Michael Goldman, Free University of Brussels (ULB) And Catherine Holmes, Catholic University of Louvain
Marketed by the name of Vaxzevria, the SARS-CoV-2 vaccine developed by the pharmaceutical company AstraZeneca in collaboration with the University of Anti-Oxford is currently monitored exclusively by healthcare institutions in various countries. Many vaccination victims are certainly victims of visceral accidents, sometimes even fatal, causing blood clots immediately after vaccine administration.
Currently, WHO considers “compromised, but not confirmed” a rare form of thrombosis apparently associated with the Oxford-Astra Zeneca vaccine, while the European Medicines Agency considers the existence of the link “possible.” General Chat Chat Lounge In France, on the 1stis the As of April 2021, more than 2,454,000 injections were reported, and 12 cases of these unconventional thrombosis were documented, resulting in four deaths.
Among the leaders that can explain these very rare side effects is an autoimmune reaction, which involves the chemical messenger produced by blood platelets, platelet factor 4 (PF4).
Auto antibody and thrombosis after antibody vaccination
The Oxford-Astra Zeneca vaccine is a viral vaccine (ChAdOx1) infected with a virus, which is responsible for inflammatory infections in monkeys (chimpanzee adenovirus). Its DNA has been changed so that it cannot reproduce the virus infected. It also contains genetic instructions for making spike protein of the SARS-CoV-2 coronary virus. Once inserted, this viral vector is inserted into some cells of the vaccine person, which will then produce SARS-CoV-2 spike protein. Detected by the immune system, it triggers an immune response that the body will remember, and it will activate again that day when it is infected with that SARS-CoV-2 coronary virus.
Shortly after receiving this vaccine, some people developed atypical thrombosis. They are actually present at abnormal sites – especially in some cerebral veins – as well as thrombocytopenia, as well as a drop in the number of platelets in the blood, which plays a major role in cracking. They are much less complicated (1,000 cases of vaccination per 1,000 cases), but many are already depressed with obesity.
Strict forms of code-19 are found to be linked to an autoimmune type of antibody response.
Research has shown that the victims of these side effects contain serum autoantibodies against their own platelets, and in particular “platelet factor 4” (platelet factor 4 – PF4), also called CNCL4. , It makes chemical messenger. However, we do know that this type of antibody is included in another reference to thrombosis, which encourages thrombocytopenia heparin (a substance that originates from a particular bloodstream cell. An anticoagulant treatment). P4 antibodies are sometimes found in other clinical situations, including severe cavity 19.
What is Platelet Factor 4?
The main role of the platelets is to ensure the integrity of the blood vessels and to prevent blood when they are damaged. These, what, disk-like cells circulate in the blood today. When they encounter an impaired vascular wall, they “activate”: they change shape and act on the surface of the vessel when they conceal the contents of those particles.
These greens contain platelet alpha granules, which contain a large amount of platelet element 4. Proteins have the ability to carry a positive electric charge. When platelets are activated, PF4 quickly records negatively charged molecules (“anionic” molecules). Heparin, which is often used as an anticoagulant treatment, is a molecule that forms complexes with PF4.
Other molecular molecules are commonly expressed on the surface of endothelial cells, which also block the blood vessels that bind to platelet-released PF4. These molecules, called glycosaminoglycans, have intracellular cells with anticoagulant properties that are important in preventing activation of aggregation. When clot formation is important, PF4 contributes to the neutralization of these extracellular antidiabetic substances and represents a mechanism by which platelets cause coagulation activation and formation of thrombosis. Since PF4 is an important player in homeostasis, this set of physiological phenogens affects the blood vessels and allows blood flow to stop.
When an anticoagulant drug causes clots
PF4 plays a central and inflammatory role in heparin-induced dystocyanopathy. The result of this severe condition is a blood clot with a decrease in platelet count following heparin injection. It achieves this anticoagulant in 1 to 5 percent of patients, usually between 4 and 10 days after starting treatment.
These paraoxygenic thrombosis produced by heparin reveals that PF4 plays a major role in this rapid occurrence. The sequence of events can be stated as follows.
- In relation to platelet activation (following an infection, surgery, etc.), PF4 is released in large quantities. Heparin administration results in the binding of anticoagulant molecules with PF4 molecules.
