1) A CERTAIN PATHWAY TO SPIKE PROTEIN MEDIATED AUTOIMMUNE/FIBROTIC DISEASE
TGF-β DRIVEN IMMUNITY, SEVERE COVID-19 OR PROLONGED SPIKE PROTEIN EXPOSURE RESULTS IN AUTOIMMUNE/FIBROTIC DISEASE (VASCULITIS)
A very interesting paper from March of 2021 made a startling observation which Image
2) was concluded with the foreboding statement: Whether or not the antibodies generated in the continued immune reactions of COVID-19 patients in the ICU are harmless, or whether they may even cause detrimental immunopathology remains to be shown.
Why is this of interest now?
3) We have been searching for a satisfactory explanation for the observed myocarditis, autoimmune issues and vasculitis which are appearing ever increasingly.
What the paper demonstrated was that they analyzed samples from six patients within the first week after ICU admission,
4) ALL EXCEPT FROM ONE (patient #11, day 7) being SERONEGATIVE FOR THE SPIKE (S) PROTEIN OF SARS-CoV-2.
Now, let’s move forward a week. All patients who had been in the ICU for MORE THAN 7 DAYS HAD in their serum SARS-CoV-2 SPIKE (S) PROTEIN-specific IgM, and IgG ANTIBODIES.
5) What we must bear in mind is that PROTRACTED VIRAL SHEDDING AND VIRAL LOAD ARE ASSOCIATED WITH ICU MORTALITY IN COVID-19.
Therefore, those patients who end up in intensive care and/or dead have a far LONGER period of and amount of EXPOSURE to the Spike Protein. This may
6) explain why so many people with mild/asymptomatic disease test negative for Spike Protein antibodies.
But this isn’t the end of the tale. What happens next is something most extraordinary. The adaptive response to the Spike Protein results in plasmablasts (stem cells which are
7) precursors of B Cells and secrete antibodies) which DO NOT TARGET SARS-CoV-2!
Even MORE bizarre is that these plasmablasts were not even prevalent in the lungs of those that died! The immune responseof these plasmablasts is also driven by TGF-β, which is the engine of
8) fibrosis.
COVID-19 patients which required prolonged ICU care (or, I believe, prolonged/high volume exposure to the Spike Protein) show a continued immune reaction reflected by egress of plasmablasts into the blood. This immune reaction is initially controlled by IFNs, IL-21,
9) and TGF-β, which target antibody class switching to IgG1 and IgA1. At later time points IFN is no longer involved, and the immune reactions are controlled by IL-21 and TGF-β, which in the end drives cells to switch to the terminal antibody class IgA2. Such cells do not
10) relocate to the lung and they contribute little to humoral immunity to SARS-CoV-2. The specificities of the antibodies generated remain to be identified, but most of them are not specific for the spike protein, its receptor-binding domain (RBD) or NP. Whether or not the
11) antibodies generated in the continued immune reactions of COVID-19 patients in the ICU are harmless, or whether they may even cause detrimental immunopathology remains to be shown. Therapeutic targeting of TGF-β may be a way to ameliorate severe COVID-19, especially, when
12) considering the fibrosis-inducing capacity of TGF-β.
At this moment, I believe we can safely say, those antibodies are real, and very pathogenic.
The Spike Protein therapies must come to a full stop. Immediately. While this is investigated.
annalsofintensivecare.springeropen.com/articles/10.11…

