REVIEW: COVID-19 and Oxidative Stress

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B. V. Chernyak¹, E. N. Popova¹, A. S. Prikhodko^1,2, O. A. Grebenchikov³, L. A. Zinovkina², and R. A. Zinovkin^1,4,5,a*

¹Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119991 Moscow, Russia

²Faculty of Bioengineering and Bioinformatics, Lomonosov Moscow State University, 119991 Moscow, Russia

³Negovsky Scientific Research Institute of General Reanimatology, 107031 Moscow, Russia

⁴Institute of Mitoengineering, Lomonosov Moscow State University, 119992 Moscow, Russia

⁵Institute of Molecular Medicine, Sechenov First Moscow State Medical University, 119991 Moscow, Russia

^* To whom correspondence should be addressed.

Received July 27, 2020; Revised August 11, 2020; Accepted August 12, 2020

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Pathogenesis of the novel coronavirus infection COVID-19 is the subject of active research around the world. COVID-19 caused by the SARS-CoV-2 is a complex disease in which interaction of the virus with target cells, action of the immune system and the body’s systemic response to these events are closely intertwined. Many respiratory viral infections, including COVID-19, cause death of the infected cells, activation of innate immune response, and secretion of inflammatory cytokines. All these processes are associated with the development of oxidative stress, which makes an important contribution to pathogenesis of the viral infections. This review analyzes information on the oxidative stress associated with the infections caused by SARS-CoV-2 and other respiratory viruses. The review also focuses on involvement of the vascular endothelium in the COVID-19 pathogenesis.

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KEY WORDS: oxidative stress, endothelium, SARS-CoV-2, COVID-19, cytokine storm, oxidative stress

DOI: 10.1134/S0006297920120068

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