About: Antagonism of dsRNA-Induced Innate Immune Pathways by NS4a and NS4b Accessory Proteins during MERS Coronavirus Infection

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About: Antagonism of dsRNA-Induced Innate Immune Pathways by NS4a and NS4b Accessory Proteins during MERS Coronavirus Infection Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Antagonism of dsRNA-Induced Innate Immune Pathways by NS4a and NS4b Accessory Proteins during MERS Coronavirus Infection
Creator	Perlman, Stanley Baric, Ralph Weiss, Susan Yount, Boyd Li, Yize Li, Y Goldstein, Stephen Ce, Citation Comar, Courtney Sa, Goldstein
Source	Medline; PMC
abstract	Middle East respiratory syndrome coronavirus (MERS-CoV) was first identified in 2012 as a novel etiological agent of severe respiratory disease in humans. As during infection by other viruses, host sensing of viral double-stranded RNA (dsRNA) induces several antiviral pathways. These include interferon (IFN), oligoadenylate synthetase (OAS)-RNase L, and protein kinase R (PKR). Coronaviruses, including MERS-CoV, potently suppress the activation of these pathways, inducing only modest host responses. Our study describes the functions of two accessory proteins unique to MERS-CoV and related viruses, NS4a and NS4b, during infection in human airway epithelium-derived A549 cells. NS4a has been previously characterized as a dsRNA binding protein, while NS4b is a 2′,5′-phosphodiesterase with structural and enzymatic similarity to NS2 encoded by mouse hepatitis virus (MHV). We found that deletion of NS4a results in increased interferon lambda (IFNL1) expression, as does mutation of either the catalytic site or nuclear localization sequence of NS4b. All of the mutant viruses we tested exhibited slight decreases in replication. We previously reported that, like MHV NS2, NS4b antagonizes OAS-RNase L, but suppression of IFN is a previously unidentified function for viral phosphodiesterases. Unexpectedly, deletion of NS4a does not result in robust activation of the PKR or OAS-RNase L pathways. Therefore, MERS-CoV likely encodes other proteins that contribute to suppression or evasion of these antiviral innate immune pathways that should be an important focus of future work. This study provides additional insight into the complex interactions between MERS-CoV and the host immune response.
has issue date	2019-03-26(xsd:dateTime)
bibo:doi	10.1128/mbio.00319-19
bibo:pmid	30914508
has license	cc-by
sha1sum (hex)	c850a9040414008da523d4ca13b8e61b36e0d98b
schema:url	https://doi.org/10.1128/mbio.00319-19
resource representing a document's title	Antagonism of dsRNA-Induced Innate Immune Pathways by NS4a and NS4b Accessory Proteins during MERS Coronavirus Infection
has PubMed Central identifier	PMC6437052
has PubMed identifier	30914508
schema:publication	mBio
resource representing a document's body	covid:c850a9040414008da523d4ca13b8e61b36e0d98b#body_text
is schema:about of	named entity 'NS4A' named entity 'encoded' named entity 'phosphodiesterase' named entity 'deletion' named entity 'similarity' named entity 'IFN' named entity 'dsRNA' named entity 'viruses' named entity 'Infection' named entity 'PATHWAYS' named entity 'ACCESSORY' named entity 'NS4A' named entity 'REPLICATION' named entity 'VIRAL' covid:arg/c850a9040414008da523d4ca13b8e61b36e0d98b named entity 'UNIQUE' named entity 'FUNCTION' named entity 'COMPLEX' named entity 'MODEST' named entity 'HOST IMMUNE RESPONSE' named entity 'DSRNA' named entity 'INCLUDING' named entity 'SENSING' named entity 'EXPRESSION' named entity 'SIMILARITY' named entity 'INTERACTIONS' named entity 'DOUBLE-STRANDED RNA' named entity 'ROBUST' named entity 'PATHWAYS' named entity 'MUTANT' named entity 'LIKELY' named entity 'CORONAVIRUSES' named entity 'FOCUS' named entity 'BUT' named entity 'RNASE L' named entity 'RESULTS' named entity 'RESPIRATORY DISEASE' named entity 'STRUCTURAL' named entity 'ENCODED' named entity 'HUMANS' named entity 'IMPORTANT' named entity 'INDUCED' named entity 'INFECTION' named entity 'HUMAN' named entity 'PREVIOUSLY' named entity 'NS2' named entity 'AIRWAY EPITHELIUM' named entity 'MERS CORONAVIRUS' named entity 'NS4B' named entity 'CORONAVIRUS INFECTION' named entity 'ANTAGONISM' named entity 'A549 CELLS' named entity 'INDUCING' named entity 'NS4B' named entity 'HOST' named entity 'ANTIVIRAL' named entity 'IDENTIFIED' named entity 'EITHER' named entity 'ADDITIONAL' named entity 'PROTEIN KINASE R' named entity 'DECREASES' named entity 'ACTIVATION' named entity 'ENZYMATIC' named entity 'FUNCTIONS' named entity 'INCREASED' named entity 'REPORTED' named entity 'NUCLEAR LOCALIZATION' named entity 'FOUND' named entity 'PROVIDES' named entity 'IFN' named entity 'SYNTHETASE' named entity 'VIRUSES'

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