About: Regulation of the ER Stress Response by the Ion Channel Activity of the Infectious Bronchitis Coronavirus Envelope Protein Modulates Virion Release, Apoptosis, Viral Fitness, and Pathogenesis

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About: Regulation of the ER Stress Response by the Ion Channel Activity of the Infectious Bronchitis Coronavirus Envelope Protein Modulates Virion Release, Apoptosis, Viral Fitness, and Pathogenesis 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	Regulation of the ER Stress Response by the Ion Channel Activity of the Infectious Bronchitis Coronavirus Envelope Protein Modulates Virion Release, Apoptosis, Viral Fitness, and Pathogenesis
Creator	Chen, Rui Huang, Kai Zheng, Chunfu Dai, Guo Li, Shumin Yuan, Lixia Aguilella, Vicente Fung, Fung, To Liu, Ding To, Sing
Source	Medline; PMC
abstract	Coronavirus (CoV) envelope (E) protein is a small structural protein critical for virion morphogenesis and release. The recently characterized E protein ion channel activity (EIC) has also been implicated in modulating viral pathogenesis. In this study, we used infectious bronchitis coronavirus (IBV) as a model to study EIC. Two recombinant IBVs (rIBVs) harboring EIC-inactivating mutations – rT16A and rA26F – were serially passaged, and several compensatory mutations were identified in the transmembrane domain (TMD). Two rIBVs harboring these putative EIC-reverting mutations – rT16A/A26V and rA26F/F14N – were recovered. Compared with the parental rIBV-p65 control, all four EIC mutants exhibited comparable levels of intracellular RNA synthesis, structural protein production, and virion assembly. Our results showed that the IBV EIC contributed to the induction of ER stress response, as up-regulation of ER stress-related genes was markedly reduced in cells infected with the EIC-defective mutants. EIC-defective mutants also formed smaller plaques, released significantly less infectious virions into the culture supernatant, and had lower levels of viral fitness in cell culture. Significantly, all these defective phenotypes were restored in cells infected with the putative EIC revertants. EIC mutations were also implicated in regulating IBV-induced apoptosis, induction of pro-inflammatory cytokines, and viral pathogenicity in vivo. Taken together, this study highlights the importance of CoV EIC in modulating virion release and various aspects of CoV – host interaction.
has issue date	2020-01-24(xsd:dateTime)
bibo:doi	10.3389/fmicb.2019.03022
bibo:pmid	32038520
has license	cc-by
sha1sum (hex)	b7b122d6d4cc409f7a22bec63936640b4cd0f334
schema:url	https://doi.org/10.3389/fmicb.2019.03022
resource representing a document's title	Regulation of the ER Stress Response by the Ion Channel Activity of the Infectious Bronchitis Coronavirus Envelope Protein Modulates Virion Release, Apoptosis, Viral Fitness, and Pathogenesis
has PubMed Central identifier	PMC6992538
has PubMed identifier	32038520
schema:publication	Front Microbiol
resource representing a document's body	covid:b7b122d6d4cc409f7a22bec63936640b4cd0f334#body_text
is schema:about of	named entity 'virions' named entity 'EIC' named entity 'control' named entity 'assembly' named entity 'interaction' named entity 'TMD' named entity 'Two' covid:arg/b7b122d6d4cc409f7a22bec63936640b4cd0f334 named entity 'transmembrane domain' named entity 'stress response' named entity 'envelope' named entity 'mutants' named entity 'RNA' named entity 'ion' named entity 'ER stress' named entity 'IBVs' named entity 'IBV' named entity 'structural protein' named entity 'ER stress' named entity 'pathogenicity' named entity 'RNA synthesis' named entity 'phenotypes' named entity 'restored' named entity 'protein' named entity 'virion' named entity 'qPCR' named entity 'hpi' named entity 'IL-6' named entity 'DMSO' named entity 'virus' named entity 'virion' named entity '0.01' named entity 'primer' named entity 'mRNA' named entity 'hpi' named entity 'IBV' named entity 'point mutations' named entity 'lung' named entity 'MERS-CoV' named entity 'chicken' named entity 'centrifugation' named entity 'virion' named entity 'chicken' named entity 'pro-inflammatory cytokines' named entity 'IBV' named entity 'IL-6' named entity 'TNF' named entity 'homologous' named entity 'VSV' named entity 'Invitrogen' named entity 'protein' named entity 'effector' named entity 'viral pathogenesis' named entity 'ATCC' named entity 'Beta-actin' named entity 'fluorescent' named entity 'Significance levels' named entity 'IBV' named entity 'caspase 3' named entity 'subgenomic' named entity 'IBV' named entity 'inflammasome' named entity 'protein' named entity 'GRP94' named entity 'ion' named entity 'formaldehyde' named entity 'SARS-CoV' named entity 'infection' named entity 'genome' named entity 'mRNA' named entity 'RNA extraction'

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