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Updated: Jun 20, 2026

MicroRNA-based Regulation of Picornavirus Tropism
Published on: February 6, 2017
Host-virus miRNA crosstalk in ebola virus disease
Ahmed S Doghish1,2, Gharieb S El-Sayyad3, Hamdi Bendif4
1Biochemistry and Molecular Biology Department, Faculty of Pharmacy (Boys), Al-Azhar University, Nasr City, Cairo, 11231, Egypt.
None:
Ebola virus disease (EVD) is a severe and often fatal illness characterized by aggressive viral replication, dysregulated immunity, and multi-organ dysfunction. Emerging evidence demonstrates that microRNAs (miRNAs), both host-derived and virus-encoded, play essential regulatory roles throughout the course of Ebola virus (EBOV) infection. Host miRNAs are widely dysregulated across different tissues and cell types during infection and contribute to antiviral defense, viral persistence, immune suppression, endothelial dysfunction, and hemorrhagic pathology. In parallel, EBOV generates its own miRNA-like molecules that target key host signaling pathways, including nuclear transport, interferon responses, apoptosis regulation, and inflammatory cascades. These dual layers of miRNA crosstalk shape infection outcomes by modulating viral replication, immune evasion, cellular adhesion, and vascular leakage. Additionally, several host and viral miRNAs show strong potential as diagnostic and prognostic biomarkers, and recent work suggests that therapeutic modulation through miRNA mimics or inhibitors may offer new antiviral strategies. This review synthesizes current evidence on miRNA interactions during EBOV infection and outlines their implications for disease pathogenesis, clinical outcomes, and translational applications.
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