SNHG15 Positively Regulates Influenza Virus Infection Through Its Association With miR-153 and RABL2A.

Influenza viruses cause seasonal epidemics, and current vaccines do not fully protect against them. This study focuses on long non-coding RNAs (lncRNAs), which are RNA molecules that do not code for proteins but play crucial roles in various biological processes. We identified 17 lncRNAs altered by the influenza virus. Among these, SNHG15 was found to enhance influenza virus infection. Knockdown of SNHG15 using CRISPR interference and RNA interference reduced influenza virus infection, while overexpression of SNHG15 increased virus replication. We found that miR-153-3p, a competitive endogenous RNA (ceRNA) for SNHG15, acts as an anti-influenza microRNA, and its overexpression negated SNHG15's proviral activity. RNA pull-down and mass spectrometry identified Rab-like protein 2A (RABL2A) as an interacting partner of SNHG15. Both SNHG15 and RABL2A facilitated influenza virus internalization. Additionally, siRNA-mediated knockdown of RABL2A reduced SNHG15-mediated virus internalization. In conclusion, SNHG15 enhances influenza A virus infection through its interactions with miR-153 and RABL2A.