Abstract
COVID-19 is a systemic infection with a significant impact on the hematopoietic system and hemostasis. Reported findings indicate that immunosuppression, endothelial activation, and direct viral-mediated tissue damage rather than hyperinflammation-related injury mediates COVID-19 induced organ dysfunction. If direct infection drives injury, the vascular tissue is expected to be quite susceptible as it highly expresses angiotensin-converting enzyme-2 (ACE-2), which is essential for coronavirus uptake. Viral injury, disordered cytokine release, and damage-associated molecular patterns (DAMPs) induce localized microvascular inflammation, which triggers endothelial activation, leading to vasodilation and pro-thrombotic conditions. It has been shown that lymphocytes express the ACE-2 receptor on their surfaces thus, SARS-CoV-2 may directly infect those cells and ultimately lead to their lysis. Furthermore, the cytokine storm is characterized by markedly increased levels of interleukins and TNF –alpha, which may promote lymphocyte apoptosis. Apoptosis mediates lymphocyte depletion and inhibitory effects of lactic acid on lymphocyte proliferation.
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