The review describes pathogenesis of the disease caused by the new SARS-CoV-2 virus. It infects the human cells by linking angiotensin-converting enzyme-2 (ACE2) and a number of other receptors. The virus imbalances the renin-angiotensin system, results to vasoconstriction and acts like pro-inflammatory agent. ACE2 is exposed on the alveolar epithelium cell surface. It is the main gates for virus entering and damaging of the respiratory system resulted in an acute respiratory distress syndrome. The injuring of the pulmonary vessel endothelium is the most important part of the COVID-19 pathogenesis. ACE2 of the endothelial and smooth muscle cell surface upon the SARS-CoV-2 infection facilitates the injury of cardiovascular system. The development of endotheliitis induced by «cytokine storm» leads to the main signs of the disease and the multiple disorder of the microcirculation. The investigation of that condition has a prognostic value and determines the treatment especially in critically ill patients. Systemic endothelial dysfunction upon the COVID-19 largely triggers the hemostasis disorders. High activity of platelets adhesion and aggregation, blood coagulation in died COVID-19 patients, disorder of fibrinolysis system functional activity could be induced by the endothelium activation. The unchanged anticoagulation blood activity in the COVID-19 patients distinguishes them from the patients with disseminated intravascular coagulation. Monitoring of the hemostasis system in COVID-19 is important for the disease severity assess and its prognosis, for justin-time correction of detected deviations.