Molecular and cellular mechanisms of central nervous system alteration in COVID-19

Abstract

The ongoing coronavirus disease 2019 (COVID-19) pandemic dictates the need to study the molecular and cellular mechanisms of interaction between the pathogen and the human body. The manifestation of neurological symptoms in some patients with COVID-19 is a problem for neuroscientists due to the insufficiently understood pathomorphogenesis of the disease. This review systematizes the literature data reflecting the ways of penetration of SARS-CoV-2 into the brain, features of its interaction with neurons, neuroglia, and immune cells. It has been shown that the main mechanisms of SARS-CoV-2 neuroinvasion are presumably retrograde axonal transport along the fibers of the olfactory and vagus nerves; penetration through the damaged blood-brain barrier (BBB) or migration of immunocompetent cells containing viral particles through the intact BBB. It was found that virusinducible neuronal death is caused not only by a direct cytotoxic effect, but also due to dysregulation of the reninangiotensin system of the brain and the release of a large amount of inflammatory cytokines as a manifestation of a “cytokine storm”. The participation of neuroglial cells in the initiation and maintenance of neuroinflammatory and neurodegenerative processes due to the activation of their proinflammatory phenotype has been demonstrated. The role of mast cells in antiviral defense mechanisms and inflammatory reactions is discussed.

Comprehensive biotechnical system for screening risk-based diagnosis of COVID-19 and post-COVID syndrome

“…Two volunteers of the control group were identified who, according to the resource www.covid19diagnosis.ru, had been ill with COVID-19 about 12 and 18 months ago. Figures 3,4 and 5,6 show that the first conclusion from the results of this study was the understanding that in the early period after COVID-19, patients showed a significant decrease in baseline impedance during light exercise. The reason for this is most likely the massive suffering of the patency of the capillaries of the hemomicrocirculatory bed (HMCB) due to micro thrombosis caused by the new coronavirus infection SARS-CoV-2, which is confirmed by numerous pathological studies [18,19].…”

“…The pathogenesis of the post-COVID syndrome is based on the systemic suffering of the hemomicrocirculatory bed of tissues and organs, triggered by the processes of thrombus formation due to a radical change in the hemorheological properties of blood [ 6 , 7 , 8 ]. And at present, there are no hardware or biochemical systems that make it possible to assess the severity of this process in vivo, only postmortem histological examination [ 9 , 10 , 11 ].…”