lncRNAs regulate the innate immune response to viral infection
Identifieur interne : 001428 ( Main/Exploration ); précédent : 001427; suivant : 001429lncRNAs regulate the innate immune response to viral infection
Auteurs : Jing Ouyang [République populaire de Chine] ; Jiayue Hu [République populaire de Chine] ; Ji-Long Chen [République populaire de Chine]Source :
- Wiley Interdisciplinary Reviews: RNA [ 1757-7004 ] ; 2016-01.
Abstract
Long noncoding RNAs (lncRNAs) are extensively expressed in mammalian cells and play a crucial role as RNA regulators in various cellular processes. Increasing data reveal that they function in innate antiviral immunity through complex mechanisms. Thousands of lncRNAs are regulated by RNA virus or DNA virus infection. The significant differential expression of lncRNAs is induced by virus or host antiviral signaling mediated by interferons (IFNs) and tumor necrosis factor‐α. In turn, these lncRNAs modulate the host immune response including the pathogen recognition receptor (PRR)‐related signaling, the translocation and activation of transcription factors, the production of IFNs and cytokines, the IFN‐activated JAK‐STAT signaling and the transcription of antiviral IFN‐stimulated genes (ISGs). Using gain‐ or loss‐of‐function analysis, the effect of lncRNAs on viral replication has been investigated to elucidate the essential role of lncRNA in the host–virus interaction. lncRNAs have shown specifically elevated or decreased levels in patients with viral diseases, suggesting the possibility of clinical application as biomarkers. Here we review the current advances of viral infection‐associated host lncRNAs, their functional significance in different aspects of antiviral immune response, the specific mechanisms and unsolved issues. We also summarize the regulation of lncRNAs by viruses, PRR agonists and cytokines. In addition, virus‐encoded lncRNAs and their functional involvement in host–virus interaction are addressed. WIREs RNA 2016, 7:129–143. doi: 10.1002/wrna.1321 For further resources related to this article, please visit the WIREs website.
Url:
DOI: 10.1002/wrna.1321
Affiliations:
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Increasing data reveal that they function in innate antiviral immunity through complex mechanisms. Thousands of lncRNAs are regulated by RNA virus or DNA virus infection. The significant differential expression of lncRNAs is induced by virus or host antiviral signaling mediated by interferons (IFNs) and tumor necrosis factor‐α. In turn, these lncRNAs modulate the host immune response including the pathogen recognition receptor (PRR)‐related signaling, the translocation and activation of transcription factors, the production of IFNs and cytokines, the IFN‐activated JAK‐STAT signaling and the transcription of antiviral IFN‐stimulated genes (ISGs). Using gain‐ or loss‐of‐function analysis, the effect of lncRNAs on viral replication has been investigated to elucidate the essential role of lncRNA in the host–virus interaction. lncRNAs have shown specifically elevated or decreased levels in patients with viral diseases, suggesting the possibility of clinical application as biomarkers. Here we review the current advances of viral infection‐associated host lncRNAs, their functional significance in different aspects of antiviral immune response, the specific mechanisms and unsolved issues. We also summarize the regulation of lncRNAs by viruses, PRR agonists and cytokines. In addition, virus‐encoded lncRNAs and their functional involvement in host–virus interaction are addressed. WIREs RNA 2016, 7:129–143. doi: 10.1002/wrna.1321 For further resources related to this article, please visit the WIREs website.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country><region><li>Fujian</li></region><settlement><li>Fuzhou</li><li>Pékin</li></settlement></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Ouyang, Jing" sort="Ouyang, Jing" uniqKey="Ouyang J" first="Jing" last="Ouyang">Jing Ouyang</name></noRegion><name sortKey="Chen, Ji Ong" sort="Chen, Ji Ong" uniqKey="Chen J" first="Ji-Long" last="Chen">Ji-Long Chen</name><name sortKey="Chen, Ji Ong" sort="Chen, Ji Ong" uniqKey="Chen J" first="Ji-Long" last="Chen">Ji-Long Chen</name><name sortKey="Chen, Ji Ong" sort="Chen, Ji Ong" uniqKey="Chen J" first="Ji-Long" last="Chen">Ji-Long Chen</name><name sortKey="Hu, Jiayue" sort="Hu, Jiayue" uniqKey="Hu J" first="Jiayue" last="Hu">Jiayue Hu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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