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

Xingjuan Liao1, Qin Liang1, Chao Xu1

  • 1Department of Pediatrics, Taihe Hospital, Affiliated Hospital of Hubei University of Medicine, No.32, Renmin South Road, Shiyan, 442000, China.

Virus Genes
|January 3, 2025
PubMed

Insights

C1RL-AS1 is elevated in children with influenza A virus (IAV) pneumonia and may serve as a diagnostic marker. It impacts viral replication and cell survival by regulating miR-16-5p and LAMP3.

Area of Science:

  • Molecular Biology
  • Virology
  • Genetics

Background:

  • Influenza A virus (IAV) poses significant public health risks.
  • Understanding the molecular mechanisms of IAV pneumonia is crucial for developing effective diagnostics and treatments.

Purpose of the Study:

  • To investigate the role of C1RL-AS1 in influenza A virus (IAV) pneumonia.
  • To explore C1RL-AS1 as a potential diagnostic biomarker for IAV pneumonia in children.

Main Methods:

  • RT-qPCR was used to measure C1RL-AS1 expression in pediatric patients and A549 cells.
  • Receiver Operating Characteristic (ROC) analysis was performed on C1RL-AS1 expression data.
  • C1RL-AS1 knockdown experiments were conducted in A549 cells to assess its functional role.
  • Bioinformatic tools were employed to predict and validate downstream miRNAs and their target genes.

Main Results:

  • C1RL-AS1 expression was significantly upregulated in children with IAV pneumonia and in IAV-infected A549 cells.
  • C1RL-AS1 expression levels effectively differentiated IAV pneumonia patients from healthy controls.
  • Knockdown of C1RL-AS1 reduced viral nucleoprotein (NP) production, enhanced cell survival, and inhibited apoptosis.
  • C1RL-AS1 was found to sponge miR-16-5p, and miR-16-5p targeted LAMP3, a gene associated with pneumonia.

Conclusions:

  • C1RL-AS1 is a potential diagnostic biomarker for pediatric IAV pneumonia.
  • C1RL-AS1 plays a role in IAV pneumonia pathogenesis by modulating the miR-16-5p/LAMP3 axis.
  • Targeting the C1RL-AS1/miR-16-5p/LAMP3 pathway may offer therapeutic strategies against IAV infection.

Keywords:
C1RL-AS1Influenza A virusLAMP3PneumoniaRespiratory failure

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