PATHOGENESIS OF CORONAVIRUS INFECTION COVID-19

Abstract

Coronavirus SARS-CoV-2, penetrates through the mucous membranes of the respiratory tract and enterocytes of the small intestine through ACE2 receptors. Most ACE2 is expressed on the surface of cells of the respiratory tract, especially on type I and II alveolocytes, which explains the lung damage in infected people. Disruption of the gas exchange process associated with damage to the alveoli and capillaries leads to hypoxemia and secondary (indirect) damage to internal organs and systems. The pathogen SARS-CoV-2, which uses the ACE2 receptor to penetrate cells, is promoted by proteases that are inside these cells. ACE2 activity is due, in particular, IFN, the role and participation of which in the infectious process is being studied. The development of systemic vasculitis due to the tropism of the glycoprotein of coronavirus to endothelial cells that have the ACE receptor also indirectly leads to pathological changes in the lungs, heart, brain, kidneys, gastrointestinal tract. As a result of endothelial dysfunction and programmed necrotic cell death (apoptosis and piroptosis) in COVID-19, there is a systemic violation of microcirculation in the vascular bed of various organs and systems, which characterizes the clinical manifestations and consequences in infected. The autoimmune mechanism of defeat of internals is not excluded also. Binding of SARS-CoV-2 to receptors on the cell surface leads to an inflammatory process with the production of pro-inflammatory cytokines, the concentration of which can be extremely high in the form of the so-called “cytokine storm” that underlies ARDS and MODS. The risk of death is directly associated with high serum IL-6 levels.

After 5-7 days from the onset of the disease there is interstitial pneumonia, initially focal, which quickly turns into drainage. The system of mononuclear phagocytes is affected; lymphopenia develops, IFN synthesis is suppressed. Coronavirus pneumonia can be complicated by the accession of bacterial flora, as evidenced by increased levels of procalcitonin in the serum, it also occurs when the patient’s condition worsens. In addition, the patient’s severity is accompanied by high levels of CRP, LDH, D-dimer, ferritin and the like. At the same time there are changes in the blood coagulation system. The level of hemoglobin decreases, which aggravates the hypoxic syndrome.

Pathomorphological changes of ARDS include acute exudative and productive phases. In the first phase, signs of diffuse alveolar damage, acute bronchiolitis, edema and hemorrhage of interstitial tissue predominate. The productive phase is characterized by the development of fibrosing alveolitis with the organization of exudate in the lumen of the alveoli and bronchioles. coronavirus infection can also cause serious damage to other internal organs and systems.

Thus, pathomorphological changes in infected SARS-CoV-2 are due to the direct action of nCoV, hyperactivity of the immune system, high levels of cytotoxicity of CD8 + T cells, autoimmune processes and the like.