The mechanism behind rona virus damage

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The key factor is the Vitamin K-dependent protein S (PROS1). While the damage is caused by the viral spike S-protein.

References:

1. "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


2. Wiki Protein S


3. "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.


4. "SARS-COV-2 mRNA Vaccine (BNT162, PF-07302048) 2.6.4 Overview of Pharmacokinetic Test",


5. "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.


6. "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


7. Talk by Dr. Byram Bridle on the "On-Point" program with Alex Pierson, 9:11, Posted on 27-May-2021


8. On-Point program with Alex Pierson, Globalnews Toronto

PROS1 has the following properties

TABLE.1: PROS1 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

TABLE.2: MECHANISM BEHIND SARS-CoV-2 (COVID-19) DAMAGE

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:

"I would probably prefer to have natural immunity" — Dr Byram Bridle (Viral Immunologist) February 24th, 2021

Alex talks with Dr. Byram Bridle, an Associate Professor on Viral Immunology at the University of Guelph about a new peer-reviewed study that suggests there may be terrifying reasons side effects such as heart inflammation, VITT, and other serious i…

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 ----

"Implications of antibody-dependent enhancement of infection for SARS-CoV-2 countermeasures", by Nikolai Eroshenko et al., Nature Biotechnology volume 38, pages789–791 (2020)

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

Hydroxychloroquine and cancer

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I am posting it as a place-holder to prompt a further digging.

The original video presentation, quoting from memory because the original video depictued in the screenshot below, has been since deleted by youtube (and my account has been blocked by Twitter).

The presenter discussed an in-vitro study using human cultured tissues, with and without Нуdrохуснlоrоquin : (1) lung cancerous tissue (HeLa) and (2) kidney tissue (non-cancerous). The study found that c0rоna virus (normal cv non c19) would attack the lung and the kidney tissue without hcq, while the virus would only attack the cancerous lung tissue but not the non-cancerous kidney tissue when hcq is added.

Further and additional referenced, not the actual presentation:

Clinical Trials Using Hydroxychloroquine.

[TO BE FINISHED LATER]