The paper considers the possible mechanism of the pathogenesis of COVID-19 caused by SARS-COV-2, associated with damage to red blood cells, which the authors attribute to the main key target that triggers a cascade of reactions leading to multiple organ failure. The paper presents morphological evidence for the presence of pathological forms of erythrocytes characteristic of various anemias in the blood vessels and parenchyma of damaged lungs of patients with COVID-19. The death of red blood cells leads to cell ischemia and anemia. The defeat of brain neurons, blood vessels and hematotissue barriers in organ systems is a consequence of ischemia due to the impossibility of transferring hemoglobin by damaged erythrocytes and ends at the terminal stages of the development of the disease with their dysfunction. Adaptive erythropoiesis with an increase in erythropoietin secretion is especially dangerous for patients suffering from hypertension, and then it is impossible, since all organs involved in the synthesis of erythropoietin are damaged. In this case, the synthesis of hemoglobin is also disrupted due to a deficiency of iron and cyancobolamin, whereas toxic iron and hemosiderin are deposited in the tissues. K E y w o r d s-COVID-19, SARS-COV-2, erythrocytes, hemoglobin, erythropoiesis, viruses, pathogenesis of COVID-19.
Rapid development in 2020 of the COVID-19 pandemic caused by SARS-CoV-2 initially indicated signifi-cant involvement of the immune system. However, information on specific changes in organs of the immune system is still limited. A wide range of alterations was revealed in our study: from pronounced devastation of B-dependent and T-dependent zones of lymphoid tissue, reminiscent of changes in HIV infection at the AIDS stage, to hyperplasia of the tissue of lymph nodes and spleen of varying degrees. Analyzing the literature data, we focused on the fact that pathomorphological changes revealed in the autopsy studies of patients with a severe COVID-19 were accompanied by premortal lymphopenia in most cases. However, the cause of lymphopenia in COVID-19 has not yet been disclosed, authors of the review hypothesized that unregulated apoptosis of circulating lymphocytes is one of the potential lymphopenia inductors. Cytokine activation (“cytokine storm”) may be associated with lymphoid organs’ atrophy, which also contributes to a decrease in the circulating lymphocyte count. There is no doubt about the relevance of further identification of the immune cell apoptosis as one of the causes of lymphopenia and immune dysfunction in COVID-19 patients, which has prospects for pharmacological developments to manage lymphocytic apoptosis. Keywords: coronavirus infection, COVID-19, pathomorphology, lymphopenia, lymph nodes, spleen, lym-phocytic apoptosis
Introduction. When studying COVID-19 pathology, considerable attention is paid to the damage to the respiratory and cardiovascular systems, which are associated with the manifestation of the infection. Data on changes in the organs of the lymphatic system are yet scarce. To date, COVID-19 is sure to cause the dysfunction of the immune system; however, information about the damage to the lymph nodes is ambiguous. The aim of the study was to characterize morphological changes in the hilar lymph nodes of patients who died from a new coronavirus infection COVID-19 in Vladivostok in 2021. Materials and methods. A morphological study of the lymph nodes was performed in 20 patients who died from the new coronavirus infection, diagnosed in vivo using a PCR test. The controls were patients who did not have diseases of the hematopoietic and lymphoid tissue in their medical histories but who died a violent death. The material for histological examination was processed according to generally accepted methods. Results. In all patients, we identified lymphadenopathy with hypoplasia of lymphoid tissue of varying severity. In the cortex, lymphatic follicles were detected, mainly without light (germinal) centers, as well as follicles with a pronounced rarefaction of cells and exposure to the reticular stroma, with no visualization of the paracortical zone. According to the severity of reactive changes in the T- and B-dependent zones of the lymph nodes, we distinguished two types of lymphadenopathy: 1) mixed follicular type; 2) follicular involution with lymphoid depletion. Conclusion. Pathological changes in the hilar lymph nodes of the lungs in patients who died from COVID-19 indicated immunosuppressive effects of the SARS-CoV-2. The pathologic changes in lymph nodes manifested with lymphocytic depletion in T- and B-dependent zones. This indicates a deficiency of cellular and humoral immunity in moderate and severe COVID-19. Keywords: coronavirus infection, COVID-19, pathomorphology, lymph nodes, lymphocytic depletion, immunodeficiency
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