6 April 2021 — Anthrax Vaccine
The Venous Sinus System, where slow blood flow apparently predisposes to clots after the Astra-Zeneca Covid vaccination
Meryl Nass, M.D
The Astra-Zeneca “cheap and easy to store” “workhorse” vaccine causes blood clots in general, and in particular clots in the venous sinuses of the brain, which have killed or wounded a number of people, especially women under 55.
Disorders caused by blood clots, including heart attacks, vein thromboses, and strokes, are common. But the types of clots that may be linked to the AstraZeneca vaccine are exceedingly rare. They have been marked by low levels of platelets — the blood cell fragments that normally cause clotting.
The types of clots seen include cerebral venous sinus thrombosis, or CVST, a type of blood clot that occurs in the veins that drain blood from the brain, and a similar condition in the abdomen, known as splanchic vein thrombosis. The clots sometimes occur in combination with bleeding.
From the Washington Post:
The European Medicines Agency, the European Union’s regulator, said it is investigating at least 44 cases of the rare brain clots and at least 14 deaths among about 9.2 million vaccinations in 30 European countries…
As of March 29, Germany’s regulator has reported 31 cases of the unusual blood clots in 2.7 million people vaccinated with the AstraZeneca vaccine, nine of whom have died.
The J and J vaccine was also associated with blood clots in the clinical trial data presented to FDA. Both vaccines use an adenovirus vector to deliver DS DNA that codes for spike protein, and human cellular machinery produces this protein, for an uncertain period of time in uncertain quantities. So blood clotting may be due to the adenovirus vector, or to the spike protein, or to something entirely different.
The mRNA vaccines use mRNA to code for the spike, also using cellular machinery to produce the spike protein. The end result of all 4 vaccines is similar, and again, we do not know for how long the body makes this protein.
If the spike itself induces clotting, which is a reasonable hypothesis scientists have put forth, but is unproven, then all 4 vaccines would be thrombogenic (induce clotting). Dr. Patrick Whelan tried to warn the FDA about this possibility, but was ignored. He wrote:
Meinhardt et al. (Nature Neuroscience 2020, in press) show that the spike protein in brain endothelial cells is associated with formation of microthrombi (clots), and like Magro et al. do not find viral RNA in brain endothelium. In other words, viral proteins appear to cause tissue damage without actively replicating virus.
Is it possible the spike protein itself causes the tissue damage associated with Covid-19? Nuovo et al (in press) have shown that in 13/13 brains from patients with fatal COVID-19, pseudovirions (spike, envelope, and membrane proteins) without viral RNA are present in the endothelia of cerebral microvessels.
This is frightening information, providing a strong hint of the spike protein’s potential toxicity.
Many countries are counting on AstraZeneca’s vaccine. The European Union alone has purchased 400 million doses of the vaccine. The United States has bought 300 million doses of the vaccine, the largest pre-purchase deal of all those contracted by Operation Warp Speed, the vaccine and therapeutics fast-tracking project started during the Trump administration.
How did 20 countries deal with the clotting issue?
First they halted the vaccinations until they could review all the available data and get their narratives aligned. They then decided the A-Z vaccine did cause clots. But you cannot waste Covid vaccine (unless you are Emergent BioSolutions) so it had to be used. But in whom? In poorer countries of course. But what about the supplies already purchased by western Europe?
The public health leaders came up with a great idea. Restrict it, just for the elderly. If they die, there is almost always a preexisting condition to blame.
But apparently that wasn’t sufficient. So they started testing this vaccine in children.
A few countries stopped the A-Z vaccine altogether.
What about the US? Despite the problems with EBS’s failed production of the Johnson and Johnson/Janssen vaccine (up to 150 million doses may need to be thrown away) the US seems to be swimming in vaccine at the moment, and any adult can sign up for a dose. It is likely that Astra-Zeneca’s 300 million doses will be written off, in addition to the failed J and J doses.
Whether it will be used here remains an open question. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, told Reuters last week that the U.S. may not need the vaccine.“My general feeling is that given the contractual relationships that we have with a number of companies, that we have enough vaccine to fulfill all of our needs without invoking AstraZeneca,” Fauci said, without referring to the clotting problem now associated with the vaccine.