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More from @Parsifaler

Jan 19,
1) miR-200, COVID-19, CANCER AND FIBROSIS

Downregulation of miR-200 is implicated in mesenchymal transformation, cancer and fibrosis as well. It is also intimately tied to ACE2.
At the time of admission to hospital, the expression levels of miR-200c-3p and miR-421-5p in COVID Image
2) patients, as well as CD4, CD25, and Foxp3 significantly decreased while IL-6 expression notably enhanced.
Regarding Fibrosis, in a 2012 study, it was found that miR-200a, miR-200b, and miR-200c are significantly down-regulated in the lungs of mice with experimental lung
3) fibrosis.
And with regards to the “oncogenic flash drive” hypothesis I have, members of the miR-200 miRNA family are downregulated in human cancer cells and tumors due to aberrant epigenetic gene silencing and play a critical role in the suppression of epithelial-to-
Read 7 tweets
Jan 16,
1) AN ENERGY-BASED MITOCHONDRIAL EXPLANATION OF SPIKE PROTEIN PATHOGENESIS: SLOWLY TURNING THE POWER OFF
As we have not yet determined the primary pathogenesis of COVID-19, I propose that the disease is one of progressive Mitochondrial Dysfunction from a pathogen (therapeutic?)
2) delivered via the Endothelium and distributed throughout the body to all organs and tissues.
PREMISE: S1 and Trimer both induced mitochondrial damage including functional deficits in mitochondrial respiration.
For example: It is well established that the brain uses more energy
3) than any other human organ, accounting for up to 20 percent of the body's total haul. Therefore, it would only be logical that one of the first signs of mitochondrial dysfunction would be brain fog. Indeed, brain fog has been theorized as being an energy, or mitochondrial
Read 5 tweets
Jan 11,
1) AN ONCOGENIC “FLASH DRIVE”: THE SPIKE PROTEIN OF SARS-CoV-2 AND CANCER
When I first began studying the SARS-CoV-2 virus I was initially concerned about its Spike Protein’s potential ability to induce prion disease, as the spike has homology with our Prion protein and it
2) induces a strong Unfolded Protein response.
However, almost two years after I reached that conclusion, I believe it is only part of the story. Yes, I am still concerned that it may induce Prion Disease. But, what concerns me more is that its interactions and mimicking of the
3) human Prion Protein may be more “effective” having a role in tumorigenesis and metastasis.
In fact, the more I look at the Spike Protein now, and with the now common knowledge that the Spike Protein mimics Trousseau Syndrome, I now believe that the Spike Protein may be a
Read 15 tweets
Jan 10,
1) COVID-19 COAGULATION ABNORMALITIES AS TROUSSEAU SYNDROME
IS THE SPIKE PROTEIN INDUCING GENERALIZED CANCER AND COULD THOSE IMMEDIATELY EXPERIENCING COAGULATION ABNORMALITIES HAVE OCCULT CANCERS?
Malignancy affects the hemostatic system and the hemostatic system affects
2) malignancy.
Cancer's "purpose" is to invade organs and disrupt their normal functioning by rendering cells dysfunctional. These dysfunctional cells then spread, disrupting further cells, and so on until the victim dies.
The way cancer accomplishes this is to spread through
3) vessels. If it spreads through blood vessels, it must cross the barrier of the blood vessels to enter organs, including blood vessels themselves. Therefore disrupting (activating) the endothelium is essential to "breaking through" that barrier.
The close relationship between
Read 11 tweets
Jan 9,
1) Guild Navigator:
You are transparent. I see many things. I see plans within plans. (DUNE)
VASCULAR DISEASE AS CAMOUFLAGE: THE SPIKE PROTEIN OF SARS-CoV-2 AS MICROTUMOR
Respiratory disease held the world in a false awe at the beginning of the COVID-19 pandemic. Health
2) authorities the world over reiterated the same narrative: We have a new Respiratory Virus. Those of us who looked closely at the disease from the beginning knew that wasn’t the true picture – or at least not the full picture.
Then, slowly, over the course of the first year of
3) the pandemic, everyone else began to realize this, too. Finally, towards the end of 2020, COVID-19 was universally recognized as a Vascular Disease. However, I have realized the virus’ deception does not stop there.
IT IS ONLY A VASCULAR DISEASE INSOMUCH AS THE SPIKE PROTEIN
Read 17 tweets
Jan 8,
1) AN EXPLANATION FOR THE SUDDEN CARDIAC DEATHS:
I believe the endocytosis of the Spike Protein is interfering with Ryanodine Receptors causing a calcium channelopathy resulting in Catecholaminergic Polymorphic Ventricular Tachycardia. This is a potentially fatal arrhythmia Image
2) which is induced when the heart rate exceeds 120 bpm.
The intracellular actions of the Spike Protein with Cathepsin L, a protease on the plasma membrane of host cells, increases Ca2+ release from the endoplasmic reticulum (ER) via the ryanodine receptors (RyRs). The associated ImageImage
3) elevation of cytosolic Ca2+ concentration, in turn, increases cathepsin L activity. Cathepsin L promotes virus fusion with host cells by cleaving and activating the spike (S) protein. High levels of extracellular and cytosolic Ca2+ concentrations are also necessary for virus
Read 6 tweets

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