Foreign Proteins and the Induction of Chronic Disease: Lessons from 1919
Understanding why introducing the Spike Protein into the body, especially repeatedly, was one of the worst “ideas” in medical history.
This is an incredibly urgent and important post. I ask you to please read it carefully and thoughtfully.
I’d like to step back in time. And this is important. I’d like for us to look at something us researchers knew back in 1919.
By a series of animal experiments Longcope believes that he has shown that repeated nonfatal poisoning with foreign protein is responsible for some cases of chronic nephritis, cirrhosis of the liver, and chronic myocarditis.
Effect of Foreign Protein on Kidney
https://www.jstor.org/stable/30080494?seq=2
Now, from later in the paper.
It is conceivable that toxic foreign protein might have a similar effect in man, but it is unlikely that such proteins ever gain access to the circulation in such relatively large amounts as are used experimentally in animals.
Effect of Foreign Protein on Kidney
https://www.jstor.org/stable/30080494?seq=2
At least it WAS unlikely...
Yet, what effect were they discussing? The effect of introducing a foreign protein repeatedly in NON-LETHAL doses. First let’s look at those that died in acute anaphylactic shock.
Inklings of the mechanisms the Spike Protein would induce were seen in 1919, as well.
Gay and Southard described hemorrhages and degeneration in guinea-pigs that died in acute anaphylactic shock and in those killed subsequent to severe shock. The hemorrhages were widely distributed, but were most commonly found in the mucosa of the stomach and in the lungs. Areas of fatty degeneration were found in capillary endothelium, in the mucosa of the stoma cardiac and voluntary muscle. The hemorrhages were the result of the degeneration of the capillary endothelium.
Effect of Foreign Protein on Kidney
https://www.jstor.org/stable/30080494?seq=2
I found the most important point of the paper to be the following observation, about non-lethal doses.
Longcope's conclusions were confirmed by Boughton to the extent that repeated injections of foreign protein may produce renal lesions. Boughton produced repeated anaphylactic shock in guinea-pigs using beef serum and egg-white as antigens. Some of the animals received as many as 19 secondary injections, and the average number of injections was 9. The average duration of the experiments was four months but some animals were under experimentation as long as 8 months. The urine was not examined systematically. Twenty-three guinea-pigs were used. Degeneration, desquamation, and necrosis of the tubular epithelium was the most striking change noted and was seen in all cases. Round cell infiltration was found in nearly all cases though it was never vary marked. There was no distinct scar formation.
Effect of Foreign Protein on Kidney
https://www.jstor.org/stable/30080494?seq=2
Another serious issue with exposure to foreign proteins is their ability to induce aberrant and deleterious signaling. I believe this is certainly the case with the Spike Protein as it mimics hyperactive RANK protein. To understand, let’s look at the mechanism.
Chronic signals lead to chronic illnesses
The RANK receptors work like switches within the cell: They generate a signal in the cell when activated by signal molecules. One such signal molecule is called RANKL, for Receptor Activator of NF-κB Ligand.
Working in the laboratory to determine the effects of hyperactive RANK receptors, the team compared healthy mice and genetically modified animals with modified RANK receptors. After only a few weeks a large portion of the mice with genetically modified receptors contracted systemic lupus erythematosus, while the animals in the control group remained healthy, proving that this autoimmune disease can be triggered by defective regulation of the RANK signals.
When Hyperactive Proteins Trigger Illnesses
https://dktk.dkfz.de/en/about-us/news/wenn-hyperaktive-proteine-krank-machen
And activating NF-kB is something the Spike Protein is a pro at.
S protein activates the NF-κB pathway
Inflammatory genes are transcriptionally regulated by transcription factors that are activated by signaling pathways such as NF-κB, MAPK, STAT3, and AKT. To obtain further insight into how S protein induces the expression of inflammatory mediators, we stimulated THP1 cells with S2 protein. Cell lysates collected at various times following stimulation were analyzed for the activation of these inflammatory pathways by Western blotting. As shown in Figure 4A, P65 and IκB were phosphorylated in cells treated with S2. MAPK pathways, including ERK, P38, and JNK, are often activated concomitant to the NF-κB pathway. Surprisingly, there was no activation of ERK and JNK in S2 stimulated cells (Figure 4A). There was also no activation of the AKT pathway (Figure 4A), but STAT3 was phosphorylated at 2 hr following stimulation (Figure 4A). Inflammatory cytokines, such as IL-6, can activate STAT3; thus, the observed activation of STAT3 could be a secondary response of S protein-mediated activation of the NF-κB pathway. S2 protein also activated the NF-κB and STAT3 pathways in A549 cells (Figure 4B). To confirm that S protein-induced inflammation was NF-κB dependent, we inhibited the NF-κB pathway using Sc514, an inhibitor of IKKβ, during stimulation with S protein. As expected, inhibition of the NF-κB pathway abrogated inflammatory responses in S protein-stimulated macrophages.
SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway
https://pmc.ncbi.nlm.nih.gov/articles/PMC8709575/
Let me be very clear. Things got MUCH WORSE for the mice discussed above.
And that wasn't all: After about a year, the transgenic mice that survived systemic lupus erythematosus contracted chronic lymphatic leukemia or CLL. "This result was a surprise to us, since it shows that activated RANK proteins are also responsible for the degeneration of B cells to cancer of the lymphatic sytem nodes," says Maike Buchner, CLL specialist, junior group leaderyoung scientist at the Institute of Clinical Chemistry and Pathobiochemistry at the university hospital TUM Klinikum rechts der Isar and DKTK scientist.
When Hyperactive Proteins Trigger Illnesses
https://dktk.dkfz.de/en/about-us/news/wenn-hyperaktive-proteine-krank-machen
Repeated exposure to the Spike Protein MUST be halted IMMEDIATELY. I implore everyone to take action by contacting your health care professionals and politicians.
Thank you, as always, for your readership, dialog and financial support. I will continue to discover what we are facing and ways we can fight back and keep our health.
Human bodies NEVER tolerate foreign proteins every transplant patient proves the point. Even twins are different enough that bone marrow from one will be foreign to the other.
Since 1999 biotech death of Jesse Gelsinger it was understood that the idea of "gene therapy" to repair fatal flaws cannot work because non-self proteins ALWAYS trigger the immune system to attack the affected cells. It is basic biology and all the fancy tech does not change the laws of Nature where immune systems are organized to destroy ALL foreign proteins.
Spike might be worse than other formulas but NONE will work ALL will cause harm this is TRANSFECTION a decades old lab tool that was always lobotomy level criminal experiment.
https://web.archive.org/web/20121025034826/https://www.nytimes.com/1999/11/28/magazine/the-biotech-death-of-jesse-gelsinger.html
https://web.archive.org/web/20150822064507/https://www.thermofisher.com/us/en/home/references/gibco-cell-culture-basics/transfection-basics.html
This was discovered and reported more than 100 years ago, and yet the idiots at Pharma, FDA, and CDC told us, hey, no problem, we will use YOUR OWN CELLS to create trillions of toxic foreign proteins so you will develop antibodies to covid. Makes me want to SCREAM that these people were so reckless and so incompetent. And they are getting away with it, getting away with mass murder.