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Transmissible Gastroenteritis Virus Papain-Like Protease 1 Antagonizes Production of Interferon-β through Its Deubiquitinase Activity

Identifieur interne : 000D47 ( Main/Exploration ); précédent : 000D46; suivant : 000D48

Transmissible Gastroenteritis Virus Papain-Like Protease 1 Antagonizes Production of Interferon-β through Its Deubiquitinase Activity

Auteurs : Xiaoliang Hu [République populaire de Chine] ; Jin Tian [République populaire de Chine] ; Hongtao Kang [République populaire de Chine] ; Dongchun Guo [République populaire de Chine] ; Jiasen Liu [République populaire de Chine] ; Dafei Liu [République populaire de Chine] ; Qian Jiang [République populaire de Chine] ; Zhijie Li [République populaire de Chine] ; Juanjuan Qu [République populaire de Chine] ; Liandong Qu [République populaire de Chine]

Source :

RBID : PMC:5672592

Descripteurs français

English descriptors

Abstract

Coronaviruses (CoVs), such as human coronavirus NL63 (HCoV-NL63), severe acute respiratory syndrome CoV (SARS-CoV), murine hepatitis virus (MHV), porcine epidemic diarrhea virus (PEDV), and Middle East Respiratory Syndrome Coronavirus (MERS-CoV), encode papain-like (PL) proteases that inhibit Sendai virus- (SeV-) induced interferon (IFN-β) production. Recently, the crystal structure of transmissible gastroenteritis virus (TGEV) PL1 has been solved, which was similar to that of SARS-CoV PL2pro, which may antagonize host innate immunity. However, very little is known about whether TGEV PL1 can antagonize host innate immune response. Here, we presented evidence that TGEV PL1 encoded by the replicase gene could suppress the IFN-β expression and inhibit the nuclear translocation of interferon regulatory factor 3 (IRF3). The ability to antagonize IFN-β production was dependent on the intact catalytic activity of PL1. Furthermore, TGEV PL1 exerted deubiquitinase (DUB) activity which strongly inhibited the retinoic acid-induced gene I- (RIG-1-) and stimulator of interferon gene- (STING-) dependent IFN expression. Our data collectively suggest that TGEV PL1 can inhibit the IFN-β expression and interfere with RIG-1- and STING-mediated signaling through a viral DUB activity. Our study has yielded strong evidence for the TGEV PL1 mechanisms that counteract the host innate immunity.


Url:
DOI: 10.1155/2017/7089091
PubMed: 29201911
PubMed Central: 5672592


Affiliations:


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Le document en format XML

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<term>Host-Pathogen Interactions (genetics)</term>
<term>Humans</term>
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<term>Animaux</term>
<term>Cellules HEK293</term>
<term>Enzymes de désubiquitinylation (génétique)</term>
<term>Facteur-3 de régulation d'interféron (génétique)</term>
<term>Humains</term>
<term>Immunité innée (génétique)</term>
<term>Interactions hôte-pathogène (génétique)</term>
<term>Interféron bêta (biosynthèse)</term>
<term>Interféron bêta (génétique)</term>
<term>Papaïne ()</term>
<term>Papaïne (génétique)</term>
<term>Papaïne (immunologie)</term>
<term>Protéine-58 à domaine DEAD (génétique)</term>
<term>Protéines membranaires (génétique)</term>
<term>RNA replicase (génétique)</term>
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<term>Virus de la gastroentérite transmissible ()</term>
<term>Virus de la gastroentérite transmissible (génétique)</term>
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<term>Papain</term>
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<term>Interferon-beta</term>
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<term>RNA Replicase</term>
<term>Ubiquitin</term>
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<term>Interféron bêta</term>
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<term>Transmissible gastroenteritis virus</term>
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<term>Host-Pathogen Interactions</term>
<term>Immunity, Innate</term>
<term>Transmissible gastroenteritis virus</term>
</keywords>
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<term>Enzymes de désubiquitinylation</term>
<term>Facteur-3 de régulation d'interféron</term>
<term>Immunité innée</term>
<term>Interactions hôte-pathogène</term>
<term>Interféron bêta</term>
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<term>Protéine-58 à domaine DEAD</term>
<term>Protéines membranaires</term>
<term>RNA replicase</term>
<term>Ubiquitine</term>
<term>Virus de la gastroentérite transmissible</term>
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<div type="abstract" xml:lang="en">
<p>Coronaviruses (CoVs), such as human coronavirus NL63 (HCoV-NL63), severe acute respiratory syndrome CoV (SARS-CoV), murine hepatitis virus (MHV), porcine epidemic diarrhea virus (PEDV), and Middle East Respiratory Syndrome Coronavirus (MERS-CoV), encode papain-like (PL) proteases that inhibit Sendai virus- (SeV-) induced interferon (IFN-
<italic>β</italic>
) production. Recently, the crystal structure of transmissible gastroenteritis virus (TGEV) PL1 has been solved, which was similar to that of SARS-CoV PL2
<sup>pro</sup>
, which may antagonize host innate immunity. However, very little is known about whether TGEV PL1 can antagonize host innate immune response. Here, we presented evidence that TGEV PL1 encoded by the replicase gene could suppress the IFN-
<italic>β</italic>
expression and inhibit the nuclear translocation of interferon regulatory factor 3 (IRF3). The ability to antagonize IFN-
<italic>β</italic>
production was dependent on the intact catalytic activity of PL1. Furthermore, TGEV PL1 exerted deubiquitinase (DUB) activity which strongly inhibited the retinoic acid-induced gene I- (RIG-1-) and stimulator of interferon gene- (STING-) dependent IFN expression. Our data collectively suggest that TGEV PL1 can inhibit the IFN-
<italic>β</italic>
expression and interfere with RIG-1- and STING-mediated signaling through a viral DUB activity. Our study has yielded strong evidence for the TGEV PL1 mechanisms that counteract the host innate immunity.</p>
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</TEI>
<affiliations>
<list>
<country>
<li>République populaire de Chine</li>
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<country name="République populaire de Chine">
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</tree>
</affiliations>
</record>

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