Analysis of the Expression Profile in COVID-19 Patients in the Russian Population Considering Disease Severity, Mortality, and Cytokine Storm

<b>Background/Objectives</b>: The COVID-19 pandemic has posed a significant challenge to global healthcare systems and has prompted a need for a better understanding of the molecular mechanisms underlying SARS-CoV-2 infection. This study aims to analyze differential gene expression in COVID-19 patients to identify regulatory genes influencing key pathways involved in disease progression. <b>Methods</b>: We conducted a transcriptomic analysis of patients admitted to the Infectious Disease Department of City Hospital No. 40, confirmed with SARS-CoV-2 via PCR. The study received ethical approval (protocol No. 171, 18 May 2020), and all participants provided informed consent. Total RNA was extracted from blood samples, followed by RNA sequencing using the DNBSEQ-G400 platform. Differential gene expression was analyzed using the Mann-Whitney test, and Gene Ontology enrichment analysis was performed to identify relevant biological processes. <b>Results</b>: Our analysis revealed significant number of differentially expressed genes within studied groups (severity, outcome, cytokine storm and paired samples). These genes are involved in key regulatory and signal transduction pathways governing immune responses, intercellular communication, and the metabolism of various compounds. Furthermore, we identified genes <i>ALOX15</i>, <i>PRL</i>, <i>FLT3</i>, <i>S100A8</i>, <i>S100A12</i>, <i>IL4</i>, <i>IL13</i>, and a few others as master regulators within the studied pathways, which represent promising candidates for further investigation as potential therapeutic targets. <b>Conclusions</b>: This study highlights critical gene expression changes associated with COVID-19 severity and outcomes, identifying potential biomarkers. Our findings contribute to the understanding of the molecular drivers of COVID-19 and suggest new avenues for therapeutic interventions aimed at modulating immune responses.