In silico approach to identify the relationships between COVİD-19 and coronary artery disease/rheumatoid arthritis

Abstract

Global public has been threatened by the coronavirus disease 2019 (COVID-19) pandemic which led to nearly 15 million deaths around the world. People with complex and chronic diseases usually have more severe COVID-19 symptoms than the general population. Mounting evidence indicates individuals with coronary artery disease (CAD) and rheumatoid arthritis (RA) have worse COVID-19 outcomes yet the underlying mechanism still needs to be explored. The aim of our study is to reveal in silico evidence for the molecular mechanisms shared by COVID-19, CAD and RA pathogenesis which may aggravate the COVID-19 disease severity. Public datasets (GSE164805 and GSE23561) were downloaded from the Gene Expression Omnibus (GEO) database and analyzed for differential expression analysis (DEG). Identified differential expressed genes (DEGs) were further analyzed to find common DEGs, common pathways, hub genes, transcription factors (TFs) and microRNAs (miRNAs). Our study identified common hub genes, miRNAs, TFs and shared mechanisms in both mild and severe COVID-19-CAD patients and mild and severe COVID-19- RA patients. We also uncovered that mild and severe forms of COVID-19 differ in potential biomarkers, mechanisms, miRNAs and TFs in both CAD and RA patients. Our study is the first study investigating the potential shared mechanisms, biomarkers, TFs and miRNAs between COVID-19 and CAD patients and COVID-19 and RA patients. Our results could shed on light to the patient management strategies with CAD with COVID-19 and patients with RA with COVID-19 based on the severity of the COVID-19 disease.