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
4) classic crown of spike proteins, but did not contain any actual virus. Exposure to this pseudovirus resulted in damage to the lungs and arteries of an animal model—proving that the spike protein alone was enough to cause disease. Tissue samples showed inflammation in
5) endothelial cells lining the pulmonary artery walls.
The team then replicated this process in the lab, exposing healthy endothelial cells (which line arteries) to the spike protein. They showed that the spike protein damaged the cells by binding ACE2. This binding disrupted
6) ACE2’s molecular signaling to mitochondria (organelles that generate energy for cells), causing the mitochondria to become damaged and fragmented.
Another paper by Lei, Zhang et al. proved SARS-CoV-2 infection impairs endothelial function and induces vascular inflammation,
7) leading to endotheliitis. SARS-CoV-2 infection relies on the binding of Spike glycoprotein (S protein) to angiotensin converting enzyme 2 (ACE2) in the host cells. We show here that S protein alone can damage vascular endothelial cells (ECs) in vitro and in vivo, manifested by
8) impaired mitochondrial function, decreased ACE2 expression and eNOS activity, and increased glycolysis.
Endothelial Injury and Repair
Prolonged and/or repeated exposure to cardiovascular risk factors can ultimately exhaust the protective effect of endogenous antiinflammatory
9) systems within endothelial cells. As a consequence, the endothelium not only becomes dysfunctional, but endothelial cells can also lose integrity, progress to senescence, and detach into the circulation28 (Figure 2). Circulating markers of such endothelial cell damage include
10) endothelial microparticles derived from activated or apoptotic cells, and whole endothelial cells.29 These markers have been found to be increased in both peripheral and coronary atherosclerosis disease, as well as other inflammatory conditions associated with increased
11) vascular risk such as rheumatoid arthritis and systemic lupus erythematosus.
Indeed, the Spike Protein also induces senescence in endothelial cells. SARS-CoV-2 Spike Protein Induces Paracrine Senescence and Leukocyte Adhesion in Endothelial Cells was the major finding and
12) title of a paper published in August in the Journal of Virology.
This then causes the endothelial cells to detach from the epithelium. The repair process is impeded as the Spike Protein furthermore, complementary increases and decreases phosphorylation of eNOS (endothelial NO
13) synthase) Thr-494 and Ser-1176 indicated impaired eNOS activity. This reduces/eliminates NO, which is necessary to repair the damaged endothelium.
Endothelial integrity depends not only on the extent of injury, but also on the endogenous capacity for repair. Mobilization of
14) these re[air cells is in part NO-dependent, and may thus be impaired in patients with cardiovascular risk factors. Conversely, factors that have been shown to improve endothelial function and NO bioavailability, such as exercise and statins, have also been shown to have a
15) potent positive effect on endothelial progenitor cell mobilization.
This damage and repair process not only results in microclotting/platelet activation, but also in the resulting fibrosis.
Vascular fibrosis, characterized by reduced lumen diameter and arterial wall
16) thickening attributable to excessive deposition of extracellular matrix (ECM), links with many clinical diseases and pathological progresses including atherosclerosis. It involves proliferation of vascular smooth muscle cell (VSMC), accumulation of ECM and inhibition of
17) matrix degradation. The risk factors associated with cardiovascular disease, including hypertension, hyperglycemia, dyslipidemia and hyperhomocysteinemia (HHcy), are also suggested as initiation and progression factors of vascular fibrosis. Vascular fibrosis has been found to
18) relate to renin-angiotensin-aldosterone system (RAAS), oxidative stress, inflammatory factors, growth factors and imbalance of endothelium-derived cytokine secretion. Angiotensin II (Ang II) and aldosterone, the circulating effector hormones of RAAS, are recognized as
19) responsible for the pathophysiology of vascular fibrosis.
Circulating endothelial cells have been found. This virtually proves a substantial portion of this hypothesis.
pubmed.ncbi.nlm.nih.gov/23375582/
ahajournals.org/doi/10.1161/ci…
ncbi.nlm.nih.gov/labs/pmc/artic…
journals.asm.org/doi/10.1128/JV…

