SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2


Senior Member

SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection relies on the binding of S protein (Spike glycoprotein) to ACE (angiotensin-converting enzyme) 2 in the host cells. Vascular endothelium can be infected by SARS-CoV-2,1 which triggers mitochondrial reactive oxygen species production and glycolytic shift.2 Paradoxically, ACE2 is protective in the cardiovascular system, and SARS-CoV-1 S protein promotes lung injury by decreasing the level of ACE2 in the infected lungs.3 In the current study, we show that S protein alone can damage vascular endothelial cells (ECs) by downregulating ACE2 and consequently inhibiting mitochondrial function.
However I found the following quite interesting for ME patients:

We next studied the impact of S protein on mitochondrial function. Confocal images of ECs treated with S1 protein revealed increased mitochondrial fragmentation, indicating altered mitochondrial dynamics (Figure [C], i)


Moreover, ACE2-L overexpression caused increased basal acidification rate, glucose-induced glycolysis, maximal glycolytic capacity, and glycolytic reserve (Figure [D], ii). Also, ECs incubated with S1 protein had attenuated mitochondrial function but increased glycolysis, when compared with control cells treated with IgG (Figure [D], iii and iv)
It is a fascinating look at what happens if a virus attacks ACE2 receptors and how that could cause what is believed to be the underlying base of ME/CFS from Ron Davis' research. It looks like they managed to induce ME in a hamster!

Endothelial cells are found in the lungs, guts and capillaries, all areas where ME/CFS research has in recent years been pointed and finding dysfunctions.
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Senior Member