Host microRNA-203a Is antagonistic to the progression of foot-and-mouth disease virus infection
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Updated: Mar 8, 2026
MicroRNA-based Regulation of Picornavirus Tropism
Published on: February 6, 2017
Joseph Gutkoska1, Michael LaRocco1, Elizabeth Ramirez-Medina1
1Plum Island Animal Disease Center Foreign Animal Disease Research Unit (FADRU) Agricultural Research Service (ARS), United States Department of Agriculture (USDA), 40550 Route 25, Orient Point, NY 11957, United States.
Abstract:
Sam68 was previously shown to be a critical host factor for foot-and-mouth disease virus (FMDV) replication. MicroRNA (miR) miR-203a is reportedly a negative regulator of Sam68 expression both in vitro and in vivo. Here, transfection of miR-203a-3p and miR-203a-5p mimics separately and in combination in a porcine cell line followed by FMDV infection resulted in diminished viral protein synthesis and a 4 and 6log reduction in virus titers relative to negative controls, respectively. Unexpectedly, Sam68 expression was increased by miR-203a-5p transfection, but not miR-203a-3p. miR-203a-5p also down-regulated Survivin expression, which was predicted to play a role in FMDV infection. Moreover, miR-203a-5p but not miR-203a-3p affected a reduction in FMDV viral RNA. These effects were not replicated with a related Picornavirus, suggesting FMDV specificity. Importantly, miR-203a-3p and miR-203a-5p impaired FMDV infection across multiple FMDV serotypes. We concluded that miR-203a-3p and miR-203a-5p represent attractive potential naturally occurring bio-therapeutics against FMDV.
Insights
MicroRNAs miR-203a-3p and miR-203a-5p significantly reduce foot-and-mouth disease virus (FMDV) replication in porcine cells. These microRNAs show potential as natural therapeutics against FMDV infection.
Area of Science:
- Virology
- Molecular Biology
- Biotechnology
Background:
- Sam68 is a crucial host factor for foot-and-mouth disease virus (FMDV) replication.
- MicroRNA (miR) miR-203a is known to negatively regulate Sam68 expression.
Purpose of the Study:
- To investigate the role of miR-203a-3p and miR-203a-5p in FMDV infection.
- To evaluate the potential of these microRNAs as antiviral therapeutics.
Main Methods:
- Transfection of miR-203a mimics into porcine cells followed by FMDV infection.
- Analysis of viral protein synthesis, viral titers, Sam68 and Survivin expression.
- Assessment of FMDV RNA levels and testing against multiple FMDV serotypes.
Main Results:
- miR-203a-3p and miR-203a-5p significantly reduced FMDV titers and viral protein synthesis.
- miR-203a-5p increased Sam68 expression and down-regulated Survivin, impacting viral RNA.
- The antiviral effects were specific to FMDV and effective across multiple serotypes.
Conclusions:
- miR-203a-3p and miR-203a-5p demonstrate potent antiviral activity against FMDV.
- These microRNAs represent promising candidates for naturally occurring bio-therapeutics against FMDV.
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