1) THE SPIKE PROTEIN OF SARS-CoV-2 RECOGNIZES THE BODY’S ENTIRE ENDOTHELIUM AS TUMOR ENDOTHELIUM. IT CAUSES THE BODY TO “TREAT” THE ENDOTHELIUM PRECISELY AS A CANCER THERAPY – BY DESTROYING IT WHILE CAUSING MASSIVE INLAMMATION AND IMMUNE CELL INFILTRATION.
First, let us look at
2) what Cancer does. Cancer wants an Anergic Endothelium. It wants an Endothelium which WILL NOT REACT. It will not cause the Endothelium to activate so that immune cells will not be “attracted” to it and remove it. It also wants to create new blood vessels to feed it.
3) This combination of “problems” it has can be easily remedied – by destroying it. Indeed, THIS IS A RECENT THERAPEUTIC UNDER DEVELOPMENT.
The following certainly is COVID-19. Would you not agree?
One important physiological function of normal endothelial cells is quiescence of
4) the inflammatory response and thus, participation in immune surveillance. Quiescent endothelial cells fail to provide the requisite signals for leukocyte recruitment; but the cells can be activated to express adhesion molecules and to release chemokines that promote capture
5) and transmigration of blood leukocytes into tissues. Endothelial cell activation can typically induced by multiple factors, including circulating inflammatory cytokines, such as tumor necrosis factors (TNF) and interleukins (IL), reactive oxygen species, oxidized low density
6) lipoprotein, autoantibodies and traditional risk factors directly and indirectly activate endothelial cells. The term activated endothelium implies a change in endothelial cell morphology. Endothelial activation was further specified as a change in surface molecules and in
7) endothelial cell functions in response to cytokine treatment, and it was emphasized that these changes does not represent endothelial cell injury or dysfunction. Components of endothelial cell activation are upregulation of surface antigens (e.g., HLA molecules) and leucocyte
8) adhesion molecules (e.g., E-selectin, ICAM-1/2, and VCAM-1), pro-thrombotic endothelial cell changes (e.g., loss of the surface anticoagulant molecules thrombomodulin and heparan sulfate), cytokine production (e.g., IL6, IL8, MCP1), and changes in the vascular tone (e.g., loss
9) of vascular integrity, expression of vasodilators, and NO). These components mutually interact in causing local inflammation. Endothelial activation also leads to an increase in angiopoietin-2, which is known to destabilize barrier function and promote inflammation (26).
10) The recruited and extravasated immune cells appear then in vicinity of the activated endothelial cells, and can further become activated. Importantly, the phenotype of activated endothelial cell is reversible and can return to the quiescent, non-activated phenotype when the
11) activating factors were removed. Prolonged activation of the endothelium can be associated with the loss of microvascular barrier integrity and subsequent vascular injury or progress to endothelial cell apoptosis.
Now, let us turn our attention to current tumor therapy theory
12) The different approaches being currently explored to increase recruitment of immune effector cells, include manipulating the expression of homing-associated molecules on T-cells and tumor endothelial cells. In a very elegant preclinical study Elia et al. showed that a
13) selective (PRE)ACTIVATION OF THE TUMOR ENDOTHELIUM WITH THE CYTOKINE TNF promoted intratumoral T-cell infiltration, and IMMUNE CHECKPOINT BLOCKADE.
And, does this not sound familiar? NGR-TNF administration was already used as a safe and therapeutic systemic administration to
14) target TNF selectively to angiogenic tumor vessels which then altered the endothelial barrier function together with an upregulation of leukocyte-endothelial cell adhesion molecules, the release of pro-inflammatory cytokines, and the infiltration of tumor-specific effector
15) CD8(+) T-cells.
And, most interestingly: Finally, the combined therapy had beneficial effects on endogenous immune surveillance, THROUGH DEPLETION OF REGULATORY T-CELLS and expansion of a fully functional, polyclonal repertoire of cytotoxic T-lymphocytes.
16) Is the entire body being viewed as a tumor?
frontiersin.org/articles/10.33…

