This article features two studies that showed that the spike proteins of the SARS-CoV-2 virus produce abnormal blood clots.
After reading, this essay will add knowledge on the clotting problems seen in COVID-19 disease, Long COVID, and post-COVID “vaccine” injuries.
Clot and Anti-Clot
In daily life, blood clots form inside the body when bleeding happens. It can be from external injury or metabolic inflammation.
The clot is essential not only to stop bleeding but also to begin the repair process. But there should be a balance. Too many huge clots can lead to blood supply loss, for example, in an arm or leg, as they block the blood vessels.
Large clots can also interfere with blood oxygenation, as in pulmonary embolism (PE), where a clot travels up the leg to the lungs.
Many people can “suddenly die” due to PE. Loss of blood supply to a limb can lead to critical limb ischemia and amputation. Clots can happen anywhere in the body. These are just examples.
To provide balance, there exists an anti-clotting mechanism to check clot formation. The anti-clotting mechanism is used in medicine to help control disease-causing blood clots.
Heparin exists in the body and can also be given as a medicine. Heparin increases the activity of the anti-clotting factors antithrombin (AT) and heparin cofactor II (HCII).
Both AT and HCII inactivate thrombin to prevent excessive clotting. Thrombin is the main effector of the clotting cascade. The clotting cascade is a series of biochemical reactions that results in blood clot formation.
A study by Zhang and colleagues showed that the spike protein of the SARS-CoV-2 virus that causes COVID-19 could bind to heparin. The result is a decrease or a loss of anti-clotting activity of AT and HCII, forming disease-causing clots.[1]
The spike protein is also made after administration of the mRNA vaccines like Pfizer and Moderna and vector vaccines like AstraZeneca and Janssen.
The authors of SARS-CoV-2 spike protein causes blood coagulation and thrombosis by competitive binding to heparan sulfate are from the Chinese Academy of Sciences, Nantong University in China, and the Imperial College London.
The research was published in the International Journal of Biological Macromolecules.
Spike Proteins Cause Abnormal Inflammatory Blood Clots
Another study, this time from the US, found another way that the SARS-CoV-2 spike protein facilitates blood clotting.[2]
Fibrinogen in the blood participates in normal clot formation. Fibrinogen gets activated to form fibrin, forming a scaffold or a skeleton where other blood, like the platelets, can adhere to and form a clot.
Thrombin which was mentioned earlier as the main effector of clotting is the one that activates fibrinogen.
The US study showed that the spike protein could activate the fibrinogen without input from the thrombin. The clots that formed were different from the usual. The authors report that,
Spike strikingly altered the fibrin clot structure resulting in thinner fibers with a rough appearance and increased clot density as shown by scanning electron microscopy (SEM).
Additionally, the spike protein formed fibrins that formed delayed fibrinolysis.
Incubation of Spike with fibrin delayed plasmin degradation of both the β-chain and the γ-γ dimer, suggesting that Spike delays fibrinolysis.
Plasmin is a substance in the body that lyses or dissolves fibrins and blood clots once the clot has done its work.
Fibrinolysis is essential to reopen an occluded vessel. Apparently, spike-formed clots do not follow normal body processes.
Spike-formed clots are inflammatory.
Further results showed that the fibrins induced by the spike proteins causes the release of reactive oxygen species that trigger more inflammation.
They confirmed those findings in mice that formed extensive lung fibrin deposits. A closer examination of the lungs showed inflammation of the endothelium, the inner lining of the blood vessels.
Additionally, inflammatory markers are also higher in the endothelium and activation of immune cells, which explains the inflamed endothelium.
In short, this study shows that the SARS-CoV-2 spike protein forms structurally abnormal blood clots that cause more inflammation.[2]
The same study demonstrated that a monoclonal antibody called 5B8n could neutralize that abnormal blood clot.
Putting together these two studies, the SARS-CoV-2 spike protein promotes the rapid formation of abnormal blood clots that cause more inflammation.
The findings help explain why severe COVID-19 patients have more complications. The formation of abnormal blood clots and prolonged inflammation due to the SARS-CoV-2 spike proteins highlight why Long COVID and COVID “vaccine” adverse effects happen.
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Related:
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- Four ways the spike protein rapidly forms blood clots resistant to breakdown
- Molecular mimicry between the spike protein and humans can shut down platelet production
- Retinal complications after COVID shots
- RNA splice study shows why AstraZeneca and Janssen jabs are clot shots
- Blood Vessel Damaging Proteins of the SARS-CoV-2
- Cerebral Thrombosis after the Pfizer Covid-19 Vaccine
- The High Risk of Deadly Brain Clots in the J & J COVID Vaccine
- This study shows a Ten-Fold Risk of Developing Blood Clots after the COVID Vaccines.
- You got the COVID shot and found that others developed blood clots. Now what?
- Platelet Changes Cause Blood Clots in COVID-19
- Unidentified Foreign Bodies in the Vaccines Form Clots
References:
- Zheng Y et al. SARS-CoV-2 spike protein causes blood coagulation and thrombosis by competitive binding to heparan sulfate. Int J Biol Macromol. 2021 Dec 15;193(Pt B):1124-1129. doi: 10.1016/j.ijbiomac.2021.10.112. Epub 2021 Oct 29. PMID: 34743814; PMCID: PMC8553634.
- Ryu JK et al. SARS-CoV-2 spike protein induces abnormal inflammatory blood clots neutralized by fibrin immunotherapy. bioRxiv [Preprint]. 2021 Oct 13:2021.10.12.464152. Doi: 10.1101/2021.10.12.464152. PMID: 34671772; PMCID: PMC8528086.
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