Middle East respiratory syndrome coronavirus-encoded ORF8b strongly antagonizes IFN-β promoter activation: its implication for vaccine design
Identifieur interne : 000463 ( Main/Exploration ); précédent : 000462; suivant : 000464Middle East respiratory syndrome coronavirus-encoded ORF8b strongly antagonizes IFN-β promoter activation: its implication for vaccine design
Auteurs : Jeong Yoon Lee ; Sojung Bae ; Jinjong MyoungSource :
- Journal of Microbiology (Seoul, Korea) [ 1225-8873 ] ; 2019.
Descripteurs français
- KwdFr :
- Arabie saoudite, Conception de médicament, Coronavirus du syndrome respiratoire du Moyen-Orient (génétique), Coronavirus du syndrome respiratoire du Moyen-Orient (métabolisme), Humains, Hélicase IFIH1 inductrice de l'interféron (génétique), Hélicase IFIH1 inductrice de l'interféron (métabolisme), Infections à coronavirus (génétique), Infections à coronavirus (métabolisme), Infections à coronavirus (virologie), Interactions hôte-pathogène, Interféron bêta (génétique), Interféron bêta (métabolisme), Protéine-58 à domaine DEAD (génétique), Protéine-58 à domaine DEAD (métabolisme), Régions promotrices (génétique), Vaccins antiviraux (génétique), Vaccins antiviraux (immunologie).
- MESH :
- génétique : Coronavirus du syndrome respiratoire du Moyen-Orient, Hélicase IFIH1 inductrice de l'interféron, Infections à coronavirus, Interféron bêta, Protéine-58 à domaine DEAD, Vaccins antiviraux.
- immunologie : Vaccins antiviraux.
- métabolisme : Coronavirus du syndrome respiratoire du Moyen-Orient, Hélicase IFIH1 inductrice de l'interféron, Infections à coronavirus, Interféron bêta, Protéine-58 à domaine DEAD.
- virologie : Infections à coronavirus.
- Arabie saoudite, Conception de médicament, Humains, Interactions hôte-pathogène, Régions promotrices (génétique).
- Wicri :
- geographic : Arabie saoudite.
English descriptors
- KwdEn :
- Coronavirus Infections (genetics), Coronavirus Infections (metabolism), Coronavirus Infections (virology), DEAD Box Protein 58 (genetics), DEAD Box Protein 58 (metabolism), Drug Design, Host-Pathogen Interactions, Humans, Interferon-Induced Helicase, IFIH1 (genetics), Interferon-Induced Helicase, IFIH1 (metabolism), Interferon-beta (genetics), Interferon-beta (metabolism), Middle East Respiratory Syndrome Coronavirus (genetics), Middle East Respiratory Syndrome Coronavirus (metabolism), Promoter Regions, Genetic, Saudi Arabia, Viral Vaccines (genetics), Viral Vaccines (immunology).
- MESH :
- chemical , genetics : DEAD Box Protein 58, Interferon-Induced Helicase, IFIH1, Interferon-beta, Viral Vaccines.
- chemical , immunology : Viral Vaccines.
- geographic : Saudi Arabia.
- genetics : Coronavirus Infections, Middle East Respiratory Syndrome Coronavirus.
- metabolism : Coronavirus Infections, DEAD Box Protein 58, Interferon-Induced Helicase, IFIH1, Interferon-beta, Middle East Respiratory Syndrome Coronavirus.
- virology : Coronavirus Infections.
- Drug Design, Host-Pathogen Interactions, Humans, Promoter Regions, Genetic.
Abstract
Middle East respiratory syndrome coronavirus (MERS-CoV) is a causative agent of severe-to-fatal pneumonia especially in patients with pre-existing conditions, such as smoking and chronic obstructive pulmonary disease (COPD). MERS-CoV transmission continues to be reported in the Saudi Arabian Peninsula since its discovery in 2012. However, it has rarely been epidemic outside the area except one large outbreak in South Korea in May 2015. The genome of the epidemic MERS-CoV isolated from a Korean patient revealed its homology to previously reported strains. MERS-CoV encodes 5 accessory proteins and generally, they do not participate in the genome transcription and replication but rather are involved in viral evasion of the host innate immune responses. Here we report that ORF8b, an accessory protein of MERS-CoV, strongly inhibits both MDA5- and RIG-I-mediated activation of interferon beta promoter activity while downstream signaling molecules were left largely unaffected. Of note, MDA5 protein levels were significantly down-regulated by ORF8b and co-expression of ORF4a and ORF4b. These novel findings will facilitate elucidation of mechanisms of virus-encoded evasion strategies, thus helping design rationale antiviral countermeasures against deadly MERS-CoV infection.
