Influenza Virus Exploits an Interferon-Independent lncRNA to Preserve Viral RNA Synthesis through Stabilizing Viral RNA Polymerase PB1.
IPAN
PB1
RdRp
degradation
hijack
influenza A virus
interferon
lncRNA
viral replication
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
11 06 2019
11 06 2019
Historique:
received:
30
08
2018
revised:
08
12
2018
accepted:
09
05
2019
entrez:
13
6
2019
pubmed:
13
6
2019
medline:
4
8
2020
Statut:
ppublish
Résumé
Long noncoding RNAs (lncRNAs) participate in host antiviral defense by modulating immune responses. However, it remains largely unexplored how viruses exploit interferon (IFN)-independent host lncRNAs to facilitate viral replication. Here, we have identified a group of human lncRNAs that modulate influenza A virus (IAV) replication in a loss-of-function screen and found that an IFN-independent lncRNA, called IPAN, is hijacked by IAV to assist IAV replication. IPAN is specifically induced by IAV infection independently of IFN and associates with and stabilizes viral RNA-dependent RNA polymerase PB1, enabling efficient viral RNA synthesis. Silencing IPAN results in PB1 degradation and severely impairs viral infection. Therefore, our data unveil an important role of host lncRNAs in promoting viral replication by modulating viral protein stability. Our findings may open avenues to the development of antiviral therapeutics.
Identifiants
pubmed: 31189112
pii: S2211-1247(19)30656-4
doi: 10.1016/j.celrep.2019.05.036
pii:
doi:
Substances chimiques
RNA, Long Noncoding
0
Viral Proteins
0
RNA-Dependent RNA Polymerase
EC 2.7.7.48
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
3295-3304.e4Informations de copyright
Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.