MicroRNA-23b inhibits enterovirus 71 replication through downregulation of EV71 VPl protein

Bai-ping Wen1, Hong-jian Dai, Yue-huang Yang

  • 1Kunming Children's Hospital, Kunming, China.

Intervirology
|April 19, 2013
PubMed

Insights

MicroRNAs (miRNAs), specifically hsa-miR-23b, show potential in combating Enterovirus 71 (EV71) infection. Upregulating miR-23b was found to inhibit EV71 replication, offering new avenues for treating hand-foot-and-mouth disease.

Area of Science:

  • Virology
  • Molecular Biology
  • Gene Regulation

Background:

  • Enterovirus 71 (EV71) causes hand-foot-and-mouth disease, with no current effective antiviral treatments.
  • MicroRNAs (miRNAs) regulate gene expression and are implicated in virus-host interactions.
  • Previous studies indicated hsa-miR-23b downregulation in EV71-infected cells.

Purpose of the Study:

  • To investigate the role of hsa-miR-23b in EV71 infection.
  • To determine if hsa-miR-23b can inhibit EV71 replication.
  • To identify the mechanism by which hsa-miR-23b affects EV71.

Main Methods:

  • Bioinformatic prediction of miR-23b target sites in the EV71 genome using miRanda.
  • Luciferase assays to confirm predicted target interactions.
  • Transfection of miR-23b mimics to assess its effect on EV71 replication.

Main Results:

  • hsa-miR-23b was predicted to target a conserved sequence in the EV71 3' untranslated region (UTR).
  • Upregulation of miR-23b significantly inhibited EV71 replication.
  • miR-23b inhibited EV71 replication by downregulating the EV71 VPl protein.

Conclusions:

  • hsa-miR-23b acts as a negative regulator of EV71 replication.
  • Targeting EV71's 3'UTR with miR-23b offers a potential therapeutic strategy.
  • This research enhances understanding for developing treatments against EV71-induced hand-foot-and-mouth disease.

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