| Literature DB >> 28152384 |
Joseph Gutkoska1, Michael LaRocco1, Elizabeth Ramirez-Medina1, Teresa de Los Santos1, Paul Lawrence2.
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. Published by Elsevier Inc.Entities:
Keywords: Bio-therapeutic; Foot-and-mouth disease virus (FMDV); MiR); MiR-203a-3p; MiR-203a-5p; MicroRNA (miRNA; Sam68; Survivin
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Year: 2017 PMID: 28152384 DOI: 10.1016/j.virol.2017.01.019
Source DB: PubMed Journal: Virology ISSN: 0042-6822 Impact factor: 3.616