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miRNA29 Promotes Viral Replication During Early Stage of PRRSV Infection In Vitro

Mengjiao Zhou1, Chuanmin Li1, Chunyan Lu1

  • 1College of Animal Science, Jilin University , Changchun, Jilin, People's Republic of China .

DNA and Cell Biology
|September 23, 2016
PubMed

Insights

MicroRNAs (miRNAs) play a role in antiviral immunity. This study shows miR-29a promotes porcine reproductive and respiratory syndrome virus (PRRSV) replication by targeting AKT3 in porcine alveolar macrophages.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • MicroRNAs (miRNAs) are crucial regulators of gene expression involved in host-virus interactions.
  • Porcine reproductive and respiratory syndrome virus (PRRSV) poses a significant threat to the swine industry, necessitating research into host factors influencing its replication.
  • Understanding the role of specific miRNAs in PRRSV infection is vital for developing novel antiviral strategies.

Purpose of the Study:

  • To investigate the role of miR-29 family members in PRRSV replication within porcine alveolar macrophages (PAMs).
  • To identify and validate target genes of miR-29 that are involved in PRRSV infection.
  • To elucidate the mechanism by which miR-29 influences PRRSV replication.

Main Methods:

  • PRRSV infection of PAMs followed by RT-qPCR to quantify miR-29a/b-1/c expression.
  • Transfection of PAMs with pre-miR-29a/b-1 lentiviral vectors to assess effects on PRRSV replication.
  • RT-qPCR and Western blot analysis to evaluate the expression of putative miR-29 target genes (AKT3, TP53INP1, RPS6KB1).
  • Luciferase reporter assays to confirm the interaction between miR-29a and its target gene 3'UTRs.

Main Results:

  • miR-29a/b-1 expression significantly increased post-PRRSV infection in PAMs, peaking around 24 hours.
  • Overexpression of miR-29a/b-1 via lentiviral vectors significantly enhanced PRRSV replication in PAMs within 24 hours.
  • miR-29a overexpression led to a significant reduction in the expression of its target genes AKT3, TP53INP1, and RPS6KB1.
  • Luciferase assays confirmed that miR-29a directly interacts with the 3'UTR of AKT3, inhibiting its expression.

Conclusions:

  • miR-29a promotes PRRSV replication during the early stages of infection in vitro.
  • AKT3 is identified as a direct target gene of miR-29a, suggesting its involvement in the viral replication process.
  • These findings provide insights into the host-miRNA-virus interplay and highlight miR-29a as a potential therapeutic target for PRRSV.
Keywords:
AKT3PAMPRRSVmiRNA29replication

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