Figures & data
Figure 2 Activation of the spike protein by TMPRSS2 at (or close to) the cell surface, leading to fusion of the viral membrane with the plasma membrane.
![Figure 2 Activation of the spike protein by TMPRSS2 at (or close to) the cell surface, leading to fusion of the viral membrane with the plasma membrane.](/cms/asset/87e2bd77-9d7a-49e3-9d08-c8c11132ff76/djbm_a_12167170_f0002_c.jpg)
Table 1 Incidence of Thrombotic Complications Among COVID-19 Patients
Figure 3 Pathogenesis of thrombotic complications of COVID-19. SARS-CoV2 infection induces endothelial damage triggering endothelial release of cytokines, increasing capillary permeability. PAMPs and DAMPs induced activation of neutrophils, and macrophages results in localized production of cytokines, procoagulants, and complement activation, leading to further endothelial damage and tissue factor release. Endothelial damage exposes collagen and other prothrombotic mediators leading to thrombus formation.
![Figure 3 Pathogenesis of thrombotic complications of COVID-19. SARS-CoV2 infection induces endothelial damage triggering endothelial release of cytokines, increasing capillary permeability. PAMPs and DAMPs induced activation of neutrophils, and macrophages results in localized production of cytokines, procoagulants, and complement activation, leading to further endothelial damage and tissue factor release. Endothelial damage exposes collagen and other prothrombotic mediators leading to thrombus formation.](/cms/asset/2c2cf0c2-9fdd-4368-b14e-d9e6030aa3e8/djbm_a_12167170_f0003_c.jpg)