tetano
Editor, Senior Moderator
J Med Virol. 2019 Apr 10. doi: 10.1002/jmv.25483. [Epub ahead of print]
[h=1]Long non-coding RNA TSPOAP1 antisense RNA 1 negatively modulates type I IFN signaling to facilitate influenza A virus replication.[/h] Wang Q[SUP]1[/SUP], Zhang D[SUP]1[/SUP], Feng W[SUP]1[/SUP], Guo Y[SUP]1[/SUP], Sun X[SUP]1[/SUP], Zhang M[SUP]1[/SUP], Guan Z[SUP]1[/SUP], Duan M[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Although the expression of thousands of host long noncoding RNAs (lncRNAs) can be regulated by viral infection, the number of lncRNAs with experimentally verified function is limited. In this study, the expression of host lncRNA TSPOAP1-AS1 was significantly induced by influenza A virus (IAV) infection in a dose and time dependent manner. Poly (I:C), a synthetic analog of double-stranded RNA, also increased TSPOAP1-AS1 expression. RNA fractionation revealed that TSPOAP1-AS1 was a nucleocytoplasmic lncRNA, and an increased nuclear/cytoplasmic ratio was detected after IAV infection. NF-κB signaling acting as a critical factor in transcription of TSPOAP1-AS1 was determined through the use of pharmacological and genetic approaches. Functionally, overexpression of TSPOAP1-AS1 resulted in a significant increase in IAV replication. In contrast, abolition of TSPOAP1-AS1 by RNA interference restricted viral replication. Furthermore, we demonstrated that TSPOAP1-AS1 negatively modulated the IAV-induced Ifnb1 transcription, ISRE activation and downstream ISG expression. Collectively, our data provides evidence for the host lncRNA utilized by viruses to support its replication. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
[h=4]KEYWORDS:[/h] TSPOAP1-AS1; influenza virus; interferon; long noncoding RNA
PMID: 30968963 DOI: 10.1002/jmv.25483
[h=1]Long non-coding RNA TSPOAP1 antisense RNA 1 negatively modulates type I IFN signaling to facilitate influenza A virus replication.[/h] Wang Q[SUP]1[/SUP], Zhang D[SUP]1[/SUP], Feng W[SUP]1[/SUP], Guo Y[SUP]1[/SUP], Sun X[SUP]1[/SUP], Zhang M[SUP]1[/SUP], Guan Z[SUP]1[/SUP], Duan M[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Although the expression of thousands of host long noncoding RNAs (lncRNAs) can be regulated by viral infection, the number of lncRNAs with experimentally verified function is limited. In this study, the expression of host lncRNA TSPOAP1-AS1 was significantly induced by influenza A virus (IAV) infection in a dose and time dependent manner. Poly (I:C), a synthetic analog of double-stranded RNA, also increased TSPOAP1-AS1 expression. RNA fractionation revealed that TSPOAP1-AS1 was a nucleocytoplasmic lncRNA, and an increased nuclear/cytoplasmic ratio was detected after IAV infection. NF-κB signaling acting as a critical factor in transcription of TSPOAP1-AS1 was determined through the use of pharmacological and genetic approaches. Functionally, overexpression of TSPOAP1-AS1 resulted in a significant increase in IAV replication. In contrast, abolition of TSPOAP1-AS1 by RNA interference restricted viral replication. Furthermore, we demonstrated that TSPOAP1-AS1 negatively modulated the IAV-induced Ifnb1 transcription, ISRE activation and downstream ISG expression. Collectively, our data provides evidence for the host lncRNA utilized by viruses to support its replication. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
[h=4]KEYWORDS:[/h] TSPOAP1-AS1; influenza virus; interferon; long noncoding RNA
PMID: 30968963 DOI: 10.1002/jmv.25483