Recently, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), has infected millions of individuals worldwide. While COVID-19 generally affects the lungs, it also damages other organs, including those of the cardiovascular system. Hypertrophic cardiomyopathy (HCM) is a common genetic cardiovascular disorder. Studies have shown that HCM patients with COVID-19 have a higher mortality rate; however, the reason for this phenomenon is not yet elucidated. Herein, we conducted transcriptomic analyses to identify shared biomarkers between HCM and COVID-19 to bridge this knowledge gap. Differentially expressed genes (DEGs) were obtained using the Gene Expression Omnibus ribonucleic acid (RNA) sequencing datasets, GSE147507 and GSE89714, to identify shared pathways and potential drug candidates. We discovered 30 DEGs that were common between these two datasets. Using a combination of statistical and biological tools, protein-protein interactions were constructed in response to these findings to support hub genes and modules. We discovered that HCM is linked to COVID-19 progression based on a functional analysis under ontology terms. Based on the DEGs identified from the datasets, a coregulatory network of transcription factors, genes, proteins, and microRNAs was also discovered. Lastly, our research suggests that the potential drugs we identified might be helpful for COVID-19 therapy.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has becoming globally public health threat. Recently studies were focus on SARS-CoV-2 RNA to design vaccine and drugs. It was demonstrated that virus RNA could play as sponge to host noncoding RNAs to regulate cellular processes. Bioinformatic research predicted a series of motif on SARS-CoV-2 genome where are targets of human miRNAs. In this study, we used dual-luciferase reporter assays to validate the interaction between 3’UTR of SARS-CoV-2 S (S-3’UTR) gene and bioinformatic predicted targeting miRNAs. The growth of 293T cells and HUVECs with overexpressed S-3’UTR was determined, while miRNAs and IL6, TNF-α levels were checked in this condition. Then, miR-296 and miR-602 mimic were introduced into 293T cells and HUVECs with overexpressed S-3’UTR, respectively, to reveal the underlying regulation mechanism. In results, we screened 19 miRNAs targeting the S-3’UTR, including miR-296 and miR-602. In 293T cell, S-3’UTR could inhibit 293T cell growth through down-regulation of miR-296. By reducing miR-602, S-3’UTR could induce HUVECs cell proliferation, alter the cell cycle, reduce apoptosis, and enhanced IL6 and TNF-αlevel. In conclusion, SARS-CoV-2 RNA could play as sponge of host miRNA to disturb cell growth and cytokine signaling. It suggests an important clue for designing COVID-19 drug and vaccine.