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Cell Rep. 2019 Jun 11;27(11):3295-3304.e4. doi: 10.1016/j.celrep.2019.05.036.
Influenza Virus Exploits an Interferon-Independent lncRNA to Preserve Viral RNA Synthesis through Stabilizing Viral RNA Polymerase PB1.
Wang J1, Zhang Y1, Li Q1, Zhao J1, Yi D1, Ding J1, Zhao F2, Hu S2, Zhou J1, Deng T2, Li X3, Guo F2, Liang C4, Cen S5.
Author information
Abstract
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.
Copyright ? 2019 The Author(s). Published by Elsevier Inc. All rights reserved.
KEYWORDS:
IPAN; PB1; RdRp; degradation; hijack; influenza A virus; interferon; lncRNA; viral replication
PMID: 31189112 DOI: 10.1016/j.celrep.2019.05.036
Influenza Virus Exploits an Interferon-Independent lncRNA to Preserve Viral RNA Synthesis through Stabilizing Viral RNA Polymerase PB1.
Wang J1, Zhang Y1, Li Q1, Zhao J1, Yi D1, Ding J1, Zhao F2, Hu S2, Zhou J1, Deng T2, Li X3, Guo F2, Liang C4, Cen S5.
Author information
Abstract
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.
Copyright ? 2019 The Author(s). Published by Elsevier Inc. All rights reserved.
KEYWORDS:
IPAN; PB1; RdRp; degradation; hijack; influenza A virus; interferon; lncRNA; viral replication
PMID: 31189112 DOI: 10.1016/j.celrep.2019.05.036