Open AccessComplex mechanism of COVID-19 development
Author(s) -
Sergey Bolevich,
C. C. Болевич
Publication year - 2020
Publication title -
sečenovskij vestnik
Language(s) - English
Resource type - Journals
eISSN - 2658-3348
pISSN - 2218-7332
DOI - 10.47093/2218-7332.2020.11.2.50-61
Subject(s) - cytokine storm , cytokine , receptor , coronaviridae , immunology , biology , ards , coronavirus , fibrosis , lung , pathology , medicine , covid-19 , disease , infectious disease (medical specialty) , biochemistry
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.