tetano
Editor, Senior Moderator
Vet Microbiol. 2019 Apr;231:238-245. doi: 10.1016/j.vetmic.2019.03.012. Epub 2019 Mar 14.
[h=1]Circular RNA GATAD2A promotes H1N1 replication through inhibiting autophagy.[/h] Yu T[SUP]1[/SUP], Ding Y[SUP]1[/SUP], Zhang Y[SUP]2[/SUP], Liu Y[SUP]1[/SUP], Li Y[SUP]1[/SUP], Lei J[SUP]1[/SUP], Zhou J[SUP]2[/SUP], Song S[SUP]1[/SUP], Hu B[SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Circular RNAs (circRNAs) play critical roles in various diseases. However, whether and how circular RNA regulates influenza A virus (IAV) infection is unknown. Here, we studied the role of circular RNA GATA Zinc Finger Domain Containing 2A (circ-GATAD2A) in the replication of IAV H1N1 in A549 cells. Circ-GATAD2A was formed upon H1N1 infection. Knockdown of circ-GATAD2A in A549 cells enhanced autophagy and inhibited H1N1 replication. By contrast, overexpression of circ-GATAD2A impaired autophagy and promoted H1N1 replication. Similarly, knockout of vacuolar protein sorting 34 (VPS34) blocked autophagy and increased H1N1 replication. However, the expression of circ-GATAD2A could not further enhance H1N1 replication in VPS34 knockout cells. Collectively, these data indicated that circ-GATAD2A promotes the replication of H1N1 by inhibiting autophagy.
Copyright ? 2019 The Authors. Published by Elsevier B.V. All rights reserved.
[h=4]KEYWORDS:[/h] Autophagy; H1N1; Replication; circ-GATAD2A
PMID: 30955816 DOI: 10.1016/j.vetmic.2019.03.012
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[h=1]Circular RNA GATAD2A promotes H1N1 replication through inhibiting autophagy.[/h] Yu T[SUP]1[/SUP], Ding Y[SUP]1[/SUP], Zhang Y[SUP]2[/SUP], Liu Y[SUP]1[/SUP], Li Y[SUP]1[/SUP], Lei J[SUP]1[/SUP], Zhou J[SUP]2[/SUP], Song S[SUP]1[/SUP], Hu B[SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Circular RNAs (circRNAs) play critical roles in various diseases. However, whether and how circular RNA regulates influenza A virus (IAV) infection is unknown. Here, we studied the role of circular RNA GATA Zinc Finger Domain Containing 2A (circ-GATAD2A) in the replication of IAV H1N1 in A549 cells. Circ-GATAD2A was formed upon H1N1 infection. Knockdown of circ-GATAD2A in A549 cells enhanced autophagy and inhibited H1N1 replication. By contrast, overexpression of circ-GATAD2A impaired autophagy and promoted H1N1 replication. Similarly, knockout of vacuolar protein sorting 34 (VPS34) blocked autophagy and increased H1N1 replication. However, the expression of circ-GATAD2A could not further enhance H1N1 replication in VPS34 knockout cells. Collectively, these data indicated that circ-GATAD2A promotes the replication of H1N1 by inhibiting autophagy.
Copyright ? 2019 The Authors. Published by Elsevier B.V. All rights reserved.
[h=4]KEYWORDS:[/h] Autophagy; H1N1; Replication; circ-GATAD2A
PMID: 30955816 DOI: 10.1016/j.vetmic.2019.03.012
Free full text