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MiR-362-3p mediates IFNα-induced antiviral viability against Enterovirus 71 (EV71)

San Wang1, Lan Chen1, Zongtao Wu1

  • 1Department of Pediatrics, The Third Affiliated Hospital of Zunyi Medical University, the First People'S Hospital of Zunyi), Guizhou, 563099, China.

Naunyn-Schmiedeberg'S Archives of Pharmacology
|March 26, 2025
PubMed

Insights

Interferon Alpha (IFNα) treatment boosts miR-362-3p, inhibiting Enterovirus 71 (EV71) replication and enhancing antiviral defense in HMC3 cells.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Enteroviruses, including Enterovirus 71 (EV71), are significant human pathogens.
  • Interferon Alpha (IFNα) is a key antiviral cytokine used in treating viral infections.
  • The specific role of IFNα-induced microRNAs in EV71 defense requires further elucidation.

Purpose of the Study:

  • To investigate the role of IFNα-induced miR-362-3p in cellular defense against EV71.
  • To determine if modulating miR-362-3p affects EV71 replication and cell viability.

Main Methods:

  • Differential miRNA expression analysis following IFNα treatment.
  • EV71 proliferation assays in RD cells.
  • Evaluation of IFNα and EV71 effects on miR-362-3p expression in HMC3 cells.
  • Assessment of antiviral activity by manipulating miR-362-3p levels (mimic and inhibitor).

Main Results:

  • IFNα treatment and miR-362-3p mimic increased miR-362-3p expression, enhanced cell viability, and reduced EV71 replication (-lgTCID50).
  • miR-362-3p mimic decreased VP1 mRNA and protein expression, while the inhibitor increased them.
  • IFNα induced miR-362-3p production and enhanced HMC3 cell viability.
  • Combined IFNα and miR-362-3p mimic further reduced viral load and VP1 expression.

Conclusions:

  • IFNα-induced upregulation of miR-362-3p contributes to the inhibition of EV71 replication in HMC3 cells.
  • miR-362-3p enhances antiviral viability, suggesting its potential as a therapeutic target against EV71 infections.
Keywords:
Antiviral activityEnterovirus 71HMC3 cellsIFNαMiR-362-3p

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