.
The key factor is the Vitamin K-dependent protein S (PROS1). While the damage is caused by the viral spike S-protein.
References:
- "Identification of the antithrombotic protein S as a potential target of the SARS-CoV-2 ...", Letter to Editor, Jan A. Ruzicka, Thrombosis Research 196 (2020) 257–259
- Wiki Protein S
- "Endothelial cell damage is the central part of C...-19 and a mouse model induced by injection of the S1 subunit of the spike protein", by Gerard J. Nuovo, et al., Ann Diagn Pathol. 2021 Apr; 51: 151682.
- "SARS-COV-2 mRNA Vaccine (BNT162, PF-07302048) 2.6.4 Overview of Pharmacokinetic Test",
- "The SARS-CoV-2 spike protein alters barrier function in 2D static and 3D microfluidic in-vitro models of the human blood-brain barrier", by Tetyana P Buzhdygan, et al., Neurobiol Dis. 2020 Dec;146:105131. doi: 10.1016/j.nbd.2020.105131. Epub 2020 Oct 11.
- "Circulating SARS-CoV-2 Vaccine Antigen Detected in the Plasma of mRNA-1273 Vaccine Recipients", by Alana F Ogata, et al., Clinical Infectious Diseases, ciab465, Published: 20 May 2021
- Talk by Dr. Byram Bridle on the "On-Point" program with Alex Pierson, 9:11, Posted on 27-May-2021
- On-Point program with Alex Pierson, Globalnews Toronto
PROS1 has the following properties
| PROS1 | |
|---|---|
| * | PROMOTES ANTI-THROMBOTIC STATE |
| * | AIDS IN SUPPRESSION OF COAGULATION |
| * | ACTIVATES TAM (RTK) DOWNREGULATING IMMUNE FUNCTION |
| * | SUPPRESSES INNATE IMMUNE FUNCTION |
| * | PREVENTS CYTOKINE STORM |
| * | IS SYNTHESIZED IN ENDOTHELIAL CELLS ALONGSIDE ACE2 |
| SARS-CoV-2 | |
|---|---|
| 1. | BINDS TO ACE2 PRODUCED IN ENDOTHELIUM, PENETRATES INTO ENDOTHELIAL CELLS |
| 2. | DESTROYS ENDOTHELIUM REDUCING PRODUCTION OF PROS1 THERE |
| 3. | REDUCTION OF PROS1 PROMOTES BOTH CLOTTING AND CYTOKINE STORM (RUNAWY IMMUNE RESPONSE) |
Tables 1 and 2 are based on my understanding of paper [1].
The study [3] shows that the viral S-protein by itself (i.e. a "virion" - that is the spike S-protein without the viral RNA) may alone cause similar damage to the endothelial cells as described in the Table 2.
It seems this may have some big implications for the anti-viral measures that are based on the spike S-protein by itself. Regardless whether this involves injecting the S-protein alone, with a weak/disabled form of viral RNA or by making the body manufacture that protein by itself. It means that such measures may pose the similar threat for some patients, as the viral infection itself.
Quote from paper [3]:
... It is concluded that ACE2+ endothelial damage is a central part of SARS-CoV2 pathology and may be induced by the spike protein alone.
--- Updated 31-May-2021 ---
The Spike Protein - Dr. Byram Bridle Professor of Viral Immunology University of Guelph, 29-May-2021
Above video was censored by You Tube, below are some alternatives:
Quote:
We have made a big mistake by incoculating people with the toxic spike-protein"
--- Updated 26-June-2021: "Bridging" or ADE (Anti-biody Dependent Enhancement) of infection ----
Quote:
To the Editor - For certain diseases, patients who have been previously infected by one strain of a virus and who are later infected by another strain can suffer outcomes that are worse than those infected only once. One explanation for this phenomenon is that differences between two viral serotypes can compromise the ability of antibodies induced by the first infection to neutralize the second one; instead, the antibodies elicited by the first infection ‘bridge’ the second viral strain to immunoglobulin G (IgG) antibody constant region (Fc) receptors on immune cells, such as macrophages. Because this bridging is believed to enable viral entry into immune cells, shifting the tropism of the virus1, the outcome manifests as an antibody-dependent enhancement (ADE) of infection and a potentially more serious recurrence of disease. This phenomenon is often observed when antibody concentrations decrease as a result of waning immunity; an antibody may neutralize potently at high concentrations but cause enhancement of infection at sub-neutralizing concentrations.More reference papers:
COVID-19 May Trigger Hyperglycemia and Worsen Disease by Harming Fat Cells OCTOBER 1, 2021
"Hyperglycemia in acute COVID-19 is characterized by insulin resistance and adipose tissue infectivity by SARS-CoV-2", by Moritz Reiterer et al., Cell Methabolism, September 15, 2021
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