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

[BrightCandle]

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC8091897/

Abstract

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.

 

[jpcv]

This paper should be of interest too
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8267916/

 

[nerd]

This paper should be of interest too
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8267916/

This supports the argument for cell cycle regulating medication.

It looks like they managed to induce ME in a hamster!

The question is how you confirm ME in an animal model without a biomarker. Sometimes, they used forced swimming as a control in animals. But I don't think this is appropriate for a variety of reasons.

 

[pattismith]

(Maybe someone could move this thread to the covid part?)

Anothe study about endothelial damages by the spike protein (this means virus or vaccine induced to me)

SARS-CoV-2 Spike Protein Destabilizes Microvascular Homeostasis | Microbiology Spectrum (asm.org)

Our studies add to this understanding by providing evidence that spike protein alone can mediate adverse effects on vascular cells. Understanding these mechanisms of pathogenesis may provide rationale for interventions that could limit microvascular events associated with SARS-CoV-2 infection.

I had three Pfizer vaccines and now I have evidences for peripheral microvascular damages...