Can you imagine what the informed consent for the Oxford A-Z clinical trial in children says? “We are testing a vaccine known to cause lethal blood clots, in children, who almost never get severe Covid–therefore the benefits won’t exceed the risks of the vaccine in this demographic. Your child is at greater risk of dying from the vaccine than the disease.” How many parents would sign? The consent form necessarily must be a dishonest document. Here is a legal case for you British barristers.
As I was writing this, the news appeared that the clinical trials of the A-Z vaccine in children were finally paused, just today. Which is 2-3 weeks after the blood clotting issue surfaced.
How well does the Astra-Zeneca vaccine work in the elderly? Only two months ago the leaders of France and Germany told us:
Officials in Germany claim the Astra-Zeneca vaccine is only 8% effective in those over 65. French President Macron has complained to Agence France Press that the A-Z vaccine was only “quasi-ineffective for people over 65.”
So, in order to use up the supply, or perhaps for other purposes, Germany will now use the vaccine only in those over 60, and France will use it only in those over 55 — which are the age groups in which they claimed it didn’t work.
Si Zhang, Yangyang Liu, Xiaofang Wang, Li Yang, Haishan Li, Yuyan Wang, Mengduan Liu, Xiaoyan Zhao, Youhua Xie, Yan Yang, Shenghui Zhang, Zhichao Fan, Jianzeng Dong, Zhenghong Yuan, Zhongren Ding, Yi Zhang & Liang Hu
- 20k Accesses
- 34 Citations
- 490 Altmetric
Critically ill patients diagnosed with COVID-19 may develop a pro-thrombotic state that places them at a dramatically increased lethal risk. Although platelet activation is critical for thrombosis and is responsible for the thrombotic events and cardiovascular complications, the role of platelets in the pathogenesis of COVID-19 remains unclear.
Using platelets from healthy volunteers, non-COVID-19 and COVID-19 patients, as well as wild-type and hACE2 transgenic mice, we evaluated the changes in platelet and coagulation parameters in COVID-19 patients. We investigated ACE2 expression and direct effect of SARS-CoV-2 virus on platelets by RT-PCR, flow cytometry, Western blot, immunofluorescence, and platelet functional studies in vitro, FeCl3-induced thrombus formation in vivo, and thrombus formation under flow conditions ex vivo.
We demonstrated that COVID-19 patients present with increased mean platelet volume (MPV) and platelet hyperactivity, which correlated with a decrease in overall platelet count. Detectable SARS-CoV-2 RNA in the blood stream was associated with platelet hyperactivity in critically ill patients. Platelets expressed ACE2, a host cell receptor for SARS-CoV-2, and TMPRSS2, a serine protease for Spike protein priming. SARS-CoV-2 and its Spike protein directly enhanced platelet activation such as platelet aggregation, PAC-1 binding, CD62P expression, α granule secretion, dense granule release, platelet spreading, and clot retraction in vitro, and thereby Spike protein enhanced thrombosis formation in wild-type mice transfused with hACE2 transgenic platelets, but this was not observed in animals transfused with wild-type platelets in vivo. Further, we provided evidence suggesting that the MAPK pathway, downstream of ACE2, mediates the potentiating role of SARS-CoV-2 on platelet activation, and that platelet ACE2 expression decreases following SARS-COV-2 stimulation. SARS-CoV-2 and its Spike protein directly stimulated platelets to facilitate the release of coagulation factors, the secretion of inflammatory factors, and the formation of leukocyte–platelet aggregates. Recombinant human ACE2 protein and anti-Spike monoclonal antibody could inhibit SARS-CoV-2 Spike protein-induced platelet activation.
Our findings uncovered a novel function of SARS-CoV-2 on platelet activation via binding of Spike to ACE2. SARS-CoV-2-induced platelet activation may participate in thrombus formation and inflammatory responses in COVID-19 patients
Posted by Meryl Nass, M.D. at 11:20 PM