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Updated: May 12, 2026

MicroRNA-based Regulation of Picornavirus Tropism
Published on: February 6, 2017
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.
Abstract:
Enterovirus 71 (EV71) is one of the causative pathogens of hand-foot-and-mouth disease and effective antiviral agents and vaccines against this virus have, to date, not been available. MicroRNAs (miRNAs) are a recently discovered class of RNAs with the function of post-transcriptional gene expression regulation. It has been demonstrated that miRNAs play important roles in the complicated interaction network between virus and host, while few studies have explored the role of miRNAs in EV71 infection. A recent study showed that hsa-miR-23b was downregulated significantly in cell-infected viruses. To address this issue, biological software miRanda was first used to predict possible target sites of miR-23b at EV71 gene sequence, then to confirm it by luciferase assay. miR-23b mimics were transfected to verify its effects on infection of EV71. These results suggest that miR-23b and upregulation of miR-23b inhibited the replication of EV71 by targeting at EV71 3'UTR conserved sequence. Taken together, miR-23b could inhibit EV71 replication through downregulation of EV71 VPl protein. These results may enhance our understanding on the prevention and treatment of hand-foot-and-mouth disease caused by EV71 infection.
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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