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inflammation and oxidative stress. Beyond augmentation of immune dysfunction and inflammation there is adverse effects on the vascular endothelium. The HIV accessory protein Nef has been shown to reduce endogenous nitric oxide production [ 24
virus itself. Endothelium damage is also a typical clinical feature in severe COVID-19 patients. Vasculitis-like manifestations, necrosis of extremities, and thrombosis could be seen in severe COVID-19 patients. Vascular damage may be caused by direct
endothelium and causes smooth muscle relaxation, thus contributes to colon relaxation and enhances colonic transit. It is produced by the nitric oxide synthase (NOS) enzyme family through the conversion of l -arginine to l -citrulline. Three main types of
regulation partly through GPR41, which is also expressed in the endothelium and is shown to mediate a hypotensive response ( 60 , 68 ). This is also supported by the finding that the GPR41 gene-deleted mice developed isolated systolic hypertension with
, Lichtman A , Libby P : Chlamydial and human heat shock protein 60s activate human vascular endothelium, smooth muscle cells, and
