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MicroRNA-23 inhibits PRRSV replication by directly targeting PRRSV RNA and possibly by upregulating type I

Qiong Zhang1, Xue-Kun Guo1, Li Gao1

  • 1State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University, Beijing 100193, China; Ministry of Agriculture Key Laboratory of Soil Microbiology, College of Biological Sciences, China Agricultural University, Beijing 100193, China; Department of Microbiology and Immunology, College of Biological Sciences, China Agricultural University, Beijing 100193, China.

Virology
|February 8, 2014
PubMed

Insights

Three microRNAs (miRNAs) act as antiviral host factors against Porcine Reproductive and Respiratory Syndrome Virus (PRRSV). These miRNAs, particularly miR-23, show potential for developing novel PRRSV therapies.

Area of Science:

  • Molecular Biology
  • Virology
  • Immunology

Background:

  • MicroRNAs (miRNAs) are key regulators of gene expression involved in host-pathogen interactions and innate immunity.
  • Porcine Reproductive and Respiratory Syndrome (PRRS) poses a significant threat to the global swine industry.

Purpose of the Study:

  • To identify specific microRNAs (miRNAs) that function as host antiviral factors against Porcine Reproductive and Respiratory Syndrome Virus (PRRSV).
  • To investigate the potential of these miRNAs as therapeutic agents for PRRSV infection.

Main Methods:

  • Over-expression and inhibition of specific miRNAs (miR-23, miR-378, miR-505) in host cells.
  • Assessment of PRRSV replication levels.
  • Analysis of conserved miRNA target sites in PRRSV strains.
  • Investigation of miR-23's role in type I interferon induction via IRF3/IRF7 activation.

Main Results:

  • miR-23, miR-378, and miR-505 were identified as antiviral host factors against PRRSV.
  • Over-expression of these miRNAs dose-dependently inhibited PRRSV infection.
  • Endogenous miRNA blockage enhanced PRRSV replication.
  • Conserved target sites for these miRNAs were found in PRRSV strains, mediating repression.
  • miR-23 induced type I interferon expression through IRF3/IRF7 activation, inhibiting viral infection.

Conclusions:

  • miR-23, miR-378, and miR-505 are crucial antiviral factors against PRRSV.
  • These miRNAs, especially miR-23, demonstrate potential for developing novel antiviral therapies against PRRSV.
Keywords:
IFNsIRFPRRSVmiR-23miR-378miR-505microRNAs

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