The family of coronaviruses represents rather extensive group of viruses which are capable to cause diseases both in the person, and in animals. At the same time coronaviruses can cause diseases which weight varies from asymptomatic forms of an acute respiratory infection to heavy respiratory syndromes like MERS in people. The virus causing a new koronavirusny infection (SARS-CoV-2) belongs to high-pathogenic viruses.
As entrance gate for infection of SARS-CoV-2 serves the epithelium of the upper airways and also an epithelium of a stomach and intestines. At the same time the first stage is infection with a virus of target cells which the corresponding receptors have (an angiotensin-converting enzyme of the II type — APF2). Further cellular transmembrane serinovy protease of the second type (TSP2) leads to linking of a virus with APF-2 and there is an activation of a virus protein of S which is necessary for penetration of SARS‑CoV‑2 into a cell. Now it is considered that high concentration of receptors for APF2 is available on cells of a respiratory system, an epithelium of a gullet and intestines and also in cells of a hypophysis, a hypothalamus, adrenal glands, hearts, an endothelium of vessels. At the same time the main target for a coronavirus of new type are cells of alveoluses of the second type, this moment explains the most often found damage of lungs at a new koronavirusny infection.
At the same time, there are data on defeat at a koronavirusny infection and an epithelium of other bodies, in particular, of a stomach, a small and large intestine. It leads to emergence of the relevant clinic of a gastroenterocolitis. Also there are data on defeat of an endothelium of vessels, kidneys, a myocardium and other bodies, leads to emergence of the relevant clinic of a disease. However all these data demand further studying, observation and assessment. The defeat subject at a koronavirusny infection of bodies and cells of the immune system is also insufficiently studied, in particular, defeat of lymphocytes on the apoptosis mechanism which leads to emergence of a lymphopenia and is predictively adverse criterion of a disease. There are data on involvement in pathological process of macrophages in and other leukocytes.
The observed picture of defeat of various bodies and systems at a new koronavirusny infection led to the theory which essence consists in existence of specific receptors for SARS-CoV-2 on a surface of cells, in addition to already mentioned APF2 receptor. As option, CD147 role in penetration of a virus into a cell is considered and studied.
Rather characteristic symptom of COVID-19 is defeat of a system of sense of smell (anosmia) that can demonstrate damage of the central nervous system and also immediate effect of a virus on olfactory receptors or vessels which carry out blood supply of a nasal cavity. Also the virus can disseminate through a sievebone plate and by that to cause damage of a brain.
The significant role in a pathogeny of a new koronavirusny infection is played by a so-called tsitokinovy storm when there is a disturbance of regulation of synthesis of pro-inflammatory, immunoregulatory, antiinflammatory cytokines and chemokines, such as IL-1, IL-2, IL-6, IL-7, IL-8, IL-9, IL-10, IL-12, IL-17, IL-18, granulotsitarny colony stimulating factor (G-KSF), granulotsitarno-macrophagic colony stimulating factor (GM-KSF), tumor necrosis factor α (ФНОα), ИФНγ-индуцируемый protein 10, IFNα and IFNβ, the monocytic hemoattraktantny protein 1 (MHP1), macrophagic inflammatory protein 1α (MVB1α) and also inflammation markers (A S-jet protein, ferritin). It leads to pathological activation of congenital and artificial immunity. The main target organ at this option of a tsitokinovy storm are lungs, it is caused by the raised SARS-CoV-2 tropnost to pulmonary fabric. On the other hand, such inadequate immune response at a new koronavirusny infection is also limited to often pulmonary fabric, leading to development acute respiratory a distress syndrome.
Syndrome of activation of macrophages or similar to it cellular inflammation is also characteristic of severe forms of a koronavirusny infection. This process which enhances severity of local vascular dysfunction which includes microthrombosis and hemorrhages that more leads to development of a pulmonary intravascular coagulopathy, than system disseminate intravascular coagulation. Considering that at patients with a critical current of COVID-19 endothelial dysfunction and a coagulopathy, fibrinferments with existence of antibodies to phospholipids develops. The clinical picture at the same time reminds an anti-phospholipidic syndrome.