Abstract

The COVID-19 pandemic has shown that the outcomes of the disease depend on many factors and, above all, genetic mutations in the immune system. A special role in the outcome of COVID-19 is attributed to a defect in the genes of inflammatory cytokines, the excess of which leads to endothelial dysfunction with damage to vital organs, often with lethal outcome. The aim of the study was to investigate polymorphisms of IL-1β (T-31C), TNF-α (G-308A), IL-10 (G-1082A), IL-17(G-197A), IL-4 (C-589T) genes in COVID-19 patients depending on the outcome of the disease. Methods. We examined 142 patients diagnosed with COVID-19, of whom 122 patients ended the disease with recovery (group 1) and 20 patients died (group 2). Polymorphisms of IL-1β (T-31C), TNF-α (G-308A), IL-10 (G-1082A), IL-17(G-197A), IL-4 (C-589T) genes by genetic method were investigated in COVID-19 patients depending on the outcome of the disease. Results. Analysis of IL-1β (Т-31С), TNF-α (G-308A), IL-10 (G-1082A), IL-17(G-197A), IL-4 (С-589Т) gene polymorphisms in COVID-19 patients showed no statistical differences in recovered patients compared to deceased patients. Statistically significant differences were found in IL-10 gene (genotype -1082A/A). It was found to be recorded 3.8 times more frequently in the group of COVID-19 deceased patients compared to recovered patients (p=0.001; OR=1.027). Conclusion. Among the studied polymorphic variants of IL-1β (T-31C), TNF-α (G-308A), IL-10 (G-1082A), IL-17(G-197A), IL-4 (C-589T) genotype -A/A polymorphism of IL-10(G-1082A) was a significant marker of increased risk of COVID-19 lethal outcome, which can be used as a possible predictor of unfavorable outcome of the disease.

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