Url:
DOI: 10.1007/s12275-019-9272-7
PubMed: 31452044
PubMed Central: 7091237
Affiliations:
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Le document en format XML
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MERS-CoV transmission continues to be reported in the Saudi Arabian Peninsula since its discovery in 2012. However, it has rarely been epidemic outside the area except one large outbreak in South Korea in May 2015. The genome of the epidemic MERS-CoV isolated from a Korean patient revealed its homology to previously reported strains. MERS-CoV encodes 5 accessory proteins and generally, they do not participate in the genome transcription and replication but rather are involved in viral evasion of the host innate immune responses. Here we report that ORF8b, an accessory protein of MERS-CoV, strongly inhibits both MDA5- and RIG-I-mediated activation of interferon beta promoter activity while downstream signaling molecules were left largely unaffected. Of note, MDA5 protein levels were significantly down-regulated by ORF8b and co-expression of ORF4a and ORF4b. These novel findings will facilitate elucidation of mechanisms of virus-encoded evasion strategies, thus helping design rationale antiviral countermeasures against deadly MERS-CoV infection.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Abdul Rasool, S" uniqKey="Abdul Rasool S">S Abdul-Rasool</name></author><author><name sortKey="Fielding, Bc" uniqKey="Fielding B">BC Fielding</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Akira, S" uniqKey="Akira S">S Akira</name></author><author><name sortKey="Uematsu, S" uniqKey="Uematsu S">S Uematsu</name></author><author><name sortKey="Takeuchi, O" uniqKey="Takeuchi O">O Takeuchi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Alraddadi, Bm" uniqKey="Alraddadi B">BM Alraddadi</name></author><author><name sortKey="Watson, Jt" uniqKey="Watson J">JT Watson</name></author><author><name sortKey="Almarashi, A" 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uniqKey="Misra V">V Misra</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bradburne, Af" uniqKey="Bradburne A">AF Bradburne</name></author><author><name sortKey="Bynoe, Ml" uniqKey="Bynoe M">ML Bynoe</name></author><author><name sortKey="Tyrrell, Da" uniqKey="Tyrrell D">DA Tyrrell</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cardenas, Wb" uniqKey="Cardenas W">WB Cardenas</name></author><author><name sortKey="Loo, Ym" uniqKey="Loo Y">YM Loo</name></author><author><name sortKey="Gale, M" uniqKey="Gale M">M Gale</name></author><author><name sortKey="Hartman, Al" uniqKey="Hartman A">AL Hartman</name></author><author><name sortKey="Kimberlin, Cr" uniqKey="Kimberlin C">CR Kimberlin</name></author><author><name sortKey="Martinez Sobrido, L" uniqKey="Martinez Sobrido L">L Martinez-Sobrido</name></author><author><name sortKey="Saphire, Eo" uniqKey="Saphire E">EO Saphire</name></author><author><name sortKey="Basler, Cf" 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Szretter</name></author><author><name sortKey="Baker, Sc" uniqKey="Baker S">SC Baker</name></author><author><name sortKey="Barchet, W" uniqKey="Barchet W">W Barchet</name></author><author><name sortKey="Diamond, Ms" uniqKey="Diamond M">MS Diamond</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list></list><tree><noCountry><name sortKey="Bae, Sojung" sort="Bae, Sojung" uniqKey="Bae S" first="Sojung" last="Bae">Sojung Bae</name><name sortKey="Lee, Jeong Yoon" sort="Lee, Jeong Yoon" uniqKey="Lee J" first="Jeong Yoon" last="Lee">Jeong Yoon Lee</name><name sortKey="Myoung, Jinjong" sort="Myoung, Jinjong" uniqKey="Myoung J" first="Jinjong" last="Myoung">Jinjong Myoung</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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