Fundamental Basis of COVID-19 Pathogenesis

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Abstract At the end of 2019, a new coronavirus infection occurred in the People’s Republic of China with an epicentre in the city of Wuhan. On February 11th, 2020, the World Health Organization assigned the official name of the infection caused by the new coronavirus – COVID-19. COVID-19 has affected people from all over the world given that the infection was noted in 200 countries resulting in annunciation of the pandemic situation. Human corona viruses cause mild to moderate respiratory infections. At the end of 2002, a new coronavirus appeared (SARS-CoV), the causal agent of atypical pneumonia, which caused acute respiratory distress syndrome (ARDS). The initial stage of COVID-19 infection is the penetration of SARS-CoV-2 into target cells that have angiotensin converting enzyme type II receptors. The virus enters the body through the respiratory tract and interacts primarily with toll-like receptors (TLRs). The events in SARS-Cov-2 induced infection follow the next scenario: epithelial cells via TLRs recognize and identify SARS-Cov-2, and after that the information is transmitted to the transcriptional NF-κB, which causes expression of the corresponding genes. Activated in this way, the epithelial cells begin to synthesize various biologically active molecules. The results obtained on preclinical material indicate that ROS generation increases and the antioxidant protection decreases, which plays a major role in the pathogenesis of SARS-CoV, as well as in the progression and severity of this respiratory disease.