miR-127-5p negatively regulates enterovirus 71 replication by directly targeting SCARB2
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Updated: Mar 1, 2026
MicroRNA-based Regulation of Picornavirus Tropism
Published on: February 6, 2017
Chunhong Feng1,2, Yuxuan Fu1, Deyan Chen1
1Center for Public Health Research Medical School Nanjing University China.
Abstract:
Enterovirus 71 (EV71) is the major causative agent of hand-foot-and-mouth disease in young children and can cause severe cerebral and pulmonary complications and even fatality. This study aimed at elucidating whether and how EV71 infection is regulated by a cellular microRNA, miR-127-5p. We found that miR-127-5p can downregulate the expression of SCARB2, a main receptor of EV71, by targeting two potential sites in its 3' UTR region and inhibit EV71 infection. Meanwhile, miR-127-5p expression was upregulated during EV71 infection. Notably, transfecting cells with miR-127-5p mimics led to a significant decrease in viral replication, while inhibition of endogenous miR-127-5p facilitated viral replication. Furthermore, our evidence showed that miR-127-5p did not affect postentry viral replication. Taken together, these results indicated that miR-127-5p inhibited EV71 replication by targeting the SCARB2 mRNA.
Insights
MicroRNA-127-5p inhibits Enterovirus 71 (EV71) infection by targeting its receptor, SCARB2. Upregulated miR-127-5p reduces viral replication, offering a potential therapeutic target for hand-foot-and-mouth disease.
Area of Science:
- Virology
- Molecular Biology
- Microbiology
Background:
- Enterovirus 71 (EV71) causes severe hand-foot-and-mouth disease in children.
- Understanding EV71 infection mechanisms is crucial for developing treatments.
Purpose of the Study:
- To investigate the role of microRNA-127-5p (miR-127-5p) in regulating EV71 infection.
- To elucidate the molecular mechanism by which miR-127-5p affects EV71.
Main Methods:
- Investigated miR-127-5p expression during EV71 infection.
- Analyzed the interaction between miR-127-5p and SCARB2 mRNA.
- Used miR-127-5p mimics and inhibitors to assess viral replication.
Main Results:
- miR-127-5p directly targets SCARB2, a key EV71 receptor.
- miR-127-5p expression increases during EV71 infection.
- Upregulating miR-127-5p inhibits EV71 replication; inhibiting it enhances replication.
- miR-127-5p acts at the pre-entry stage of viral infection.
Conclusions:
- miR-127-5p acts as a negative regulator of EV71 infection.
- Targeting SCARB2 mRNA by miR-127-5p is a key mechanism for inhibiting EV71.
- miR-127-5p represents a potential therapeutic target for EV71-related diseases.
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