Problem issues of the pathogenesis of inflammatory reaction and the course of coronavirus infection

Objective — to analysis and systematization of literature data about pathogenesis of the inflammatory reaction and the clinical course of coronavirus infection caused by SARS-CoV-2. Materials and methods. Access to various full-text and abstract databases was used for the search query «coronavirus», «COVID-19», «SARS-CoV-2» and their systematic evaluation was carried out. The most complete database of available literature sources (about 70) was obtainedon the molecular pathophysiology of COVID-19. Results and discussion. The results of the analysis of the molecular pathophysiology of COVID-19 showed that the biomedical terms associated with COVID-19/SARS-CoV-2 form several clusters: cluster 1 is inflammation and the formation of a cytokine storm; cluster 2 — pathophysiological justification of the treatment of coronavirus infection, cluster 3 — comorbid conditions. Analytics of cluster 1 showed one of the most interesting working hypotheses today is model of bradykinin storm. This hypothesis can explain the multisymptomatic nature of COVID-19, including some of its strangest manifestations. The essence of the theory of bradykinin is that, when the virus begins to affect the regulation of renin-angiotensin-aldosterone system (RAAS) through the activation of angio­tensin-converting enzyme type II, it causes the mechanisms that regulate bradykinin levels to fail. Bradykinin’s receptors repeatedly are sensitized and the body also ceases to efficiently break down bradykinin. ACE break down bradykinin, but when the virus suppresses its activity, it cannot work with the same efficiency. The end result of such an imbalance is the release of excessive amounts of bradykinin, due to its mass unrestrained accumulation with the formation of a phenomenon — bradykinin storm. According to the bradykinin hypothesis, this particular variant of the storm is ultimately responsible for the polymorbidity of the clinical picture and the fatal effects cause d by COVID-19. Conclusions. The bradykinin hypothesis of the development of a systemic inflammatory response in SARS-CoV-2 virus is a model that contributes to a better understanding of the pathogenesis and course of COVID-19 and adds novelty to data that are already known. It predicts almost all known symptoms today and offers quality treatments for the disease. Analysis of the processed data from the literature of cluster 2, devoted to the pathophysiological rationale treatment of coronavirus infection led to the role of vitamin D — as a nutrient involved in regulatory processes with participation of RAAS.