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Mir-302c mediates influenza A virus-induced IFNβ expression by targeting NF-κB inducing kinase

Shulin Gui1, Xueyuan Chen1, Mo Zhang1

  • 1State Key Laboratory of Virology and College of Life Sciences, Wuhan University, Wuhan 430072, China.

FEBS Letters
|November 26, 2015
PubMed

Insights

MicroRNA-302c regulates influenza A virus (IAV) replication by controlling Nuclear Factor-kappa B (NF-κB) signaling and Interferon-beta (IFNβ) expression. IAV infection downregulates miR-302c, activating IFNβ and inhibiting viral growth.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • The role of microRNAs (miRNAs) in influenza A virus (IAV) infection remains largely unexplored.
  • NIK (NF-κB-inducing kinase) is a key regulator in inflammatory and immune responses.

Purpose of the Study:

  • To elucidate the function of specific miRNAs in modulating IAV infection.
  • To identify novel molecular pathways involved in the host response to IAV.

Main Methods:

  • Luciferase reporter assays to measure NIK 3'UTR activity.
  • Quantitative real-time PCR (qRT-PCR) to assess mRNA expression levels (IFNβ).
  • Western blotting or similar techniques to analyze protein translocation (NF-κB).

Main Results:

  • IAV infection elevated NIK 3'UTR luciferase activity.
  • miR-302c was found to reduce NIK expression, subsequently decreasing IFNβ mRNA.
  • miR-302c inhibited NF-κB translocation to the nucleus.
  • IAV infection led to decreased miR-302c expression, enhancing IFNβ expression and suppressing viral replication.
  • miR-520e, despite targeting the same NIK site, did not promote viral replication.

Conclusions:

  • A novel signaling pathway involving miR-302c, NIK, NF-κB, and IFNβ in controlling IAV replication has been identified.
  • miR-302c acts as a negative regulator of the antiviral response during IAV infection.
  • Targeting this pathway could offer new therapeutic strategies against influenza.
Keywords:
Influenza A virusInnate immuneMiR-302cNF-κB-inducing kinaseType I IFN

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