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MicroRNA-30c targets the interferon-alpha/beta receptor beta chain to promote type 2 PRRSV infection

Fang Liu1,2, Honglei Wang1,2, Li Du1,2

  • 11​State Key Laboratory of Agrobiotechnology and Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Biological Sciences, China Agricultural University, Beijing 100193, PR China.

The Journal of General Virology
|November 2, 2018
PubMed

Insights

MicroRNAs (miRNAs) like miR-30c promote Porcine reproductive and respiratory syndrome virus (PRRSV) replication by down-regulating IFNAR2, a key component of the antiviral response. This study elucidates a novel mechanism of PRRSV pathogenesis.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Porcine reproductive and respiratory syndrome (PRRS) is a significant swine disease.
  • MicroRNAs (miRNAs) regulate virus-host interactions; miR-30c is implicated in PRRSV replication.
  • Interferon-alpha/beta receptor beta chain (IFNAR2) plays a crucial role in antiviral immunity.

Purpose of the Study:

  • To investigate the regulatory role of miR-30c in PRRSV infection.
  • To identify the molecular targets of miR-30c during PRRSV infection.
  • To elucidate the mechanism by which miR-30c promotes PRRSV replication.

Main Methods:

  • Bioinformatics analysis to predict miRNA-target interactions.
  • Luciferase reporter assays to validate targeting of IFNAR2 by miR-30c.
  • Co-localization studies to confirm miR-30c and IFNAR2 mRNA interaction within the RISC complex.

Main Results:

  • IFNAR2 expression was down-regulated, while miR-30c was up-regulated during PRRSV infection.
  • miR-30c directly targets the 3' UTR of IFNAR2.
  • miR-30c impairs the induction of interferon-stimulated genes (ISGs) by targeting IFNAR2, thereby promoting PRRSV replication.

Conclusions:

  • miR-30c promotes PRRSV replication by targeting and down-regulating IFNAR2.
  • This mechanism inhibits the host's interferon-mediated antiviral response.
  • Understanding this interaction provides insights into PRRSV pathogenesis and potential therapeutic strategies.
Keywords:
IFN-IIFNAR2PRRSVmiR-30c

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