New Science: How SARS CoV2 and the Genetic Jabs Cause Blood Clots
New research shows how the engineered SARS C0V2 virus as well as the genetic jabs sabotage blood cell properties that help fight natural coronaviruses, to cause deadly blood clots instead.
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Transcript
New revelations explain the unusual lung pathology found among the sickest of COVID-19 infection patients and a much bigger problem which is the extensive blood clotting among COVID “vaccine” victims.
We understand the important role of ACE2 receptors for both SARS CoV2 infection and much of the disease and death resulting from the genetic injections that induce mass production of the virus’s spike protein in their victims. Autopsies of persons who died in the weeks or months following the injections, often show that ACE2 receptor-rich tissues like young people’s hearts, are heavily laden with spike protein and then attacked by the victims’ own immune systems.
Blood clots, especially in small blood vessels are another common finding in injection victims which accounts for much of their suffering and death. Many microscopic images have circulated showing red blood cells and platelets clumping together. These seemingly sticky blood cells can not deliver oxygen effectively. Instead, they plug small blood vessels causing many tissues to suffer and die.
In WHO-occupied countries like Canada, we were obstructed from performing autopsies on people who died with COVID-19 pneumonia in 2020. Thankfully we were able to access information from rare autopsies that were performed elsewhere. These autopsies revealed that the victims’ lungs did not appear like normal cases of pneumonia. Pneumonia is generally a disease of the smallest airways and alveolar sacs in the lung. These airways are swollen and mucous accumulates there. However, with COVID-19 pneumonia, the airways and alveoli were spared. Instead, it was predominantly in the tiny blood vessels of the lungs where the pathology was found. There was blood clotting and obstruction of the capillaries as well as the smallest arterioles and veins that supply these capillaries.
This knowledge resulted in the inclusion of aspirin and other platelet-inhibiting drugs in the multi-sequential repurposed drug treatment protocols for covid-19 developed by The World Council For Health https://worldcouncilforhealth.org/resources/early-covid-19-treatment-guide/ , the FLCCC https://covid19criticalcare.com/protocol/i-care-early-covid-treatment/, and other excellent groups. These treatments were very successful in countries where the authorities did not prevent their use.
Since 2021, we have a much bigger problem than COVID-19 infections. These problems are resulting from the COVID injections being mislabelled as “safe, effective vaccines.” The clumping of blood cells and clotting of small blood vessels is one of the main pathologies seen both clinically and on autopsies.
What has made this puzzling is that red blood cells and platelets have no ACE2 receptors at all. The endothelial cells lining the small blood vessels have very few ACE2 receptors. So how did the SARS C0V2 virus cause the unusual small blood clotting pathology of COVID-19 pneumonia? And… How are the spike protein-producing genetic injections or so-called “covid-19 vaccines” causing the clumping of blood cells, and the plethora of blot clots and microvascular clotting pathology seen in their victims?
This is why we are now particularly grateful to four scientists who recently published this paper: “Sialylated Glycan Bindings from SARS-C0V2 Spike Protein to Blood and Endothelial Cells Govern the Severe Morbidities of COVID-19.” Thanks to David Scheim, Paola Vottero, Alessandro Santin, and Allen Hirsch for this work. Thanks also to my friends and colleagues Dr Roger Hodkinson and Dr Peter McCullough for bringing this to our attention.
Here are some of the key insights:
Coronavirus spike protein surfaces are rich with molecules called sialylated glycans.
Coronaviruses initially adhere to our cells by their sialylated glycans on their spike protein adhering to Sialoglycoproteins on the coating of our cells. Once adhered in this way, the virus migrates to its replication receptor. In the case of SARS CoV2 the dominant receptors for this are ACE2 receptors. Once the spike protein engages the ACE2 receptor, then the actual process of infection of the cell and replication of the virus begins. If there are no ACE2 receptors on the cell, the virus can stick to the cell but not infect it or replicate.
Red blood cells and platelets have no ACE2 receptors; and endothelial cells that line small blood vessels have very few.
The SARS C0V2 virus can stick to the red blood cells and platelets, but it can not infect these cells nor be replicated there.
Before coronavirus gain of function research (aka viral bioweapons development), there were two coronaviruses that infected humans. These were two of the viruses causing “common colds” . These colds were much milder diseases than those of the newer coronaviruses: MERS, SARS, or SARS C0V2.
Naturally, the sialylated glycan-rich surface of red blood cells and platelets actually served a natural protective function. Viral particles get stuck to them, but can not actually infect them for lack of replication receptors such as the ACE2. Thus these viral particles were sequestered by the blood cells which prevented them from infecting other cells. The red blood cells and platelets could carry a reasonable amount of these viruses, and these viruses would be disposed of along with the blood cells when they were old and broken down by the liver and spleen.
The natural mild disease-causing coronaviruses have an enzyme expressed on their surface called hemagglutin esterase. This enzyme disrupts the adherence of the spike protein sialylated glycans to the Sialoglycoproteins on the blood cells’ surfaces. So the red blood cells and platelets would pick up viral particles, and the viral particles would also free themselves by the action of this enzyme. This resulted in a balance whereby the red blood cells and platelets help to reduce the viral load to a reasonable degree.
The modern gain of function cornavirus SARS C0V2 as well as SARS and MERS do not express the hemagglutin esterase enzyme on their surface. The result is red blood cells and platelets become excessively coated with the virus, and the viruses act like glue, sticking red blood cells and platelets to each other. Hence we see the microvascular clotting in the lungs and other organs in the rare people who became very ill or died with SARS C0V2.
Since the rollout of the forced and coerced covid-19 spike producing genetic injections, or so-called
“safe and effective vaccines” we have unprecedented disease, death, and disability in all heavily injected nations.
These injections have multiple mechanisms by which they cause injury and death. Among them are: 1. immune system disruptions; 2. spike protein coating ACE2-receptor-rich-tissues and triggering an autoimmune attack on these tissues; and 3. blood clots.
We now have a deeper understanding of how the spike proteins are causing the clumping of blood cells, and both microvascular and large vessel blood clotting.
Ivermectin has a strong ability to bind to multiple spike protein glycan-binding sites, and this accounts for at least some of its tremendous value both in treating COVID-19 infections and treating or preventing blood clotting caused by COVID-19 genetic injections.
Aspiring also remains very relevant.
There are many more details to the science of sialylated glycan binding of spike proteins to red blood cells, platelets, and blood vessels. To explore those, the in-depth article by Scheim, Vottero, Santin, and Hirsh is below.
Here place the official-looking title of the article and the authors. I have attached it as an image
Source: https://www.mdpi.com/1422-0067/24/23/17039
Related Material and Links:
Covid-19 Infection Treatment:
Covid “Vaccine” and Spike Protein Detoxification:
Dr Peter McCullough: How Does SARS-CoV-2 and COVID-19 Vaccination Cause Hemagglutination?
Mark, did you notice that this review paper that you’ve cited (which is not a detailed study and hence has no Methods section) has no reference for their opening line about “the virus”?
“The virus that caused COVID-19 was first named “severe acute respiratory syndrome coronavirus 2” (SARS-CoV-2) in February 2020 in recognition of the disease’s pulmonary symptoms and the lung’s role as its initial target organ, as with its SARS predecessor.”
The authors didn’t attempt to give a reference to a study showing the existence of the alleged “virus” – probably because there are none… and if they were to cite the pseudoscientific “isolation” studies we could easily pull them apart.
It’s distressing that are you still promoting this scary weaponized “virus” narrative that has zero valid scientific evidence behind it.
That was an awesome presentation clearly explaining a complex topic. Thank you.