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MicroRNA-21-3p modulates FGF2 to facilitate influenza A virus H5N1 replication by refraining type I interferon

Jianli Shi1, Ping Feng1, Tingting Gu1

  • 1Department of Paediatrics, The Fourth People's Hospital of Jinan, Jinan 250031, Shandong, China.

Bioscience Reports
|May 21, 2020
PubMed
Abstract

Insights

MicroRNA-21-3p reduction accelerates H5N1 influenza virus replication by down-regulating fibroblast growth factor 2 and suppressing the interferon response. Restoring miR-21-3p levels inhibits viral load and enhances antiviral immunity.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Influenza A virus (IAV) poses a significant public health threat.
  • Host microRNAs (miRNAs) play a role in IAV replication.
  • This study investigates microRNA-21-3p (miR-21-3p) in H5N1 influenza virus replication.

Purpose of the Study:

  • To elucidate the role of miR-21-3p in H5N1 virus replication.
  • To determine the molecular mechanisms underlying miR-21-3p's effect on H5N1.
  • To identify potential therapeutic targets for H5N1 infection.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) for gene and miRNA expression.
  • Western blot for protein analysis.
  • TCID50 assay for virus titration.
  • Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays for target validation.

Main Results:

  • miR-21-3p levels were decreased in H5N1-infected patients and cells.
  • miR-21-3p overexpression enhanced viral factors (M1, NP, TCID50) and reduced interferon responses (IFN-β, IFN-α, PKR, MxA, OAS).
  • Fibroblast growth factor 2 (FGF2) was identified as a direct target of miR-21-3p; FGF2 introduction reversed miR-21-3p's effects.

Conclusions:

  • miR-21-3p down-regulates FGF2 expression, promoting H5N1 replication.
  • miR-21-3p suppresses the host's interferon response during H5N1 infection.
  • Targeting miR-21-3p or its interaction with FGF2 may offer a strategy against H5N1.
Keywords:
FGF2H5N1miR-21-3preplicationtype I IFN response

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