic in humans, with a death rate near 10%. This high pathogenicity suggests that SARS-CoV has developed mechanisms to overcome the host innate immune response. It has now been determined that SARS-CoV open reading frame (ORF) 3b, ORF 6, and N proteins antagonize interferon, a key component of the innate immune response. All three proteins inhibit the expression of beta interferon (IFN-β), and further examination revealed that these SARS-CoV proteins inhibit a key protein necessary for the expression of IFN-β, IRF-3. N protein dramatically inhibited expression from an NF-KB-responsive promoter. All three proteins were able to inhibit expression from an interferon-stimulated response element (ISRE) promoter after infection with Sendai virus, while only ORF 3b and ORF 6 proteins were able to inhibit expression from the ISRE promoter after treatment with interferon. This indicates that N protein inhibits only the synthesis of interferon, while ORF 3b and ORF 6 proteins inhibit both interferon synthesis and signaling. ORF 6 protein, but not ORF 3b or N protein, inhibited nuclear translocation but not phosphorylation of STAT1. Thus, it appears that these three interferon antagonists of SARS-CoV inhibit the interferon response by different mechanisms.
Affiliations:
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Le document en format XML
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<term>Cell Line</term>
<term>Coronavirus</term>
<term>Humans</term>
<term>Interferon</term>
<term>Interferon Regulatory Factor-3 (antagonists & inhibitors)</term>
<term>Interferon-beta (antagonists & inhibitors)</term>
<term>Interferon-beta (biosynthesis)</term>
<term>Microscopy, Confocal</term>
<term>NF-kappa B (antagonists & inhibitors)</term>
<term>Nucleocapsid</term>
<term>Nucleocapsid Proteins (genetics)</term>
<term>Nucleocapsid Proteins (metabolism)</term>
<term>Open Reading Frames (genetics)</term>
<term>Open Reading Frames (physiology)</term>
<term>Open reading frame</term>
<term>Protein</term>
<term>SARS Virus (genetics)</term>
<term>SARS Virus (metabolism)</term>
<term>SARS Virus (pathogenicity)</term>
<term>Severe acute respiratory syndrome</term>
<term>Transfection</term>
<term>Viral Proteins (genetics)</term>
<term>Viral Proteins (metabolism)</term>
<term>Virology</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Apoptose</term>
<term>Cadres ouverts de lecture (génétique)</term>
<term>Cadres ouverts de lecture (physiologie)</term>
<term>Facteur de transcription NF-kappa B (antagonistes et inhibiteurs)</term>
<term>Facteur-3 de régulation d'interféron (antagonistes et inhibiteurs)</term>
<term>Humains</term>
<term>Interféron bêta (antagonistes et inhibiteurs)</term>
<term>Interféron bêta (biosynthèse)</term>
<term>Lignée cellulaire</term>
<term>Microscopie confocale</term>
<term>Protéines nucléocapside (génétique)</term>
<term>Protéines nucléocapside (métabolisme)</term>
<term>Protéines virales (génétique)</term>
<term>Protéines virales (métabolisme)</term>
<term>Transfection</term>
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<term>NF-kappa B</term>
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<term>Facteur-3 de régulation d'interféron</term>
<term>Interféron bêta</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Open Reading Frames</term>
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<front><div type="abstract" xml:lang="en">The severe acute respiratory syndrome coronavirus (SARS-CoV) is highly pathogenic in humans, with a death rate near 10%. This high pathogenicity suggests that SARS-CoV has developed mechanisms to overcome the host innate immune response. It has now been determined that SARS-CoV open reading frame (ORF) 3b, ORF 6, and N proteins antagonize interferon, a key component of the innate immune response. All three proteins inhibit the expression of beta interferon (IFN-β), and further examination revealed that these SARS-CoV proteins inhibit a key protein necessary for the expression of IFN-β, IRF-3. N protein dramatically inhibited expression from an NF-KB-responsive promoter. All three proteins were able to inhibit expression from an interferon-stimulated response element (ISRE) promoter after infection with Sendai virus, while only ORF 3b and ORF 6 proteins were able to inhibit expression from the ISRE promoter after treatment with interferon. This indicates that N protein inhibits only the synthesis of interferon, while ORF 3b and ORF 6 proteins inhibit both interferon synthesis and signaling. ORF 6 protein, but not ORF 3b or N protein, inhibited nuclear translocation but not phosphorylation of STAT1. Thus, it appears that these three interferon antagonists of SARS-CoV inhibit the interferon response by different mechanisms.</div>
</front>
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<affiliations><list><country><li>États-Unis</li>
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<tree><country name="États-Unis"><noRegion><name sortKey="Kopecky Bromberg, Sarah A" sort="Kopecky Bromberg, Sarah A" uniqKey="Kopecky Bromberg S" first="Sarah A." last="Kopecky-Bromberg">Sarah A. Kopecky-Bromberg</name>
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<name sortKey="Baric, Ralph A" sort="Baric, Ralph A" uniqKey="Baric R" first="Ralph A." last="Baric">Ralph A. Baric</name>
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<name sortKey="Martinez Sobrido, Luis" sort="Martinez Sobrido, Luis" uniqKey="Martinez Sobrido L" first="Luis" last="Martinez-Sobrido">Luis Martinez-Sobrido</name>
<name sortKey="Palese, Peter" sort="Palese, Peter" uniqKey="Palese P" first="Peter" last="Palese">Peter Palese</name>
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