CHANGES IN CELLULAR PARAMETERS IN PERIPHERAL BLOOD ANALYSIS DURING COVID-19 INFECTION AND THEIR PATHOGENETIC ASPECTS
DOI:
https://doi.org/10.32782/2306-2436.15.1.2025.322Keywords:
peripheral blood, cellular composition, coronavirus infection, pathogenesisAbstract
Peripheral blood disorders and the mechanisms of their occurrence in severe acute respiratory syndrome caused by the SARS-CoV-2 coronavirus remain not fully understood, but are of practical importance. The aim of the study was to review the literature containing data on changes in cellular parameters in the analysis of peripheral blood and their pathogenesis in COVID-19 infection. The most common hematological changes included: lymphocytosis and lymphocytopenia, neutrophilia, mild thrombocytopenia, and less commonly thrombocytosis. The ratio of lymphocytes to monocytes is usually low, but could be normal or elevated. SARS-CoV-2 RNA load and lymphocyte count, CD4+ T-lymphocyte count, and CD8+ T-lymphocyte count had a linear negative correlation. Researcher reports vary on white blood cell counts in patients with COVID-19. Patients with COVID-19 are predisposed to eosinopenia. Potential mechanisms leading to a deficiency of lymphocytes include the following: the virus can directly affect lymphocytes, which leads to their death; lymphocytes express the coronavirus receptor, angiotensin-converting enzyme, which is the target of the virus; apoptosis of lymphocytes can be caused by a cytokine storm, the activation of which is associated with atrophy of lymphoid organs, including the spleen, by the direct influence of the virus; the concomitant lactic acidosis inhibits lymphocyte proliferation by blocking the export of lactic acid in T cells. The indicator of lymphocytopenia is an undoubted marker of the severity of the course of COVID 19. Like most viruses that affect the hematopoiesis and the immune system, COVID-19, due to inflammatory mechanisms and effects on the myelopoiesis system, optimizes the release of immature blood cells from the bone marrow. SARS-CoV-2 can enter hematopoietic stem/progenitor cells and the microenvironment via ACE2, CD13, or CD66a receptors, resulting in cell apoptosis, inhibition of cell proliferation, and pancytopenia.
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