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
4) incredibly VIRULENT. But not SARS or SARS-CoV-2. Nothing like Nipah or Ebola or Marburg. Yet, bat viruses are perhaps THE BEST at spreading RAPIDLY in humans. Their virulence is testament to how difficult it is for our human immune systems to deal with bat viruses.
5) Next. Let’s look at ACE2. As I have previously stated, and as I summarize (even this is only a partial summary) in the graphic, ACE2 is the foundation upon which virtually all diseases of old age are modulated. Remove ACE2 – and you are suddenly, biologically speaking,
6) in your 90s.
It has already been observed that ACE2 autoantibodies develop after SARS-CoV-2 infection. This has been attributed to the abundance of antibodies that recognize the SARS-CoV-2 RBD (Spike Protein) and ACE2 protein in plasma or serum.
Also, it has been theorized
7) that some of the Ab2 binding regions, or paratopes, can also mirror the spike protein itself and bind to the same target as the spike protein, the ACE2 receptor.
I cannot stress the importance of this. I also cannot express the utmost urgency to test those who have received
8) Spike Protein therapies and the recovered for the presence of ACE2 Autoantibodies.
To me, this is too delicately horrific to have “evolved.”
sciencenews.org/article/bats-i…
journals.plos.org/plosone/articl…
nejm.org/doi/full/10.10…

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More from @Parsifaler

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
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

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