«After the virus (covid-19) enters the airways, its replication occurs, and the immune innate response begins with the activation of macrophage and dendritic cell via Toll-like and NOD receptors against the production of inflammatory cytokine and reactive oxygen species (ROS). The consequent spread to the blood has two consequences: 1) erythrocytes are damaged by ROS and other inflammatory mechanisms leading to the generation of heme and free iron; and 2) activated macrophages and neutrophil produce respiratory bursts generating superoxide radicals and H2O2 leading to oxidative stress. Oxidative stress plus free iron converts soluble plasma fibrinogen into abnormal fibrin clots in the form of dense matted deposits (DMD resistant to the enzymatic degradation; blood clots), leading to microthrombosis in the vascular system and the pulmonary microcirculation. The cytokine storm occurs through the upregulation of cytokine expression via NF-κB. After this scenario is established, the cytokine storm induces oxidative stress via macrophage and neutrophil respiratory burst activity, and oxidative stress induces the cytokine storm. This cycle provokes serious tissue damage independent of the virus. In addition, mitochondria produce ROS, which increases iNOS expression via NF-κB and, consequently, NO formation. NO induces dysfunctional mitochondria that, in turn, results in cytopathic hypoxia. Moreover, the virus inhibits Nrf2, responsible for the increase in enzymatic antioxidants, establishing the oxidative stress. Overall, low hemoglobin-carrier, high lung proteinaceous exudate lead to pulmonary hypoxia, cytopathic hypoxia and endothelium damage, and disseminated coagulation results in multiple organ collapse.»