Schematic representation of mechanisms by which the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes mild disease in some patients and severe disease in others. In both cases, the virus enters human cells via binding to angiotensin-converting enzyme 2 (ACE2), a transmembrane receptor widely expressed in type II pneumocytes, macrophages, endothelial and other pulmonary cells [24, 25]. a) Mild disease (low incidence of coagulopathy and thrombosis, shorter hospital stay, low critical illness and mortality): these patients have low serum inflammatory cytokines and high tissue reparative growth factors such as epidermal growth factor (EGF), platelet derived growth factor (PDGF), and interleukin (IL)-7 [5]. VEGF: vascular endothelial growth factor. b) Severe disease (high incidence of micro- and macrovascular thrombosis, longer hospital stay, high critical illness, and mortality): many of these patients have cytokine storm, with high serum inflammatory cytokines (such as IL-6, IL-1, IFN-γ) and markers of endothelial activation such as von Willebrand factor (vWF), factor 8 coagulant (F8) and soluble P-selectin (sP-sel), resulting in endothelialitis and microvascular thrombosis [5, 15, 27]. Markedly elevated IL-6 leads to lymphopenia and immunoparalysis which is partially restored by IL-6 blockade [4, 32]. NET: neutrophil extracellular trap; CRP: C-reactive protein.