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
4) intimately related. In both diseases, the body deposits c3 complement (and most likely other immune complexes/antibodies) into the endothelium. Except, in the case of COVID-19, the “Graft” and the “Host” are virtually synonymous as the “reaction” is replicated sans transplant.
5) This progressive deposition of IgM, IgG, C3, and prominent infiltration of cytotoxic T cells and macrophages, with a small number of NK cells is behind the progressive destruction of the MICROVASCULATURE. It also leads to the Thrombotic Microangiopathy we are observing and may
6) contribute to the deaths of healthy young people throughout the world.
Another major contributing factor is the induction of AT1 Receptor Antibodies. It is suggested that AT1-receptor antibodies have similarities to anti–endothelial-cell antibodies since endothelial cells
7) have one AT1 receptor, and AT1-receptor antibodies induced phosphorylation of ERK 1/2 in endothelial cells. It is further suggested that binding of AT1-receptor antibodies to the AT1 receptor is a critical step for activating the downstream signaling cascade, mimicking the
8) action of angiotensin II and inducing damage to the allograft. Emerging information has established that angiotensin II acts as an inflammatory cytokine participating in various vascular disorders.
In conclusion, at the heart of both diseases is the induction of multiple
9) autoantibodies. In GvHD the body rejects a foreign substance with immense molecular mimicry. In COVID-19 the body rejects a foreign substance with immense molecular mimicry.
nejm.org/doi/full/10.10…
nature.com/articles/37800…
pubmed.ncbi.nlm.nih.gov/26718/
kidney-international.org/article/S0085-…

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More from @Parsifaler

26 Dec
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
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
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
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
5 Dec
1) SARS-CoV-2 AND MICROVASCULAR DESTRUCTION: IS THE SPIKE PROTEIN SIMPLY CAUSING THE “REMOVAL” (DESTRUCTION) OF THE MICROVASCULATURE? THE RELATION TO SYNDROME X
SYNDROME X was a disease that resembled coronary artery disease but the patients had clear coronary arteries. It was Image
2) dismissed as PSYCHOLOGICAL! It was discovered that the symptoms were of MICROVASCULAR CORONARY ARTERY DISEASE and a VERY REAL disease. Just like Long COVID. And, I believe, caused by the same pathologies – except they are for EVERY organ and system in the body in the case of
3) Long COVID. Please watch the referenced video. THE VESSELS ARE TOO SMALL TO REGISTER ON CONVENTIONAL TESTS.
A very interesting paper published in Nature Neuroscience 21 October 21 describes structural changes in cerebral small vessels of patients with COVID-19 and elucidate
Read 14 tweets
3 Dec
1) TODAY: A mathematical model supporting my hypothesis that it is the debris of damaged cells that does not undergo EFFEROCYTOSIS by the body which is causing the fatal cytokine storms.



The model focuses on cells that trigger inflammation
2) through molecular patterns: infected cells carrying pathogen-associated molecular patterns (PAMPs) and damaged cells producing damage-associated molecular patterns (DAMPs). The former signals the presence of pathogens while the latter signals danger such as hypoxia or the lack
3) of nutrients. Analyses show that SARS-CoV-2 infections can lead to a self-perpetuating feedback loop between DAMP expressing cells and inflammation. It identifies the inability to quickly clear PAMPs and DAMPs as the main contributor to hyperinflammation.
Read 4 tweets

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