Virus-induced lncRNA-BTX allows viral replication by regulating intracellular translocation of DHX9 and ILF3 to induce innate escape
Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved..
The roles of long noncoding RNA (lncRNA) and RNA-binding proteins (RBPs) in antiviral innate response warrant further investigation. Here, we identify an lncRNA, termed lncRNA-BTX (between Tbk1 and Xpot), which is upregulated upon viral infection via an IRF3-type I interferon-independent pathway, promoting viral innate immune escape. Deletion of lncRNA-BTX in cells or mice significantly reduces viral load in vitro or in vivo, respectively. Mechanistically, lncRNA-BTX strengthens the interactions between DHX9 or ILF3 (two RBPs that have opposite functions in regulating the replication of RNA virus) and their respective partner, JMJD6 or ILF2, which regulates intracellular translocations of DHX9 and ILF3 from the nucleus to the cytoplasm. Put simply, lncRNA-BTX facilitates DHX9's return to the cytoplasm and retains ILF3 within the nucleus, promoting viral replication. This work unveils a strategy developed by the virus to bypass host innate immunity, thus providing a potential target for antiviral therapeutics.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:42 |
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| Enthalten in: |
Cell reports - 42(2023), 10 vom: 31. Okt., Seite 113262 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Cao, Yang [VerfasserIn] |
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| Links: |
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| Themen: |
Antiviral Agents |
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| Anmerkungen: |
Date Completed 06.11.2023 Date Revised 13.11.2023 published: Print Citation Status MEDLINE |
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| doi: |
10.1016/j.celrep.2023.113262 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM363571213 |
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| 100 | 1 | |a Cao, Yang |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Virus-induced lncRNA-BTX allows viral replication by regulating intracellular translocation of DHX9 and ILF3 to induce innate escape |
| 264 | 1 | |c 2023 | |
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| 500 | |a Date Completed 06.11.2023 | ||
| 500 | |a Date Revised 13.11.2023 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved. | ||
| 520 | |a The roles of long noncoding RNA (lncRNA) and RNA-binding proteins (RBPs) in antiviral innate response warrant further investigation. Here, we identify an lncRNA, termed lncRNA-BTX (between Tbk1 and Xpot), which is upregulated upon viral infection via an IRF3-type I interferon-independent pathway, promoting viral innate immune escape. Deletion of lncRNA-BTX in cells or mice significantly reduces viral load in vitro or in vivo, respectively. Mechanistically, lncRNA-BTX strengthens the interactions between DHX9 or ILF3 (two RBPs that have opposite functions in regulating the replication of RNA virus) and their respective partner, JMJD6 or ILF2, which regulates intracellular translocations of DHX9 and ILF3 from the nucleus to the cytoplasm. Put simply, lncRNA-BTX facilitates DHX9's return to the cytoplasm and retains ILF3 within the nucleus, promoting viral replication. This work unveils a strategy developed by the virus to bypass host innate immunity, thus providing a potential target for antiviral therapeutics | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a CP: Immunology | |
| 650 | 4 | |a DHX9 | |
| 650 | 4 | |a ILF3 | |
| 650 | 4 | |a RBPs | |
| 650 | 4 | |a immune escape | |
| 650 | 4 | |a lncRNA-BTX | |
| 650 | 4 | |a viral infection | |
| 650 | 7 | |a RNA, Long Noncoding |2 NLM | |
| 650 | 7 | |a Antiviral Agents |2 NLM | |
| 700 | 1 | |a Wu, Jiacheng |e verfasserin |4 aut | |
| 700 | 1 | |a Hu, Ye |e verfasserin |4 aut | |
| 700 | 1 | |a Chai, Yangyang |e verfasserin |4 aut | |
| 700 | 1 | |a Song, Jiaying |e verfasserin |4 aut | |
| 700 | 1 | |a Duan, Jiaqi |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Song |e verfasserin |4 aut | |
| 700 | 1 | |a Xu, Xiaoqing |e verfasserin |4 aut | |
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| 856 | 4 | 0 | |u http://dx.doi.org/10.1016/j.celrep.2023.113262 |3 Volltext |
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