This study states that Cellular invasion by the SARS-CoV-2 begins with binding of the viral spike protein to a transmembrane receptor, followed by viral membrane fusion with the cellular membrane after activation of the spike protein by cellular proteases. SARS-CoV-2 binds to the angiotensin-converting enzyme (ACE) 2 receptor, a protein coexpressed with the protease transmembrane serine protease 2 (TMPRSS2) in endothelial cells throughout the body. ACE2 is particularly abundant in the small intestine, kidney, lungs, and heart (5). ACE2 is also present in human adult and fetal brain, with highest expression in the pons and medulla oblongata (6). In mice, brain ACE2 protein is higher in the early postnatal period than in the adult, whereas ACE2 activity is similar (7). ACE2 is also expressed in components of the cerebral vasculature and blood-brain barrier (BBB): that is, the endothelium, pericytes, and contractile cells (8–10). Purkinje cells, cortical layer V neurons, astrocytes, and micrglia also express ACE2 and TMPRSS2 (10). SARS-CoV-2 may bind instead, or also, to the neuronal adhesion molecule neuropilin (1 and undergo activation by Furin, an ubiquitous protease, to allow entry into the host cell (11). Neuropilin 1 is a glycoprotein essential for normal nervous and cardiovascular system formation and function in vertebrates.

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