IN SILICO APPROACH TO PREDICT HUMAN-DERIVED MIRNA TARGETS AGAINST COVID-19

Background: MicroRNAs (miRNAs), small noncoding RNAs, regulate gene expression and play a crucial role in antiviral defense. Computational tools, including RNA22, RNAhybrid, and miRanda, were used to predict miRNA–mRNA interactions and identify human miRNAs with potential activity against the SARS-CoV-2 genome. Among the candidates, hsa-miR-6515-5p and hsa-let-7c-3p were selected for further analysis based on predicted binding sites within the viral genome. Objectives: By targeting viral RNA, this study aims to identify human miRNAs with potential antiviral activity against COVID-19. Additionally, molecular docking was employed to assess interactions between selected miRNAs and the viral genome and to predict their binding sites. Methodology: The SARS-CoV-2 genome and human miRNA sequences were retrieved and analyzed using CLC Workbench and miRBase. Potential target sites were predicted using RNA22, miRanda, and RNAhybrid, visualized in RStudio, and modeled in three dimensions using MC-Fold, RNAComposer, and UCSF Chimera. miRNA–mRNA interactions were evaluated through HNADOCK, while expression profiles were validated using the EVmiRNA and miRmine databases. Results: Multiple putative miRNA binding sites were identified across the SARS-CoV-2 genome, with frequent targeting of RNA-dependent RNA polymerase (RdRp) and other nonstructural proteins. Molecular docking revealed strong binding interactions between hsa-let-7c-3p and RdRp, as well as between hsa-miR-6515-5p and NSP3, suggesting their potential to inhibit viral replication. Conclusion: This study highlights the potential of human miRNAs to regulate SARS-CoV-2 transcription. The identified miRNAs, particularly hsa-miR-6515-5p and hsa-let-7c-3p, emerge as promising candidates for antiviral intervention. However, further in vivo validation is required to confirm their efficacy in inhibiting viral replication and to support the development of miRNA-based therapeutic strategies against COVID-19.