About: Porcine transmissible gastroenteritis virus inhibits NF-κB activity via nonstructural protein 3 to evade host immune system

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About: Porcine transmissible gastroenteritis virus inhibits NF-κB activity via nonstructural protein 3 to evade host immune system Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Porcine transmissible gastroenteritis virus inhibits NF-κB activity via nonstructural protein 3 to evade host immune system
Creator	Wang, Li Sun, Yu Cui, Wen Guo, Tiantian Hao, Zhenye Jiang, Yanping Li, Yijing Qiao, Xinyuan Sun, Aoying Sun, Li Tang, Lijie Wang, Yanan Xia, Tian Xu, Yigang Zhang, Sijia
Source	Medline; PMC
abstract	BACKGROUND: Transmissible gastroenteritis virus (TGEV), a member of the family Coronaviridae, causes lethal watery diarrhea in piglets. Previous studies have revealed that the coronaviruses develop various strategies to evade the host innate immunity through the inhibition of nuclear factor kappa B (NF-κB) signaling pathway. However, the ability of TGEV to inhibit the host innate immune response by modulating the NF-κB signaling pathway is not clear. METHODS: In this study, a dual luciferase reporter assay was used to confirm the inhibition of NF-κB by TGEV infection and to identify the major viral proteins involved in the inhibition of NF-κB signaling. Real-time quantitative PCR was used to quantify the mRNA expression of inflammatory factors. The deubiquitination of Nsp3 domains and its effect on IκBα and p65 were analyzed by western blotting. The ubiquitination level of IκBα was analyzed by immunoprecipitation. RESULTS: In ST and IPEC-J2 cells, TGEV exhibited a dose-dependent inhibition of NF-κB activity. Individual TGEV protein screening revealed the high potential of non-structural protein 3 (Nsp3) to inhibit NF-κB signaling, and leading to the downregulation of the NF-κB-induced cytokine production. We demonstrated that the inhibitory effect of Nsp3 was mainly mediated through the suppression of IκBα degradation as well as the inhibition of p65 phosphorylation and nuclear translocation. Furthermore, the amino acid residues at positions 590–1,215 in Nsp3 were demonstrated to inhibit the degradation of IκBα by inhibiting the IκBα ubiquitination. CONCLUSION: TGEV infection can inhibit the activation of the NF-κB signaling pathway, which is mainly mediated by Nsp3 through the canonical pathway. The amino acid residues at positions 590–1,215 in Nsp3 compose the critical domain that mediates NF-κB inhibition. We speculate that this inhibitory effect is likely to be related to the structure of PLP2 with deubiquitinating enzyme activity of the amino acid residues at positions 590–1,215 in Nsp3. Our study provides a better understanding of the TGEV-mediated innate immune modulation and lays the basis for studies on the pathogenesis of coronavirus.
has issue date	2019-08-05(xsd:dateTime)
bibo:doi	10.1186/s12985-019-1206-9
bibo:pmid	31382996
has license	cc-by
sha1sum (hex)	62a510dfb56136e79dbfcb424fae13b47c476635
schema:url	https://doi.org/10.1186/s12985-019-1206-9
resource representing a document's title	Porcine transmissible gastroenteritis virus inhibits NF-κB activity via nonstructural protein 3 to evade host immune system
has PubMed Central identifier	PMC6683377
has PubMed identifier	31382996
schema:publication	Virol J
resource representing a document's body	covid:62a510dfb56136e79dbfcb424fae13b47c476635#body_text
is schema:about of	named entity 'BAB' named entity 'gastroenteritis' named entity 'PREVIOUS' named entity 'HOST' named entity 'REVEALED' named entity 'CAUSES' named entity 'FAMILY CORONAVIRIDAE' covid:arg/62a510dfb56136e79dbfcb424fae13b47c476635 named entity 'ACTIVITY' named entity 'IMMUNE SYSTEM' named entity 'VARIOUS' named entity 'MODULATING' named entity 'NUCLEAR FACTOR KAPPA B' named entity 'INNATE IMMUNITY' named entity 'TO INHIBIT' named entity 'WATERY DIARRHEA' named entity 'TRANSMISSIBLE GASTROENTERITIS VIRUS' named entity 'STUDIES' named entity 'CLEAR' named entity 'BACKGROUND' named entity 'CORONAVIRUSES' named entity 'SIGNALING PATHWAY' named entity 'MEMBER OF' named entity 'HAVE' named entity 'BAB' named entity 'INNATE IMMUNE RESPONSE' named entity 'STRATEGIES' named entity 'PORCINE TRANSMISSIBLE GASTROENTERITIS VIRUS' named entity 'PROTEIN 3' named entity 'HOST' named entity 'ABILITY' named entity 'INHIBITION' named entity 'LETHAL' named entity 'However' named entity 'immunity' named entity 'p65' named entity 'immune response' named entity 'canonical pathway' named entity 'piglets' named entity 'TGEV' named entity 'innate immune response' named entity 'signaling pathway' named entity 'nonstructural protein 3' named entity 'NF-κB' named entity 'NF-κB' named entity 'IκBα' named entity 'amino acid residues' named entity 'SARS' named entity 'PLP2' named entity 'phosphorylation' named entity 'positively correlated' named entity 'intracellular' named entity 'RelA' named entity 'NF-κB' named entity 'NDV' named entity 'nucleus' named entity 'TGEV' named entity 'TGEV' named entity 'NF-κB' named entity 'transcription of genes' named entity 'enteric disease' named entity 'NF-κB' named entity 'plasmids' named entity 'infection' named entity 'nuclear translocation' named entity 'Nsp3' named entity 'IκBα'

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