September 13, 2021
A collateral circulation developing to compensate for the vascular thickening caused by the transdifferentiation actions of the Spike Protein may be behind the vasculopathy of COVID-19.
This is manifest in almost precisely the same way as in MOYAMOYA DISEASE. Interestingly, those with DOWN SYNDROME are extremely susceptible to this. I believe the spike protein is transdifferentiating endothelial to mesenchymal cells. SARS-CoV-2 is also dedifferentiating at least multiciliated cells and monocytes. The virus is erasing/changing cellular identities.
Unlike the flu or SARS-1 which left NO vascular thickening, SARS-CoV-2 is leaving its victims with vascular thickening of 15.4μm. Let us compare that
to those that died of flu, which was 6.7μm. It has been a point of argument as to why. I believe it is because the spike protein signaling (please see The
Viral Fragment Theory paper referenced below) is inducing the cells to become SMOOTH MUSCLE CELLS. This is called TRANSDIFFERENTIATION. To put it in layman’s terms, it is one more way SARS-CoV-2 makes a Jackson Pollack with your genes.
Just as in Moyamoya disease, I believe the rapidly developing collateral circulation is small, weak, and prone to bleeding, aneurysm and thrombosis. TIAs, seizures and strokes are all common complications of this disease. Just as in COVID-19 and post spike protein therapies.
The similarities with Moyamoya are, indeed, striking:
Impaired cGMP signaling leads to VSMC proliferation, impaired vasodilation, and fibrosis as well as endothelial dysfunction. These events will account for intimal hyperplasia with fibrous thickening, a typical pathological feature of MMD. Because impaired cGMP signaling can cause VSMC dedifferentiation and endothelial-to-mesenchymal transition, these cells can be potential sources of fibrosis.
Impaired protection from vascular insults is also a potential mechanism of arterial stenosis in MMD. As mentioned in the previous section, sGC acts protective against homocysteine, and RNF213 regulates lipotoxicity and has antiviral and antibacterial properties. Viral or bacterial infection causes type I IFN production and mitochondrial dysfunction, and they increase the RNF213 expression. When patient mutations induce dysfunction of RNF213 or sGC, vascular damage caused by homocysteine, dyslipidemia or infection may be amplified, leading to chronic inflammation. RNF213 mutations also induce inflammation via NF-κB. This may cause damaged VSMCs, which is another typical pathological feature of MMD.
A thorough examination of post spike protein recipient’s vasculature must be immediately commenced. We must look further into other aspects of dedifferentiation with regards to COVID and the Spike Protein. Have we been lied to? Most likely. So much more progress could have been made if we knew what the Spike Protein was doing to the vasculature. How can these therapies be allowed to continue? Will doctors please unite? Corporations and governments cannot function without doctors, so, please, save us, your patients.
Referenced/Related Papers
RNF213 and GUCY1A3 in Moyamoya Disease: Key Regulators of Metabolism, Inflammation, and Vascular Stability
https://www.frontiersin.org/articles/10.3389/fneur.2021.687088/full
Moyamoya disease
https://en.wikipedia.org/wiki/Moyamoya_disease
SARS-CoV-2 infection induces the dedifferentiation of multiciliated cells and impairs mucociliary clearance
https://www.nature.com/articles/s41467-021-24521-x
The Viral Fragment Theory of Covid-19 Vascular Complications
Endothelial to mesenchymal transition: a precursor to post-COVID-19 interstitial pulmonary fibrosis and vascular obliteration?