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More from @Parsifaler

31 Dec 21
1) A HYPOTHETICAL FATAL PATHOGENIC FEEDBACK LOOP OF THE SARS-CoV-2 SPIKE PROTEIN
Heretofore the global medical community has been mainly concerned with the Acute phase of COVID-19. This is in both aspects of treatment and prevention. However, I believe that the Acute phase of
2) COVID-19 is only the very tip of a massive pathogenic iceberg. And one that continues to “build” upon itself.
A paper published November 12 identified kidney disease as the leading risk factor for hospitalization in confirmed COVID-19 patients. The phenome-wide association
3) study also identified Type 2 Diabetes, Congestive Heart Failure, COPD in addition to Chronic Kidney Disease.
What is it that ties all of these diseases together? Please remember that Schizophrenia is also considered to be a major risk factor for severe COVID. All of the above
Read 7 tweets
27 Dec 21
1) My Christmas gift of understanding to the world. May it help.
Breakthrough. Finally. Mechanisms found.
Eexecutive (non-techincal) Summary: The Spike Protein of COVID-19 most likely cases the body to reject iteself.
COVID-19 mimics Graft vs Host Disease via Anti-Angiotenisn II
2) Type 1 Receptor Antibody induction and complement/immune complex deposition in the microvasculature mediated by the Spike Protein.
If you have been following my posts, you know that for the better part of the past year I have been focused on the observation that COVID-19 and
3) its sequelae look VERY MUCH like Graft vs Host disease. We see identical endothelial/multisystemic destruction in both COVID-19 and GvHD. However, as you know, I have been working to find the mechanism for this parallel.
I believe I can now explain why COVID-19 and GvHD are
Read 10 tweets
26 Dec 21
1) FIFO (First In First Obliterated) Hypothesis of the SARS-CoV-2 Spike Protein:

Given the paper out yesterday that the Spike is found in all organs of even asymptomatic patients and that the Spike has been proven to cause Sensecence in Endothelial cells, is it possible that we
2) only NOTICE the destruction of the Endothelium FIRST as it is a MONOLAYER of cells and the FIRST the Spike is widely exposed to? Is the Spike conducting a "Sherman's March Through Georgia" of our organs?

Especially with CONSTANT REINFORCEMENTS?

journals.asm.org/doi/10.1128/JV…
Read 4 tweets
22 Dec 21
1) @JikkyKjj @WambierMD @KathMLee1 OK. I am now thinking Pericytes are at the nexus of COVID.

Pericytes (previously Rouget cells) are multi-functional mural cells of the microcirculation that wrap around the endothelial cells that line the capillaries throughout the body.
2) Pericytes are embedded in the basement membrane of blood capillaries, where they communicate with endothelial cells by means of both direct physical contact and paracrine signaling. The morphology, distribution, density and molecular fingerprints of pericytes vary between
3) organs and vascular beds. Pericytes help to maintain homeostatic and hemostatic functions in the brain, one of the organs with higher pericyte coverage, and also sustain the blood–brain barrier. These cells are also a key component of the neurovascular unit, which includes
Read 4 tweets
20 Dec 21
1) URGENT: MY MOST IMPORTANT FINDING TO DATE
COVID-19, LONG COVID, INITIATED AND ACCELERATED DISEASES OF AGING AND ACE2 AUTOANTIBODIES
When Joseph Tritto wrote his work early in the pandemic about COVID-19, Cina COVID-19, he quoted a UK virologist who wished to remain anonymous.
2) This virologist stated that, once infected with COVID-19, the virus would never let its victim go, even if it didn’t kill upon initial infection.
That statement, which I had read elsewhere in February of 2020, has been one of the forces driving my search for what SARS-CoV-2
3) actually is.
First and foremost. BEFORE SARS THERE WERE NO KNOWN BAT CORONAVIRUSES THAT USED ACE2 FOR CELLULAR ENTRY. None. Not one. None of them used ACE2. Not for entering a single cell.
Secondly, bat viruses which have previously spilled over to human populations have been
Read 8 tweets
14 Dec 21
1) PROGRESS. NEW MOST IMPORTANT FINDING. URGENT.
IN A NUTSHELL: ALMOST INSTANTANEOUS, LETHAL, SYSTEMIC ARTHEROSCLEROTIC DISEASE. IF THE PATIENT SUVIVES, THEN SYSTEMIC FIBROSIS
A THEORY OF COVID-19 DISEASE: THE SPIKE PROTEIN INJURES VASCULAR ENDOTHELIUM CAUSING ENDOTHELIAL CELLS
2) TO DETACH, DESTROYING THE MICROVASCULATURE, RESULTING IN SEVERE MICROCLOTTING. THE SPIKE PROTEIN ALSO DAMAGES BONE MARROW STEM/PROGENITOR CELLS. THE COMBINATION CAUSES ABERRANT WOUND REPAIR, RESULTING IN FIBROSIS. THIS EXPLAINS SEVERE DISEASE AND LONG COVID. IT IS A SYSTEMIC
3) MICROVASCULAR “BRAIN/HEART/LUNG/KJDNEY ETC. ATTACK!” FOLLOWED BY ORGAN FIBROSIS, IF THE PATIENT SURVIVES.
One of the most important findings of the Salk Institute paper on the Spike Protein is that the researchers created a “pseudovirus” that was surrounded by SARS-CoV-2
Read 20 tweets

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