Complex mechanism of COVID-19 development

Abstract

Coronavirus infection (COVID-19) is an acute viral disease, which affects all vital organs and is caused by an RNA-genomic virus of the genus Betacoronavirus of the family Coronaviridae. This virus (SARS-CoV-2) enters the body through the respiratory tract and interacts primarily with Toll-like receptors of epithelial cells of the bronchi, alveoli, intestines and vascular endotheliocytes, as well as with angiotensin-converting enzyme 2 receptors. Toll-like receptors activate nuclear factor Kappa B in these cells, which initiates the formation of many cytokines (“cytokine storm”). SARS-CoV-2 affects type II pneumocytes by causing a termination of surfactant formation and, accordingly, alveolar shrinking and the formation of acute respiratory distress syndrome and also fibrosis on the interalveolar-capillary membrane and the formation of acute respiratory failure. SARS-CoV-2 and cytokines disrupt the function of vascular endothelial cells, which leads to endothelial dysfunction. In microvessels forms a mass formation of microthrombi, which causes the failure of organs and systems. “Cytokine storm” turns into cytokine sepsis with the formation of multiple organ dysfunction syndrome.