tetano
Editor, Senior Moderator
PLoS Pathog
. 2025 Jan 8;21(1):e1012854.
doi: 10.1371/journal.ppat.1012854. Online ahead of print. An interferon-stimulated long non-coding RNA USP30-AS1 as an immune modulator in influenza A virus infection
Yi Cao[SUP] 1 [/SUP], Alex W H Chin[SUP] 1 2 [/SUP], Haogao Gu[SUP] 1 [/SUP], Mengting Li[SUP] 1 [/SUP], Yuner Gu[SUP] 1 [/SUP], Sylvia P N Lau[SUP] 1 [/SUP], Kenrie P Y Hui[SUP] 1 2 [/SUP], Michael C W Chan[SUP] 1 2 [/SUP], Leo L M Poon[SUP] 1 2 3 4 [/SUP]
Affiliations
Long non-coding RNAs (lncRNAs) are essential components of innate immunity, maintaining the functionality of immune systems that control virus infection. However, how lncRNAs engage immune responses during influenza A virus (IAV) infection remains unclear. Here, we show that lncRNA USP30-AS1 is up-regulated by infection of multiple different IAV subtypes and is required for tuning inflammatory and antiviral response in IAV infection. Genetically inactivation of USP30-AS1 enhances viral protein synthesis and viral growth. USP30-AS1 is an interferon-stimulated gene, and the induction of USP30-AS1 can be achieved by JAK-STAT mediated signaling activation. The immune regulation of USP30-AS1 is independent of its proximal protein-coding gene USP30. In IAV infection, deletion of USP30-AS1 unleashes high systemic inflammatory responses involving a broad range of pro-inflammatory factors, suggesting USP30-AS1 as a critical modulator of immune responses in IAV infection. Furthermore, we established a database providing well-annotated host gene expression profiles IAV infection or immune stimulation.
. 2025 Jan 8;21(1):e1012854.
doi: 10.1371/journal.ppat.1012854. Online ahead of print. An interferon-stimulated long non-coding RNA USP30-AS1 as an immune modulator in influenza A virus infection
Yi Cao[SUP] 1 [/SUP], Alex W H Chin[SUP] 1 2 [/SUP], Haogao Gu[SUP] 1 [/SUP], Mengting Li[SUP] 1 [/SUP], Yuner Gu[SUP] 1 [/SUP], Sylvia P N Lau[SUP] 1 [/SUP], Kenrie P Y Hui[SUP] 1 2 [/SUP], Michael C W Chan[SUP] 1 2 [/SUP], Leo L M Poon[SUP] 1 2 3 4 [/SUP]
Affiliations
- PMID: 39777915
- DOI: 10.1371/journal.ppat.1012854
Long non-coding RNAs (lncRNAs) are essential components of innate immunity, maintaining the functionality of immune systems that control virus infection. However, how lncRNAs engage immune responses during influenza A virus (IAV) infection remains unclear. Here, we show that lncRNA USP30-AS1 is up-regulated by infection of multiple different IAV subtypes and is required for tuning inflammatory and antiviral response in IAV infection. Genetically inactivation of USP30-AS1 enhances viral protein synthesis and viral growth. USP30-AS1 is an interferon-stimulated gene, and the induction of USP30-AS1 can be achieved by JAK-STAT mediated signaling activation. The immune regulation of USP30-AS1 is independent of its proximal protein-coding gene USP30. In IAV infection, deletion of USP30-AS1 unleashes high systemic inflammatory responses involving a broad range of pro-inflammatory factors, suggesting USP30-AS1 as a critical modulator of immune responses in IAV infection. Furthermore, we established a database providing well-annotated host gene expression profiles IAV infection or immune stimulation.