About: The Strategy of Picornavirus Evading Host Antiviral Responses: Non-structural Proteins Suppress the Production of IFNs

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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	The Strategy of Picornavirus Evading Host Antiviral Responses: Non-structural Proteins Suppress the Production of IFNs
Creator	Liu, Yongsheng Ma, Lina Wang, Penghua Stipkovits, Laszlo Li, Xuerui Wang, Yining Szathmary, Susan Cn, Lixuerui@caas
Source	PMC
abstract	Viral infections trigger the innate immune system to produce interferons (IFNs), which play important role in host antiviral responses. Co-evolution of viruses with their hosts has favored development of various strategies to evade the effects of IFNs, enabling viruses to survive inside host cells. One such strategy involves inhibition of IFN signaling pathways by non-structural proteins. In this review, we provide a brief overview of host signaling pathways inducing IFN production and their suppression by picornavirus non-structural proteins. Using this strategy, picornaviruses can evade the host immune response and replicate inside host cells.
has issue date	2018-12-11(xsd:dateTime)
bibo:doi	10.3389/fmicb.2018.02943
bibo:pmid	30619109
has license	cc-by
sha1sum (hex)	f72c004e5517cc9cf54b882cb1b817f21cce515c
schema:url	https://doi.org/10.3389/fmicb.2018.02943
resource representing a document's title	The Strategy of Picornavirus Evading Host Antiviral Responses: Non-structural Proteins Suppress the Production of IFNs
has PubMed Central identifier	PMC6297142
has PubMed identifier	30619109
schema:publication	Front Microbiol
resource representing a document's body	covid:f72c004e5517cc9cf54b882cb1b817f21cce515c#body_text
is schema:about of	named entity 'host cells' named entity 'IFN' named entity 'IFN' named entity 'Viral infections' named entity 'innate immune' named entity 'Picornavirus' named entity 'IFNGR1' named entity 'viral capsids' named entity 'phosphorylation' named entity 'epithelial cells' named entity 'RNA genome' named entity 'immune response' named entity 'type I IFNs' named entity 'JAK1' named entity 'coxsackievirus' named entity 'light-chain' named entity 'Hepatitis A virus' named entity 'cell type' named entity 'signaling pathways' named entity 'ISGs' named entity 'FMDV' named entity 'mRNA translation' named entity 'Papon' named entity 'protein kinase' named entity 'type I IFN' named entity 'RNA helicases' named entity 'RNA replication' named entity 'Beck' named entity 'MAVS' named entity 'structural proteins' named entity 'IFN-γ' named entity 'EV71' named entity 'type I IFN' named entity 'IFN' named entity 'STAT1' named entity 'Enterovirus 71' named entity 'viral pathogens' named entity 'picornavirus' named entity 'phosphorylation' named entity 'RIG-I' named entity 'homologous sequence' named entity 'eukaryotic translation initiation factor' named entity 'poliovirus' named entity 'enteroviruses' named entity 'IFN' named entity 'IRF7' named entity 'kDa' named entity 'receptor' named entity 'activated B cells' named entity 'PRRs' named entity 'RIG-I' named entity 'protease' named entity 'ISGs' named entity 'adaptor proteins' named entity 'IFNAR1' named entity 'antiviral' named entity 'type I IFNs' named entity 'TAK1' named entity 'transcription factors' named entity 'picornaviruses' named entity 'IFN' named entity 'Encephalomyocarditis virus' named entity 'signaling pathways' named entity 'miR' named entity 'ORF' named entity 'phosphorylation' named entity 'receptor' named entity 'specific sites' named entity 'antiviral' named entity 'leukocytes' named entity 'picornaviruses' named entity 'dimerization' named entity 'EV71' named entity 'IRF3'

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