PLP2, a potent deubiquitinase from murine hepatitis virus, strongly inhibits cellular type I interferon production.
Identifieur interne : 003066 ( Main/Exploration ); précédent : 003065; suivant : 003067PLP2, a potent deubiquitinase from murine hepatitis virus, strongly inhibits cellular type I interferon production.
Auteurs : Dahai Zheng [République populaire de Chine] ; Gang Chen ; Beichu Guo ; Genhong Cheng ; Hong TangSource :
- Cell research [ 1748-7838 ] ; 2008.
Descripteurs français
- KwdFr :
- Animaux, Cellules HeLa, Cellules cultivées, Coronavirus (génétique), Coronavirus (métabolisme), Facteur-3 de régulation d'interféron (métabolisme), Humains, Interféron alpha (génétique), Interféron alpha (métabolisme), Interféron bêta (génétique), Interféron bêta (métabolisme), Interféron de type I (génétique), Interféron de type I (métabolisme), Lignée cellulaire, Papaïne (métabolisme), Protéines virales non structurales (génétique), Protéines virales non structurales (métabolisme), Souris, Syndrome respiratoire aigu sévère (génétique), Syndrome respiratoire aigu sévère (métabolisme), Syndrome respiratoire aigu sévère (virologie), Ubiquitinylation, Virus de l'hépatite murine (génétique), Virus de l'hépatite murine (métabolisme), Virus du SRAS (génétique), Virus du SRAS (métabolisme).
- MESH :
- génétique : Coronavirus, Interféron alpha, Interféron bêta, Interféron de type I, Protéines virales non structurales, Syndrome respiratoire aigu sévère, Virus de l'hépatite murine, Virus du SRAS.
- métabolisme : Coronavirus, Facteur-3 de régulation d'interféron, Interféron alpha, Interféron bêta, Interféron de type I, Papaïne, Protéines virales non structurales, Syndrome respiratoire aigu sévère, Virus de l'hépatite murine, Virus du SRAS.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Cellules HeLa, Cellules cultivées, Humains, Lignée cellulaire, Souris, Ubiquitinylation.
English descriptors
- KwdEn :
- Animals, Cell Line, Cells, Cultured, Coronavirus (genetics), Coronavirus (metabolism), HeLa Cells, Humans, Interferon Regulatory Factor-3 (metabolism), Interferon Type I (genetics), Interferon Type I (metabolism), Interferon-alpha (genetics), Interferon-alpha (metabolism), Interferon-beta (genetics), Interferon-beta (metabolism), Mice, Murine hepatitis virus (genetics), Murine hepatitis virus (metabolism), Papain (metabolism), SARS Virus (genetics), SARS Virus (metabolism), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (virology), Ubiquitination, Viral Nonstructural Proteins (genetics), Viral Nonstructural Proteins (metabolism).
- MESH :
- chemical , genetics : Interferon Type I, Interferon-alpha, Interferon-beta, Viral Nonstructural Proteins.
- chemical , metabolism : Interferon Regulatory Factor-3, Interferon Type I, Interferon-alpha, Interferon-beta, Papain, Viral Nonstructural Proteins.
- genetics : Coronavirus, Murine hepatitis virus, SARS Virus, Severe Acute Respiratory Syndrome.
- metabolism : Coronavirus, Murine hepatitis virus, SARS Virus, Severe Acute Respiratory Syndrome.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Cell Line, Cells, Cultured, HeLa Cells, Humans, Mice, Ubiquitination.
Abstract
Infections by coronaviruses such as severe acute respiratory syndrome (SARS) coronavirus (SCoV) and mouse hepatitis virus A59 (MHV-A59) result in very little type I interferon (IFN) production by host cells, which is potentially responsible for the rapid viral growth and severe immunopathology associated with SARS. However, the molecular mechanisms for the low IFN production in cells infected with coronaviruses remain unclear. Here, we provide evidence that Papain-like protease domain 2 (PLP2), a catalytic domain of the nonstructural protein 3 (nsp3) of MHV-A59, can bind to IRF3, cause its deubiquitination and prevent its nuclear translocation. As a consequence, co-expression of PLP2 strongly inhibits CARDIF-, TBK1- and IRF3-mediated IFNbeta reporter activities. In addition, we show that wild-type PLP2 but not the mutant PLP2 lacking the deubiquitinase (DUB) activity can reduce IFN induction and promote viral growth in cells infected with VSV. Thus, our study uncovered a viral DUB which coronaviruses may use to escape from the host innate antiviral responses.
DOI: 10.1038/cr.2008.294
PubMed: 18957937
Affiliations:
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Le document en format XML
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Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Cells, Cultured</term><term>HeLa Cells</term><term>Humans</term><term>Mice</term><term>Ubiquitination</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules HeLa</term><term>Cellules cultivées</term><term>Humains</term><term>Lignée cellulaire</term><term>Souris</term><term>Ubiquitinylation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Infections by coronaviruses such as severe acute respiratory syndrome (SARS) coronavirus (SCoV) and mouse hepatitis virus A59 (MHV-A59) result in very little type I interferon (IFN) production by host cells, which is potentially responsible for the rapid viral growth and severe immunopathology associated with SARS. However, the molecular mechanisms for the low IFN production in cells infected with coronaviruses remain unclear. Here, we provide evidence that Papain-like protease domain 2 (PLP2), a catalytic domain of the nonstructural protein 3 (nsp3) of MHV-A59, can bind to IRF3, cause its deubiquitination and prevent its nuclear translocation. As a consequence, co-expression of PLP2 strongly inhibits CARDIF-, TBK1- and IRF3-mediated IFNbeta reporter activities. In addition, we show that wild-type PLP2 but not the mutant PLP2 lacking the deubiquitinase (DUB) activity can reduce IFN induction and promote viral growth in cells infected with VSV. Thus, our study uncovered a viral DUB which coronaviruses may use to escape from the host innate antiviral responses.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country><settlement><li>Pékin</li></settlement></list><tree><noCountry><name sortKey="Chen, Gang" sort="Chen, Gang" uniqKey="Chen G" first="Gang" last="Chen">Gang Chen</name><name sortKey="Cheng, Genhong" sort="Cheng, Genhong" uniqKey="Cheng G" first="Genhong" last="Cheng">Genhong Cheng</name><name sortKey="Guo, Beichu" sort="Guo, Beichu" uniqKey="Guo B" first="Beichu" last="Guo">Beichu Guo</name><name sortKey="Tang, Hong" sort="Tang, Hong" uniqKey="Tang H" first="Hong" last="Tang">Hong Tang</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Zheng, Dahai" sort="Zheng, Dahai" uniqKey="Zheng D" first="Dahai" last="Zheng">Dahai Zheng</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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