- This leads to heparin-2, EL, PF4 immunogenic, saying that it initiates an immune response that manifests itself by producing antibodies directed against PF4 / heparin complexes. This phenomenon is equivalent to a drop in the natural tolerance of a protein that we normally associate. This is because our immune system does not normally show up in our own cells and their products. However, some antibodies also attack PF4 molecules, which are not bound to heparin.
- The Pf4 inhibitors present at the platform and cell surface attack the Pf4 antibodies that line the blood vessels.
- Anti-PF4 antibodies also bind to the receptors of antibodies present on the platform called FcgammaRIIA, which activates them;
- The plates are influenced by platelet activation and on contact with antidial cells to which the anti-PF4 antibody is also attached.
- Platelets exposed to anti-PF4 antibodies are free from rotation and die, which contributes to the decrease in the number of platelets.
Lastly, it is a catastrophic condition such as anticoagulant, administration of heparin, leading to blood clot formation. The diagnosis of this complication of heparin therapy is directed at antibiotics directed against anti-PDs, thrombosis and FF4 h / / epeparin directed complexes. One in the other is the other in the demonstration.
Similar thrombotic phylogenies associated with low platelet levels and anti-Pfx anemics autoantibodies have been reported in the absence of heparin exposure. These ointments are known to be non-hipper immunombomagopepinic droppings, thought to be damaged or damaged cells on the molecular molecule of bacteria. These substances are generally that they interact with PF4, change its adaptation and automatically generate a reaction that causes clot formation.
The abnormal incidence of clots associated with a decrease in the level of blood platelets is sometimes observed 4 to 16 days after vaccine injection, suggesting a trend of this type.
What happens after injecting AstraZeneca’s Vaxzevria vaccine?
Could it be that anti-PF4 autoimmune reactions are sometimes the cause of thrombotic side effects after administration of voxiviria? This hypothesis is only confirmed by activation of platelets in the serum of other infected patients with the demonstration of pf4 antibiotics.
However, the mechanism of the post-vaccine autoimmune response remains unclear. Possible involvement of adenovirus vectors has been reported in terms of its ability to activate adenovirus. This leads to questions about the anti-HIV-19 adenoviral vector vaccine available on European markets, developed by Johnson & Johnson. Activation of platelets is also linked to their ACE2 receptor motif by being linked to the vaccine by the Spc protein.
But how can an intramuscular injection be possible with this activation of the platform that circulates in the blood? We speculate that endothelial cells of muscle are one of the targets of adenoviral vectors, which will enhance their spike protein production. The blood vessels, therefore, may be infected with the “transmitted” antidial cells, ie, infected with the viral vectors contained in the vaccine. Platelets can activate spike protein interaction and release PF4. This was complicated by the anionic glycosaminoglycan released following local inflammation induced by PF4 vacuolation.
Thus, the combined action of adenovirus and spike protein on the platelets and epithelial cells acts together to cause formation of plexus to stimulate LB lymphocytes antagonizing PP4 antibiotics.
Identify risk factors for adoption of vaccination strategies
Given the extremely low prevalence of these dermatocytopenic thrombosis, research should focus on identifying individual risk factors that may determine the specific subjects to develop this type of response. These include genetic susceptibility factors.
Traps are present, among others, at the level of surface receptors that are actually different from one person to another, due to genetic variation. This element probably includes the presence of a “memory” immune cell that we know of information from previous contacts with PF4. They are therefore able to produce faster and stronger immune responses to these additives.
The past week has demonstrated the efficacy and the great potential of many international pharmacokines, among millions of vaccine subjects, a new, much less rare clinical entity. Although not all the mechanisms involved have been identified yet, autoimunity is a major breakthrough in the discovery of the role of PF4 and their understanding of the occurrence of these side effects.
These stombs are unusual, their inspection and management have now become standard. This new knowledge will make it possible to effectively and safely manage the vaccination campaign, in order to maintain or restore the climatic climate necessary for its success.
Michael Goldman, Chair Professor, Free University of Brussels (ULB) And Cedric Hermans, Chair Professor, Catholic University of Louvain
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