Thread by @Parsifaler

1) UPDATED SYNTHESIS: EXTREMELY URGENT
IT’S COMPLICATED, BUT CLEAR – LOOKING ONE MOVE DEEPER
THE SPIKE PROTEIN PATHOGENIC ALGORITHM – DUAL PATHS TO TERMINAL SYSTEMIC FIBROSIS: IMMEDIATE FOR THOSE WITH SIGNIFICANT COMORBIDITIES, INDUCED FOR THOSE WITHOUT
The Spike Protein is

2) inducing terminal systemic fibrosis of all organs, including the blood, via two principal mechanisms.
The first is a direct, immediate path via binding to RGD-binding integrins, which includes several TGF-β -activating integrins. This this activates Myofibroblasts which

3) induces Fibrosis. Indeed, in autopsies of COVID-19 patients with advanced disease, 38% collagen deposition was found in their lungs.
This is a rapid and certainly fatal circumstance.
But, this is not limited to the lungs. In a series of cardiac autopsies conducted in

4) Washington state, the most common changes observed were fibrosis in 14 (100%) patients and myocyte hypertrophy in 13 (93%) patients.
Let that sink in. In 100%. In EVERY SINGLE CARDIAC AUTOPSY, FIBROSIS WAS OBSERVED.
The other mechanism is via DNA Double Strand Breaks and

5) Impaired DNA Repair Mechanisms. This induces fatal systemic fibrosis in those who do not succumb to the initial assault.
In mice that have their DNA Repair Mechanisms genetically deleted (this kind of mouse was developed to study Alzheimer’s) they experience THE SAME LEVEL OF

6) DNA DAMAGE AS NORMAL TYPE MICE. HOWEVER, THEY ACCUMLATE DNA LESIONS FASTER DUE TO THEIR IMPAIRED DNA REPAIR RESPONSE.
What is the effect of this?
THEIR AGING IS ACCELERATED 6-FOLD OVER NORMAL TYPE MICE.
What happens to these mice?
They develop conditions common in elderly

7) humans such as osteoporosis, pulmonary fibrosis, chronic kidney disease, cardiovascular disease, muscle wasting, peripheral neuropathy, hepatic fibrosis, urinary incontinence, intervertebral disc degeneration, cognitive decline, and loss of hearing and vision.

8) Sounds like Long COVID, doesn’t it?
How does this happen?
SARS–CoV–2 full–length spike protein inhibits DNA damage repair by hindering DNA repair protein recruitment.
Why should this happen in some faster than others? Let us look at Diabetics.
Diabetes-induced, persistent DNA

9) damage is associated with organ fibrosis. Non-diabetics are accumulating DNA damage lesions, which will result in terminal fibrosis, but Diabetics are accumulating them FASTER as they already experience HIGHER LEVELS OF DNA DAMAGE, WHICH IS ALSO NOT. BEING. REPAIRED.

10) Let us look at Obesity.
Altered DNA repair; an early pathogenic pathway in Alzheimer’s disease and obesity. In an inverted mechanism to Diabetes, the Obese already have an impaired DNA Repair Response, so, their DNA Repair Response becomes DYSREGULATED INCREASINGLY FASTER

11) than those without this common comorbidity.
What is the ultimate point of the Spike Protein’s inhibition of DNA repair?
Loss of the DNA repair potential results in persistent DNA damage signaling, senescence, SASP, fibrosis, and organ failure.
embopress.org/doi/full/10.15…

12) journals.asm.org/doi/10.1128/JV…
ncbi.nlm.nih.gov/pmc/articles/P…
nature.com/articles/s4159…
pubmed.ncbi.nlm.nih.gov/26440363/
onlinelibrary.wiley.com/doi/full/10.11…
ncbi.nlm.nih.gov/pmc/articles/P…
ncbi.nlm.nih.gov/pmc/articles/P…
ncbi.nlm.nih.gov/pmc/articles/P…