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More from @Parsifaler

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
3 Dec
1) THE SPIKE PROTEIN, MICROVASCULAR DESTRUCTION/DYSFUNCTION/VIT D
YOU CANNOT FIND WHAT YOU ARE NOT LOOKING FOR!
There is no easy way to measure MICROVASCULAR DISEASE. IT HAS NOT BEEN LOOKED FOR! We have missed the forest for the trees. PLEASE READ WHY VITAMIN D IS SO IMPORTANT! ImageImage
2) Vitamin D is known to elicit a vasoprotective effect, while vitamin D deficiency is a risk factor for endothelial dysfunction (ED). ED is characterized by reduced bioavailability of a potent endothelium-dependent vasodilator, nitric oxide (NO), and is an early event in the
3) development of atherosclerosis. In endothelial cells, vitamin D regulates NO synthesis by mediating the activity of the endothelial NO synthase (eNOS). Under pathogenic conditions, the oxidative stress caused by excessive production of reactive oxygen species (ROS) facilitates
Read 7 tweets
2 Dec
1) IMPORTANT EVIDENCE SUPPORTING THE HYPOTHESIS THAT SARS-CoV-2 IS PRIMARILY A DISEASE OF THE SPIKE PROTEIN’S INTERACTION WITH THE MICROVASCULATURE
A large study was posted today, which I believe greatly supports the hypothesis that COVID-19 is not only a Vascular Disease, but,
2) specifically, a disease of the MICROVASCULATURE. This is due, mainly, to the Spike Protein’s injury to the endothelium.
If we look at the mortality rates from the Trends and associated factors for Covid-19 hospitalisation and fatality risk in 2.3 million adults in England
3) study, we find that OBESITY IS ACTUALLY A VERY, VERY SLIGHT RISK FOR MORTALITY. HOWEVER, UNDERWEIGHT IS A VERY, VERY SIGNIFICANT RISK FOR MORTALITY.
If we look at the other major mortality risks, we observe that they are CHRONIC KIDNEY DISEASE, SEVERE MENTAL ILLNESS
Read 12 tweets
30 Nov
1) MY MOST IMPORTANT FINDING TO DATE
MORE FOCUS > WHY COVID-19 LOOKS LIKE RADIATION POISONING
COVID-19: NOT JUST A VASCULAR DISEASE BUT A DISEASE OF SYSTEMIC MICROANGIOPATHY FOLLOWED BY SYSTEMIC FIBROSIS, ALMOST CERTAINLY INDUCED BY THE TISSUE-DAMAGING EFFECTS OF THE SPIKE
2) PROTEIN
Please review the first image. It is the most important image about the pathogenesis of COVID-19 we will ever see. Please note that SUPEROXIDE PRODUCTION CORRESPONDS DIRECTLY WITH SPIKE PROTEIN LEVELS. SARS-CoV-2 Spike protein (S protein) induced an excessive ROS
3) production in a dose dependent manner in endothelial cells.
Next, please replace Ionizing Radiation in the second image with Spike Protein. Now we understand why pathologists are observing that COVID-19 patients appear to be dying of “Radiation Poisoning.” The Spike Protein
Read 16 tweets
26 Nov
1) SONATA ALLEGRO FORM: DEVELOPMENT – SKEWED T CELL RECEPTOR REPERTOIRE AND THE SPIKE PROTEIN – SEVERE HYPERINLAMMATORY REACTION AND AUTOIMMUNE DISEASE/SEVERE COMBINED IMMUNODEFICIENCY
Continuing with our study of the Graft vs Host Disease (GVHD) “response” to the SARS-CoV-2
2) Spike Protein.
Upon further investigation, I believe the GVHD-like response being observed in those exposed to the Spike Protein of SARS-CoV-2 is due to the Spike’s ability to SKEW TCR (T Cell Receptor) repertoire. This appears to occur via a variety of mechanisms.
First, and
3) ironically, there is a massive T-Cell activation and proliferation due to a super-antigenic portion of the Spike Protein. Using in silico modeling and analysis, it was found that SARS-CoV-2 encodes a superantigen motif near its S1/S2 cleavage site. This region is highly
Read 11 tweets

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