July 30, 2021

One remarkable finding among severe COVID-19 patients is that 18/66 (27%) patients with severe COVID-19 were found to have IgM autoantibodies recognizing ACE2. This explains the sudden increase of recent widespread severe disease in heretofore mild viruses, such as RSV.

The importance of ACE2 for the immune systems is the following: ACE2 attenuates the formation of aortic plaques in vivo and also limits macrophage expression of several proinflammmatory cytokines in vitro, including TNF-α and IL-6, after an LPS challenge, suggesting that ACE2 can directly blunt the proinflammatory polarization of myeloid cells.

TNF-α and IL-6. By now, these terms are in our daily vocabulary. And they are PRECISELY what knockout ACE2 leads to an increased expression of.

In ACE2 knockout mice, this knockout was associated with increased expression of adhesion molecules and inflammatory cytokines, including interleukin-6, monocyte chemoattractant protein-1, and vascular cell adhesion molecule-1, and an early increase in white cell adhesion across the whole aortae on dynamic flow assay. In the absence of a proatherosclerotic (ApoEKO) genotype, ACE2 deficiency was also associated with increased expression of these markers, suggesting that these differences were not an epiphenomenon.

Given that even 3.8% of non-ventilated patients developed these autoantibodies, it would seem only a matter of time before all do.

I believe the spike protein's rabid attachment to ACE2 toxifies the protein, and causes the body to view uld raising levels of Ang 1–7 help attenuate? We need to find out. We MUST stop the spike protein therapies this instant. The damage is incalculable.

Referenced/Related Papers

Genetic Ace2 Deficiency Accentuates Vascular Inflammation and Atherosclerosis in the ApoE Knockout Mouse

Immunologic Effects of the Renin-Angiotensin System

IgM autoantibodies recognizing ACE2 are associated with severe COVID-19