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Cellular microRNAs influence replication of H3N2 canine influenza virus in infected cells

Xing Xie1, Maoda Pang2, Shan Liang3

  • 1Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, China; Institute of Veterinary Medicine, Jiangsu Academy of Agricultural Sciences, Key Laboratory of Veterinary Biological Engineering and Technology, Ministry of Agriculture, Nanjing, 210014, China.

Veterinary Microbiology
|April 24, 2021
PubMed

Insights

Two canine microRNAs, cfa-miR-125b and cfa-miR-151, were found to inhibit H3N2 canine influenza virus (CIV) replication. These microRNAs are crucial negative regulators in host-pathogen interactions during CIV infection.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • MicroRNAs (miRNAs) are key regulators in host-virus interactions.
  • Avian-origin H3N2 canine influenza virus (CIV) is prevalent in Asia.
  • Understanding host miRNA roles in CIV infection is crucial for canine health.

Purpose of the Study:

  • To investigate the role of host miRNAs in H3N2 CIV infection.
  • To identify specific miRNAs involved in the host response to CIV.
  • To elucidate the regulatory mechanisms of miRNAs in CIV pathogenesis.

Main Methods:

  • Comparison of miRNA profiles in canine primary cells (CBECs and CAMCs) after H3N2 CIV infection.
  • Bioinformatics analysis to predict miRNA targets within CIV.
  • Experimental validation using miRNA overexpression and inhibition assays, including qRT-PCR and western blotting.

Main Results:

  • Expressions of cfa-miR-125b and cfa-miR-151 were significantly decreased in CIV-infected canine cells.
  • These miRNAs target the nucleoprotein (NP) and non-structural protein 1 (NS1) mRNAs of H3N2 CIV.
  • Overexpression of cfa-miR-125b and cfa-miR-151 inhibited CIV replication, while their inhibition enhanced it.

Conclusions:

  • Cfa-miR-125b and cfa-miR-151 act as negative regulators of H3N2 CIV replication.
  • These findings contribute to understanding host resistance mechanisms against viral infections.
  • The study clarifies the pathogenesis of H3N2 CIV and highlights potential therapeutic targets.
Keywords:
Canine alveolar macrophagesCanine bronchiolar epithelial cellsCanine influenza virusH3N2Virus replicationmicroRNAs

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