Long non-coding RNA C1RL-AS1 aggravates influenza A virus pneumonia through miR-16-5p/LAMP3.

Influenza A viruses continue to pose a serious threat to public health and economic stability. To investigate the role of C1RL-AS1 in influenza A virus (IAV) pneumonia. Using RT-qPCR analysis, we determined C1RL-AS1 expression levels in children with IAV-infected pneumonia and A549 cells. C1RL-AS1 expression levels in children were subjected to ROC analysis. C1RL-AS1 was knocked down to investigate its role in IAV-infected A549 cells, including effects on viral nucleoprotein (NP) production, cell survival, and apoptosis. Downstream miRNAs of C1RL-AS1 were predicted and validated. MiR-16-5p target genes were predicted and validated. C1RL-AS1 was up-regulated in IAV-infected children and A549 cells. C1RL-AS1 expression levels distinguished children with IAV pneumonia from healthy children. Knockdown of C1RL-AS1 attenuated viral NP production, promoted A549 cell survival, and inhibited apoptosis. MiR-16-5p was a downstream C1RL-AS1 miRNA. miR-16-5p counteracted the anti-IAV infection effect brought about by C1RL-AS1 knockdown. LAMP3 was a miR-16-5p target gene associated with pneumonia. LAMP3 restored the cellular effects brought about by C1RL-AS1/miR-16-5p co-knockdown. C1RL-AS1 is a possible diagnostic factor for IAV pneumonia in children. C1RL-AS1 may participate in IAV pneumonia by sponging miR-16-5p and then moderating LAMP3.