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COVID-19 kills people like this: the Spike binds to ACE2, downregulating ACE2. ACE2 can no longer inactivate bradykinin. Bradykinin promotes intracellular calcium rise and cAMP/cGMP activity, triggering various factors that lead to ROS and prostaglandin production. Superoxide reacts with nitric oxide to make peroxynitrite. Peroxynitrite uncouples nitric oxide synthase so that it produces tons of extra superoxide in a vicious cycle that destroys all available NO. The virus's own proteins down-regulate Nrf2 antioxidant activity. Superoxide, hydrogen peroxide, and hypochlorous acid start building up. Iron is stripped out of heme by hypochlorous acid. Iron, superoxide, and hydrogen peroxide make hydroxyl radicals through the Haber-Weiss and Fenton reactions. Hydroxyl radicals attack various lipids/PUFAs and produce various lipid peroxidation byproducts. Oxidized lipids feed into toll-like receptors and trigger autoantibody production and ferroptosis. The extreme oxidative stress promotes the phosphorylation of various triggers of NF-kB and AP-1, promoting IL-6 and TNF-alpha release, along with numerous other inflammatory cytokines and chemokines. This process continuously summons neutrophils, which blast everything in sight with NETs and degranulation products (superoxide dismutase and myeloperoxidase that make more hydrogen peroxide and hypochlorous acid), and monocytes, which actually get infected by the virus and start the same vicious cycle over. Neutrophilia and sepsis set in, along with pulmonary angioedema, coagulopathy, and ARDS. The endothelial lining of blood vessels and the lining of the alveoli in the lungs are utterly ruined by inflammation, edema, and oxidative stress. In extreme cases, multiple organ failure and catastrophic clotting sets in.