Antagonism of dsRNA-Induced Innate Immune Pathways by NS4a and NS4b Accessory Proteins during MERS Coronavirus Infection
Identifieur interne : 000697 ( Main/Exploration ); précédent : 000696; suivant : 000698Antagonism of dsRNA-Induced Innate Immune Pathways by NS4a and NS4b Accessory Proteins during MERS Coronavirus Infection
Auteurs : Courtney E. Comar [États-Unis] ; Stephen A. Goldstein [États-Unis] ; Yize Li [États-Unis] ; Boyd Yount [États-Unis] ; Ralph S. Baric [États-Unis] ; Susan R. Weiss [États-Unis]Source :
- mBio [ 2150-7511 ] ; 2019.
Descripteurs français
- KwdFr :
- ARN double brin (immunologie), ARN viral (immunologie), Cellules A549, Cellules épithéliales (virologie), Coronavirus du syndrome respiratoire du Moyen-Orient (immunologie), Coronavirus du syndrome respiratoire du Moyen-Orient (pathogénicité), Délétion de gène, Humains, Immunité innée, Interactions hôte-pathogène, Mutation, Protéines virales non structurales (génétique), Protéines virales non structurales (métabolisme), Protéines virales régulatrices ou accessoires (génétique), Protéines virales régulatrices ou accessoires (métabolisme), Réplication virale, Échappement immunitaire.
- MESH :
- génétique : Protéines virales non structurales, Protéines virales régulatrices ou accessoires.
- immunologie : ARN double brin, ARN viral, Coronavirus du syndrome respiratoire du Moyen-Orient.
- métabolisme : Protéines virales non structurales, Protéines virales régulatrices ou accessoires.
- pathogénicité : Coronavirus du syndrome respiratoire du Moyen-Orient.
- virologie : Cellules épithéliales.
- Cellules A549, Délétion de gène, Humains, Immunité innée, Interactions hôte-pathogène, Mutation, Réplication virale, Échappement immunitaire.
English descriptors
- KwdEn :
- A549 Cells, Epithelial Cells (virology), Gene Deletion, Host-Pathogen Interactions, Humans, Immune Evasion, Immunity, Innate, Middle East Respiratory Syndrome Coronavirus (immunology), Middle East Respiratory Syndrome Coronavirus (pathogenicity), Mutation, RNA, Double-Stranded (immunology), RNA, Viral (immunology), Viral Nonstructural Proteins (genetics), Viral Nonstructural Proteins (metabolism), Viral Regulatory and Accessory Proteins (genetics), Viral Regulatory and Accessory Proteins (metabolism), Virus Replication.
- MESH :
- chemical , genetics : Viral Nonstructural Proteins, Viral Regulatory and Accessory Proteins.
- chemical , immunology : RNA, Double-Stranded, RNA, Viral.
- immunology : Middle East Respiratory Syndrome Coronavirus.
- chemical , metabolism : Viral Nonstructural Proteins, Viral Regulatory and Accessory Proteins.
- pathogenicity : Middle East Respiratory Syndrome Coronavirus.
- virology : Epithelial Cells.
- A549 Cells, Gene Deletion, Host-Pathogen Interactions, Humans, Immune Evasion, Immunity, Innate, Mutation, Virus Replication.
Abstract
Middle East respiratory syndrome coronavirus (MERS-CoV) is the second novel zoonotic coronavirus to emerge in the 21st century and cause outbreaks of severe respiratory disease. More than 2,200 cases and 800 deaths have been reported to date, yet there are no licensed vaccines or treatments. Coronaviruses encode unique accessory proteins that are not required for replication but most likely play roles in immune antagonism and/or pathogenesis. Our study describes the functions of MERS-CoV accessory proteins NS4a and NS4b during infection of a human airway-derived cell line. Loss of these accessory proteins during MERS-CoV infection leads to host antiviral activation and modestly attenuates replication. In the case of both NS4a and NS4b, we have identified roles during infection not previously described, yet the lack of robust activation suggests much remains to be learned about the interactions between MERS-CoV and the infected host.
Url:
DOI: 10.1128/mBio.00319-19
PubMed: 30914508
PubMed Central: 6437052
Affiliations:
- États-Unis
- Caroline du Nord, Pennsylvanie
- Chapel Hill (Caroline du Nord)
- Université de Caroline du Nord à Chapel Hill
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Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>Middle East respiratory syndrome coronavirus (MERS-CoV) is the second novel zoonotic coronavirus to emerge in the 21st century and cause outbreaks of severe respiratory disease. More than 2,200 cases and 800 deaths have been reported to date, yet there are no licensed vaccines or treatments. Coronaviruses encode unique accessory proteins that are not required for replication but most likely play roles in immune antagonism and/or pathogenesis. Our study describes the functions of MERS-CoV accessory proteins NS4a and NS4b during infection of a human airway-derived cell line. Loss of these accessory proteins during MERS-CoV infection leads to host antiviral activation and modestly attenuates replication. In the case of both NS4a and NS4b, we have identified roles during infection not previously described, yet the lack of robust activation suggests much remains to be learned about the interactions between MERS-CoV and the infected host.</p>
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