COVID-19 and its implications for thrombosis

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