THE SPIKE PROTEIN AND EXPERIMENTAL PRODUCTION OF AMYLOIDOSIS IN HUMANS

If you want to know the future, look at the past. – Albert Einstein

This is my most important finding to date.

I believe I have made a very significant breakthrough this evening. As I am certain we are dealing with a lab created pathogen that induces amyloidosis in humans (at least, perhaps other species, too?) I decided to investigate what has been done in the past, as the mechanisms I am looking for, I do not believe I would find in the natural pathogenesis of amyloidosis.

Indeed, there is an extensive history of amyloidosis being experimentally induced in lab animals.

Let us go back to the year 1965. In this year, in the American Journal of Pathology, a paper was published with the simple title Experimental Amyloidosis. What this paper demonstrated was that mice REPEATEDLY INJECTED WITH CASEIN seven days a week for 3-4 weeks all developed amyloidosis. Specifically, they attributed the development of Amyloidosis to the ANTIGENICITY of Casein.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1920408/pdf/amjpathol00284-0165.pdf

However, we now know that Casein has a very special property. In 2013 a paper was published in Protein Nanotechnology (!). This paper describes how casein proteins have the propensity to SELF-ASSEMBLE into AMYLOID FIBRILS.

https://link.springer.com/protocol/10.1007/978-1-62703-354-1_6

What is most important here is that the SPIKE PROTEIN also has the ability to SELF-ASSEMBLE into AMYLOID FIBRILS.

https://pubs.acs.org/doi/10.1021/acsnano.1c10658

There is another mechanism which I believe is also at work.

Let us turn the clock ahead. This time to the year 1992. In this year the Guangdong Provincial Poultry Science Research Institute published a Short Communication entitled Experimental production of amyloidosis in ducks.

Ducks were REPEATEDLY INOCULATED with crude extracts of E Coli and Salmonella Tryphimurium, or both. The results were that between 30%-60% of the ducks developed amyloid deposition in a variety of tissues.

The authors posited two main hypotheses - that amyloidosis was induced by “a disturbance in the immune system” and that amyloidosis results from “over-stimulation by antigens.”

https://www.tandfonline.com/doi/pdf/10.1080/03079459208418827

The concern with the Spike Protein is far more profound. The Spike Protein is a Superantigen, and is Amyloidogenic in and of itself. This almost certainly accelerates and increases the severity of amyloidosis induction and progression.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7263503/

This published just seven hours ago:

https://pubs.acs.org/doi/10.1021/jacs.2c03925