Over the past 20 years, aggressive coronavirus infections have invaded the world at least twice: in 2002—2003, when 26 countries were affected by the SARS-CoV (Severe Acute Respiratory Syndrome) epidemic with a main peak in February 2003 and a lethality rate of 10%, and in 2012—2013, when 27 countries of the world were attacked by the MERS-CoV (Middle East respiratory syndrome) coronavirus with a lethality of up to 35%. However, none of the epidemics has caused such a violent global reaction as the pandemic-announced invasion of the coronavirus SARS-CoV-2 (COVID-19) in 2019. The insidiousness of this virus is recognized in that, the majority carries the disease in a mild form, in severe cases, the percentage of which has yet to be established, often including patients with chronic pathologies, a week after the onset, the disease can developed a) cytokine storm, b) synthesis of prostaglandins, c) induction of secondary bacterial infection, d) hypercoagulation, in case of developing pulmonary insufficiency as therapeutic targets of the initial stage of SARS-CoV-2 coronavirus infection. This review introduces the reader to inflammatory mediators based on the interaction between the virus, bacteria and the host’s immune system. Inflammation spread’ mechanisms include: a) «cytokine storm»; b) synthesis of prostaglandins; c) induction of secondary bacterial infection; d) hypercoagulation, in case of developing pulmonary insufficiency as a target of therapeutic effects of the initial stage of coronavirus SARS-CoV-2. This review also discusses initial drug therapy, with a focus on the benefits of aspirin, aimed at suppressing the development of inflammatory processes.