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.

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 heavilly laden with spike protein and then attacked by the victims’ own immune systems.

Blood clots, especially in  small blood vessels is another common finding in the 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, the FLCCC 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 mislabeled 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 proteins 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 cornaviruses: 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 cornaviruses 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 a glue sticking reb 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 roll out 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 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 micro-vascular 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.

Source: https://www.mdpi.com/1422-0067/24/23/17039

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The post New Science: How SARS CoV2 & Genetic Jabs Cause Blood Clots first appeared on Dr Mark Trozzi.

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