November 16, 2021
LESSONS FROM THE PAST INTENTIONALLY SUPPRESSED: PRE SARS-CoV-2 KNOWLEDGE OF ACE2, ITS FUNCTIONS AND THE SARS-CoV SPIKE PROTEIN
To begin with, please read the following paragraph:
To further clarify whether the intraperitoneally injected Spike-Fc protein directly affected lung pathology in mice, we examined the localization of the injected Spike-Fc protein in lung. Spike-Fc was detected in lung homogenates by western blot using human Fc–specific antibody, whereas injected control-Fc was not detected. In addition, using immunohistochemistry, we found that Spike-Fc protein localized to bronchial epithelial cells, inflammatory exudates and alveolar pneumocytes. Notably, Spike-Fc primarily localized to severe lesions. This localization of Spike-Fc protein is similar to Spike antigen staining in SARS-CoV–infected mice. Spike-Fc treatment resulted in downregulation of ACE2 protein expression in lungs of acid-treated wild-type mice in vivo, consistent with ACE2 protein downregulation in SARS-CoV–infected mice and Spike-Fc protein–treated cells in vitro. These results show that the SARS-CoV Spike protein can directly affect the development of severe acute lung failure through ACE2.
This is not new. This was written in 2005. It was known then that the Spike Protein of SARS-CoV downregulated ACE2 and enhanced the severity of acute lung injury. The Spike Protein of SARS-CoV-2 interacts FAR MORE STRONGLY with ACE2 than does the Spike Protein of SARS-CoV.
To be clear, the Spike Protein of SARS-CoV worsened ANY acute lung injury: Treatment with Spike(S318-510)-Fc again worsened acid-induced acute lung injury in wild-type mice. Notably, in vivo Spike-Fc protein administration did not affect the severity of lung failure in Ace2 knockout mice, indicating that the effect of Spike protein on acute lung injury is ACE2 specific.
Now, what have we learned since 2005 about ACE2? The answer is: quite a lot.
PROGRESSIVE CARDIAC DYSFUNCTION
The progressive cardiac dysfunction observed in the first ACE2 mouse knockout model resembled that of tissue subjected to long-term hypoxia of the type that occurs after coronary artery disease or bypass surgery in humans.
Perhaps more can be learned by observing what ACE2 CAN do:
Viral delivery of ACE2 after induction of myocardial infarction is protective, reducing the adverse cardiac remodelling and fibrosis. Similar antifibrotic effects have been seen with an ACE2 activator along with attenuation of Ang-II-induced thrombus in hypertensive rats and a modest reduction in the blood pressure of spontaneously hypertensive rats. Over the past 18 months a number of studies have been carried out examining the effect of recombinant human ACE2 on a range of disease conditions. To date, administration of ACE2 to mouse models of Ang-II-induced diseases has been shown to reverse the pathological effects of Ang II in diabetic nephropathy, heart disease, renal oxidative stress as well as reversal of Ang-II-induced hypertension.
Do the math if we invert the observations of the above paragraph.
DIABETES
ACE2 hydrolyzes the octapeptide angiotensin (Ang)-II to heptapeptide Ang-(1-7), which has an important protective effect on blood sugar. ACE2 knockout mice respond to glucose with impaired glucose tolerance and impaired insulin secretion.
SYMPATHETIC NERVOUS SYSTEM (SUDDEN CARDIAC DEATH, NEURODEGENERATION)
Brain ANG II plays an important role in modulating sympathetic function and homeostasis. The generation and degradation of ANG II are carried out, to a large extent, through the angiotensin-converting enzyme (ACE) and ACE2, respectively. In disease states, such as hypertension and chronic heart failure, central expression of ACE is upregulated and ACE2 is decreased in central sympathoregulatory neurons. In this study, researcher determined the expression of ACE and ACE2 in response to ANG II in a neuronal cell culture and the subsequent signaling mechanism(s) involved.
There are additional implications for ACE2 in the prevention of cancer metastasis and further beneficial biological function.
I am horrified by the medical establishment. Either I am one of the greatest medical geniuses the world has ever seen, or people with desperately needed knowledge are maliciously hiding the truth and/or are actively lying. Which is it? As much as anyone would like to be the GOAT of anything, human nature may be the Occam’s Razor which quickly and efficiently answers this question.
Referenced/Related Papers
Angiotensin-Converting Enzyme 2: The First Decade
https://www.hindawi.com/journals/ijhy/2012/307315/
ACE2 knockout cell line
https://www.ubigene.us/about/article/2931.html
A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus–induced lung injury