A paper published in 2017 provides some compelling evidence for the SARS nCoV-2 spike-amyloid theory
Can we stop infectious amyloid production if it ensues?
A paper was sent to me today entitled: “Pathogenesis and diagnosis of viral infections of the nervous system” published in 2017 in the The FASEB Journal.1
The paper provides evidence to show that a species of bacteria named Pseudomonas aeruginosa (P. aeruginosa) - the etiological agent for many hospital-acquired pneumonias - induces the release of a degradation-resistant cytotoxin that acts as a prion.
We show that infection of pulmonary endothelial cells by P. aeruginosa induces production and release of a cytotoxic amyloid molecule2 with prion characteristics, including resistance to various nucleases and proteases.
What this means is that infection of pulmonary endothelial cells by this pathogen causes the cells to produce and release durable, self-replicating amyloid cytotoxins that act as prions to induce mis-folding of other proteins. A by-product of production and release of these cytotoxins is the destruction of endothelial cells as well as non-endothelial cells and lung tissue that can eventually lead to death even after pneumonia resolution ensues. This is an amazing finding in that the initiating agent of the prion-like substances was clearly identified to be P. aeruginosa.
This begs 2 questions:
Is the SARS-nCoV-2 virus the initiating agent of a prion-like substances in humans?
More precisely, is the initiating agent of SARS-nCoV-2 the spike protein, or spike protein peptides?3
https://www.youtube.com/watch?v=lXZsWTUjV7Q
Balczon R, Morrow KA, Zhou C, Edmonds B, Alexeyev M, Pittet JF, Wagener BM, Moser SA, Leavesley S, Zha X, Frank DW, Stevens T. Pseudomonas aeruginosa infection liberates transmissible, cytotoxic prion amyloids. FASEB J. 2017 Jul;31(7):2785-2796. doi: 10.1096/fj.201601042RR. Epub 2017 Mar 17. PMID: 28314768; PMCID: PMC5471513.
Amyloid plaques form when pieces of protein called beta-amyloid aggregate. https://www.news-medical.net/health/What-are-Amyloid-Plaques.aspx
Stephanie Seneff, Anthony M Kyriakopoulos, Greg Nigh, et al. SARS-CoV-2 Spike Protein in the Pathogenesis of Prion-like Diseases. Authorea. August 16, 2022.
DOI: 10.22541/au.166069342.27133443/v1
I wonder if this has anything to do with the self-assembling nature of the "blood clots" (not made with normal clotting material, but with electrically conductive elements).
Edit: Just after I wrote the above, I found this in an article on The Epoch Times:
“The very large blood clots that are being removed before and after death are unlike anything we have ever seen in medicine,” Dr. James Thorp, a maternal-fetal medicine expert who has been observing anomalies in pregnant women and fetuses, told The Epoch Times.
“The COVID-19 vaccine diverts energy away from the physiologic processes in the body towards the production of the toxic spike protein. This directs energy away from the normal process of internal digestion also known as autophagy. This results in protein misfolding and propagation of large intravascular blood clots and also a variety of related diseases including prion disease, Creutzfeldt-Jakob disease, amyloidosis, and dementias including Alzheimer’s and others. While it is possible that COVID-19 illness in itself could potentially contribute to these diseases, it is unlikely and if so the effect of the vaccine would be 100 to a 1,000-fold greater than that of COVID-19 disease.” Thorp said.
https://www.theepochtimes.com/embalmers-have-been-finding-numerous-long-fibrous-clots-that-lack-post-mortem-characteristics_4696015.html?est=F7G0nVQqlGpvAXWMTzvR8%2BxwSCxN3hIvLfTgD1aOIhQHpYITNCshBxt2ZWibTvWf8g%3D%3D
The work has been done for SARS cov2. Yes, indeed, the S1 subunit of the spike protein induces amyloid-like (beta sheet) configurational change in the fibrin molecule, causing our fibrin clots to be much more resistant to plasmin and the therapeutic anticoagulants. A good review of these findings can be found at https://portlandpress.com/biochemj/article/479/4/537/230829/A-central-role-for-amyloid-fibrin-microclots-in . This would also explain the pathological clots that are formed in some people after the m-RNA inoculations.