tetano
Editor, Senior Moderator
Cell Microbiol. 2019 May 2:e13036. doi: 10.1111/cmi.13036. [Epub ahead of print]
[h=1]Identification of lncRNA-155 encoded by MIR155HG as a novel regulator of innate immunity against influenza A virus infection.[/h] Maarouf M[SUP]1,[/SUP][SUP]2[/SUP], Chen B[SUP]1,[/SUP][SUP]2[/SUP], Chen Y[SUP]1[/SUP], Wang X[SUP]1,[/SUP][SUP]2[/SUP], Rai KR[SUP]1,[/SUP][SUP]2[/SUP], Zhao Z[SUP]1,[/SUP][SUP]2[/SUP], Liu S[SUP]1,[/SUP][SUP]2[/SUP], Li Y[SUP]1,[/SUP][SUP]2[/SUP], Xiao M[SUP]1,[/SUP][SUP]2[/SUP], Chen JL[SUP]1,[/SUP][SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Long non-coding RNAs (lncRNAs) are single-stranded RNA molecules longer than 200 nt that regulate many cellular processes. MicroRNA 155 host gene (MIR155HG) encodes the microRNA (miR)-155 which regulates various signaling pathways of innate and adaptive immune responses against viral infections. MIR155HG also encodes a lncRNA that we call lncRNA-155. Here we observed that expression of lncRNA-155 was markedly upregulated during influenza A virus (IAV) infection both in vitro (several cell lines) and in vivo (mouse model). Interestingly, robust expression of lncRNA-155 was also induced by infections with several other viruses. Disruption of lncRNA-155 expression in A549 cells diminished the antiviral innate immunity against IAV. Furthermore, knockout of lncRNA-155 in mice significantly increased IAV replication and virulence in the animals. In contrast, overexpression of lncRNA-155 in human cells suppressed IAV replication, suggesting that lncRNA-155 is involved in host antiviral innate immunity induced by IAV infection. Moreover, we found that lncRNA-155 had profound effect on expression of protein tyrosine phosphatase 1B (PTP1B) during the infection with IAV. Inhibition of PTP1B by lncRNA-155 resulted in higher production of interferon-beta (IFN-β) and several critical interferon-stimulated genes (ISGs). Together, these observations reveal that MIR155HG derived lncRNA-155 can be induced by IAV, which modulates host innate immunity during the virus infection via regulation of PTP1B-mediated interferon response.
This article is protected by copyright. All rights reserved.
[h=4]KEYWORDS:[/h] Influenza A virus; Innate immunity; MIR155HG; PTP1B; lncRNA; miR-155
PMID: 31045320 DOI: 10.1111/cmi.13036
[h=1]Identification of lncRNA-155 encoded by MIR155HG as a novel regulator of innate immunity against influenza A virus infection.[/h] Maarouf M[SUP]1,[/SUP][SUP]2[/SUP], Chen B[SUP]1,[/SUP][SUP]2[/SUP], Chen Y[SUP]1[/SUP], Wang X[SUP]1,[/SUP][SUP]2[/SUP], Rai KR[SUP]1,[/SUP][SUP]2[/SUP], Zhao Z[SUP]1,[/SUP][SUP]2[/SUP], Liu S[SUP]1,[/SUP][SUP]2[/SUP], Li Y[SUP]1,[/SUP][SUP]2[/SUP], Xiao M[SUP]1,[/SUP][SUP]2[/SUP], Chen JL[SUP]1,[/SUP][SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Long non-coding RNAs (lncRNAs) are single-stranded RNA molecules longer than 200 nt that regulate many cellular processes. MicroRNA 155 host gene (MIR155HG) encodes the microRNA (miR)-155 which regulates various signaling pathways of innate and adaptive immune responses against viral infections. MIR155HG also encodes a lncRNA that we call lncRNA-155. Here we observed that expression of lncRNA-155 was markedly upregulated during influenza A virus (IAV) infection both in vitro (several cell lines) and in vivo (mouse model). Interestingly, robust expression of lncRNA-155 was also induced by infections with several other viruses. Disruption of lncRNA-155 expression in A549 cells diminished the antiviral innate immunity against IAV. Furthermore, knockout of lncRNA-155 in mice significantly increased IAV replication and virulence in the animals. In contrast, overexpression of lncRNA-155 in human cells suppressed IAV replication, suggesting that lncRNA-155 is involved in host antiviral innate immunity induced by IAV infection. Moreover, we found that lncRNA-155 had profound effect on expression of protein tyrosine phosphatase 1B (PTP1B) during the infection with IAV. Inhibition of PTP1B by lncRNA-155 resulted in higher production of interferon-beta (IFN-β) and several critical interferon-stimulated genes (ISGs). Together, these observations reveal that MIR155HG derived lncRNA-155 can be induced by IAV, which modulates host innate immunity during the virus infection via regulation of PTP1B-mediated interferon response.
This article is protected by copyright. All rights reserved.
[h=4]KEYWORDS:[/h] Influenza A virus; Innate immunity; MIR155HG; PTP1B; lncRNA; miR-155
PMID: 31045320 DOI: 10.1111/cmi.13036