About: The Long Noncoding RNA NEAT1 Exerts Antihantaviral Effects by Acting as Positive Feedback for RIG-I Signaling

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About: The Long Noncoding RNA NEAT1 Exerts Antihantaviral Effects by Acting as Positive Feedback for RIG-I Signaling 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	The Long Noncoding RNA NEAT1 Exerts Antihantaviral Effects by Acting as Positive Feedback for RIG-I Signaling
Creator	Zhang, Liang Cheng, Linfeng Zhang, Fanglin Zheng, Xuyang Yu, Lan Ye, Wei Ma, Hongwei Lei, Yingfeng Chen, Hesong Han, Peijun Xu, Zhikai Williams, Bryan Zhang, Y An Wu, Xing Lei, Xu
Source	Medline; PMC
abstract	Hantavirus infection, which causes zoonotic diseases with a high mortality rate in humans, has long been a global public health concern. Over the past decades, accumulating evidence suggests that long noncoding RNAs (lncRNAs) play key regulatory roles in innate immunity. However, the involvement of host lncRNAs in hantaviral control remains uncharacterized. In this study, we identified the lncRNA NEAT1 as a vital antiviral modulator. NEAT1 was dramatically upregulated after Hantaan virus (HTNV) infection, whereas its downregulation in vitro or in vivo delayed host innate immune responses and aggravated HTNV replication. Ectopic expression of NEAT1 enhanced beta interferon (IFN-β) production and suppressed HTNV infection. Further investigation suggested that NEAT1 served as positive feedback for RIG-I signaling. HTNV infection activated NEAT1 transcription through the RIG-I–IRF7 pathway, whereas NEAT1 removed the transcriptional inhibitory effects of the splicing factor proline- and glutamine-rich protein (SFPQ) by relocating SFPQ to paraspeckles, thus promoting the expression of RIG-I and DDX60. RIG-I and DDX60 had synergic effects on IFN production. Taken together, our findings demonstrate that NEAT1 modulates the innate immune response against HTNV infection, providing another layer of information about the role of lncRNAs in controlling viral infections. IMPORTANCE Hantaviruses have attracted worldwide attention as archetypal emerging pathogens. Recently, increasing evidence has highlighted long noncoding RNAs (lncRNAs) as key regulators of innate immunity; however, their roles in hantavirus infection remain unknown. In the present work, a new unexplored function of lncRNA NEAT1 in controlling HTNV replication was found. NEAT1 promoted interferon (IFN) responses by acting as positive feedback for RIG-I signaling. This lncRNA was induced by HTNV through the RIG-I–IRF7 pathway in a time- and dose-dependent manner and promoted HTNV-induced IFN production by facilitating RIG-I and DDX60 expression. Intriguingly, NEAT1 relocated SFPQ and formed paraspeckles after HTNV infection, which might reverse inhibitive effects of SFPQ on the transcription of RIG-I and DDX60. To the best of our knowledge, this is the first study to address the regulatory role of the lncRNA NEAT1 in host innate immunity after HTNV infection. In summary, our findings provide additional insights regarding the role of lncRNAs in controlling viral infections.
has issue date	2017-04-13(xsd:dateTime)
bibo:doi	10.1128/jvi.02250-16
bibo:pmid	28202761
has license	cc-by
sha1sum (hex)	d18636f47e3c7dd93da309d556ba464d964fd24f
schema:url	https://doi.org/10.1128/jvi.02250-16
resource representing a document's title	The Long Noncoding RNA NEAT1 Exerts Antihantaviral Effects by Acting as Positive Feedback for RIG-I Signaling
has PubMed Central identifier	PMC5391460
has PubMed identifier	28202761
schema:publication	J Virol
resource representing a document's body	covid:d18636f47e3c7dd93da309d556ba464d964fd24f#body_text
is schema:about of	named entity 'transcription' named entity 'family' named entity 'control' named entity 'This' named entity 'IFN' named entity 'activated' named entity 'innate' named entity 'play' named entity 'Virology' named entity 'vivo' named entity 'aggravated' named entity 'EXERTS' named entity 'EFFECTS' named entity 'WORLDWIDE' named entity 'JOURNAL ' named entity 'MORTALITY RATE' named entity '90%' named entity 'VOLUME' named entity 'UPREGULATED' named entity 'INNATE IMMUNITY' named entity 'IN VITRO' named entity 'ITS' named entity 'PROTEIN ' named entity 'ECTOPIC EXPRESSION' named entity 'PUBLIC HEALTH' named entity 'PATHOGENS' named entity 'ATTENTION' named entity 'REPLICATION' named entity 'RESPONSES' named entity 'SINGLE-STRANDED RNA' named entity 'NEGATIVE' named entity 'IDENTIFIED' named entity 'EVIDENCE' named entity 'CONCERN' named entity 'UNKNOWN' named entity 'NUCLEOCAPSID PROTEIN' named entity 'ADDITIONAL' named entity 'DDX60' named entity 'INSIGHTS' named entity 'STUDY' named entity 'PATHWAY' named entity 'PRESENT' named entity 'POSITIVE FEEDBACK' named entity 'REVERSE' named entity 'LONG' named entity 'ACCUMULATING' named entity 'ROLE' named entity 'HUMANS' named entity 'ANTIVIRAL' named entity 'ABOUT' named entity 'SMALL' named entity 'INVOLVEMENT' named entity 'OUR' named entity 'INDUCED' named entity 'REGULATORY ROLE' named entity 'DOSE-DEPENDENT' named entity 'AGGRAVATED' named entity 'PROMOTING' named entity 'VIROLOGY' named entity 'MEDIUM' named entity 'HANTAVIRUSES' named entity 'REMOVED' named entity 'SENSE' named entity 'HANTAVIRUS INFECTION' named entity 'FUNCTION' named entity 'ZOONOTIC DISEASES' named entity 'LARGE'

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