Cytokine storm and oxidative stress in severe COVID-19

Some patients infected with the SARS-CoV-2 virus show rapid progress to acute respiratory distress syndrome, multi-organ failure, and death. Acute respiratory distress syndrome is a large concern of death in COVID-19. Current therapeutic strategies focus on the virus itself and antiviral drugs are used to manage the disease. Unfortunately, the benefits of antiviral drugs are not satisfactory in every patient. It seems that the excessive inflammatory response rather than the virus titer is more relevant to the death. A brisk immune response generally destroys the virus but can cause significant local and longterm damage in tissues. In severe COVID-19, acute respiratory distress syndrome and multi-organ failure are associated with cytokine storm. Cytokine storm triggers the production of reactive oxygen species storm in immune system cells to destroy the virus. Although a certain amount of reactive oxygen species is helpful in the regulation of immune response and killing viruses, an excessive amount of reactive oxygen species damages the cellular lipids, proteins, and DNA. Extensive damage by reactive oxygen species results in apoptosis. Apoptotic death of endothelial and epithelial cells in the lungs plays important role in the development of acute respiratory distress syndrome in COVID-19 patients. Here, we will summarize the current molecular understanding of the vicious circle between the cytokine storm and oxidative stress that is an executive factor for cells. © 2021 Nova Science Publishers, Inc.