Intralipid blocks the entry of the SARS-Cov2/COVID/19 virus into cells by maintaining receptor a leucine-rich repeat containing 15 (LRRC15), an angiotensin-converting enzyme 2 receptor competitor.

The effectiveness of Intralipid against SARS-Cov2/COVID/19 with Multiple Organ Dysfunction Syndrome (MODS) prevention or regression is described in the original scientific paper [1]. Intralipid at Oxidative and Nitro-Galogenic stress in patients with SARS-Cov2 / COVID /19, favors the predominance of the membrane-cytoprotective action of Reactive Oxygen Species (ROS) / Reactive Nitrogen Species (ROS/RNS) over the membrane-to-destructive action, restoring the balance between [ROS /AS] / [RNS / ANOS]. Membrane-cytoprotective mechanism Intralipid is due to a decrease in ROS and RNS and an increase in the activity of the Antioxidant System (AS) and Anti Nitro Oxidant System (ANOS), stopping lipid peroxidation (LPO), reducing Electro-Ion Membrane Distress Syndrome (Maria&Irina Vasilieva syndrome) [2], accelerates the regeneration of endothelial and epithelial cells of the alveolar acinus, restoring gas-respiratory metabolism and the predominance of physiological cell apoptosis over necrosis. Intralipid at SARS-Cov 2 / COVID / 19 opposes Microcirculatory Mitochondrial Distress syndrome (MMDS) by Microcirculatory - Mitochondrial Recruitment; as a result of which pCO2 (AVgap) <6 mm Hg, since LPO decreases and at the level of mitochondrial membranes, improving the function of Mitochondrial permeability transition pore-dependent Ca uniporter, mPT pore, support energy metabolism, eliminating energy deficits, restoring Extreme / Abnormal myelopoiesis and impaired autophagy (mitophagy). Thus, Intralipid has been shown in the strategy of targeted treatment of LPO in Oxidative and Nitro-Galogenic stress in patients with SARS-Cov2 /COVID / 19.