Figure 1. a) Docking approach of the spike protein with the host cell membrane, which presents three main receptors: ACE2, CD147 and Sialic Acid (SA); SA is expressed on the membrane glycoproteins and on the outer site of the other two receptors. b) The two subunits of the spike protein (S1 and S2), derived from priming and cleavage by hydrolases (TMPRSS2) and furins, contact host cell membrane: S1 receptor binding domain (RBD) attach ACE2 and CD147 through SA and directly SA on the membrane glycoproteins; S2 enters the lipid layer of the cell membrane. c) Upper part: normal hepcidin-ferroportin axis; lower part: COVID-19 situation, with hyper-concentrated plasma hepcidin molecules that bind the extracellular portion of the transmembrane ferroportin, thus blocking iron extracellular transport and favoring intracellular ferritin accumulation. d) Decrease of the membrane potential (less negatively charged), which is altered by the formation of several dipoles between SA negative and S1 positive; consequent opening of the cation channels, especially of the voltage gated calcium channels (VGCC), with intracellular entry of cations, primarily calcium and iron. e) Cell homeostasis, after cation entry, rapidly brings closure of VGCC and cation channels (1 intracellular oscillation with one peak of cations); simultaneous viroporin action of membrane channeling which brings opening of new channels and re-entry of cations (2 intracellular oscillation with a second peak of cations). f) Ferroptosis: excessive cation concentration, increase of free radicals, depletion of glutathione peroxidase 4 (GPX4), lipoperoxidation of membranes and organelles, mitochondria degeneration.