Misrepresents source: None of the studies reported harmful effects from spike protein produced by COVID-19 vaccination. On the contrary, one study suggested that COVID-19 vaccines targeting the spike protein might prevent blood vessel damage.
Lack of context: The spike protein produced by COVID-19 vaccination behaves differently from spike protein produced during infection. While some spike protein produced through vaccination might enter the bloodstream, it is at a much lower level compared to the amount associated with damage in infected animals.
AFFIRMATION COMPLETE: “The infamous spike protein of the coronavirus gets into the blood where it circulates for several days post-vaccination and then accumulated in organs and tissues including the spleen, bone marrow, the liver, adrenal glands, and in quite high concentrations in the ovaries”; “a large number of studies has shown that the most severe effects of SARS-CoV-2, the virus that causes COVID-19, such as blood clotting and bleeding, are due to the effects of the spike protein of the virus itself”
REVIEW
In late May 2021, the claim that COVID-19 vaccines could cause blood vessel damage to vaccinated people went viral on social media platforms, including Facebook, Instagram, Reddit, and Twitter. Many posts and articles (see examples here and here), like this article from LifeSiteNews, based this claim on a 28 May 2021 radio interview between the Canadian broadcaster Alex Pierson and the immunologist Byram Bridle. The interview received more than 39,000 interactions on Facebook, according to the social media analytics tool CrowdTangle.
During the interview, Bridle claimed that the spike protein produced through COVID-19 vaccination, which generates immunity against the disease, enters the bloodstream and can damage the blood vessels and brain. Scientists who reviewed this claim for Health Feedback found it misleading because it misrepresented the results from scientific studies and was based on cherry-picked information.
Bridle’s claim was based on three assumptions:
- The spike protein from SARS-CoV-2 alone is the main cause of blood vessel damage in COVID-19 patients.
- The vaccine-derived spike protein damages the body in the same way as the spike protein produced during viral infection.
- The vaccine-derived spike protein enters the bloodstream and accumulates at harmful levels in tissues, such as the spleen, bone marrow, liver, adrenal glands, and ovaries.
In this review, we explain why these three assumptions are unsupported by current evidence.
What is the spike protein?
Coronaviruses are a large family of viruses that cause respiratory illnesses in animals and humans. They receive their name from a crown (corona, in Latin) of spikes made of protein that cover the surface of the virus when observed under an electron microscope. The spike protein allows the virus to enter the cells by binding to a receptor called angiotensin-converting enzyme 2 (ACE2) that sits on the surface of some cells[1].
An immune response against the spike protein could eliminate infected cells while preventing the virus from entering the cells and producing more viral particles. That is why the majority of COVID-19 vaccines target this protein[2]. These vaccines work by exposing the body to the spike protein of SARS-CoV-2, the virus that causes COVID-19, thereby training the immune system to respond more rapidly and effectively when it encounters the virus in the future.
None of the COVID-19 vaccines authorized for emergency use by the U.S. Food and Drug Administration (FDA) contains the spike protein. Instead, they instruct the cells to produce the protein on their own. Viral vector-based COVID-19 vaccines (Johnson & Johnson and the Oxford-AstraZeneca vaccine, authorized for emergency use in the European Union and other countries but not in the U.S.) deliver the genetic instructions for making the protein in the form of DNA. The genetic instructions are delivered within a modified harmless version of an adenovirus similar to the one that causes the common cold. In contrast, mRNA COVID-19 vaccines (Pfizer-BioNTech and Moderna) use mRNA carried within fat droplets called lipid nanoparticles.
Evidence that the spike protein from SARS-CoV-2 cause cardiovascular damage is preliminary
Although COVID-19 is primarily a respiratory disease, several studies showed that the disease causes cardiovascular damage in many patients. Complications such as irregular heartbeat, blood clots, heart failure, and stroke can occur even after the patient recovers[3]. Bridle claimed that the spike protein alone is responsible for most of these vascular complications in COVID-19 patients. He based his claim on several studies that we discuss below, which evaluated the effect of the spike protein on blood vessels. However, these studies provide insufficient data to support this claim.
Some studies found that SARS-CoV-2 can indeed infect and damage endothelial cells[4-6]. These cells line the inside of blood vessels and have the ACE2 receptors, making them susceptible to SARS-CoV-2 infection.
One of these studies found signs of endothelial damage and fragments of SARS-CoV-2, including the spike protein, in the brains of 13 deceased COVID-19 patients[5]. When the researchers injected the spike protein into mice, the animals developed neurological symptoms and brain inflammation similar to that observed in COVID-19 patients.
Later, a small study by Lei et al. at the Salk Institute reported endothelial damage in the lungs of hamsters injected with an engineered pseudovirus, a particle that carried the SARS-CoV-2 spike protein on its surface[6]. In an email to Health Feedback, Peter Hotez, an expert in vaccinology and professor at Baylor College of Medicine, explained that this study « looks at cellular mechanisms of how viral spike protein works, not the immune response from a vaccine ».
Julie Bettinger, an associate professor at the Vaccine Evaluation Centre at the University of British Columbia, pointed out to Health Feedback [read Bettinger’s comment in full below]:
“[The Lei et al. study] actually concludes by stating, ‘vaccination-generated antibody and/or exogenous antibody against S protein not only protects the host from SARS-CoV-2 infectivity but also inhibits S protein-imposed endothelial injury’. That is, COVID-19 vaccines may actually prevent vascular damage.”
Therefore, COVID-19 vaccines targeting the spike protein might protect the cells not only from SARS-CoV-2 infection but also from the endothelial damage caused by the spike protein if the infection occurs, contradicting Bridle’s claim.
Although the findings from both studies suggest that the spike protein of SARS-CoV-2 could damage blood vessels, they don’t provide evidence that this does occur in COVID-19 patients. Abraham Al-Ahmad, an assistant professor of pharmaceutical sciences at the Texas Tech University, highlighted several limitations of this study in his response to Health Feedback [read Al-Ahmad’s comment in full below].
The first limitation is that the authors of the study didn’t provide information about the type of pseudovirus they used in their study, which determines the behavior of the pseudovirus and how similar it is to the spike protein from SARS-CoV-2.
The second limitation is that we don’t know the viral load, which is the amount of virus, injected into the animals and how it compares with the viral load in COVID-19 patients. The third limitation is that results from animal studies often don’t reflect what happens in human patients and require further validation in humans. Al-Ahmad explained:
“We have some indications that SARS-CoV-2 can be detrimental to endothelial cells, but at this point, we are lacking two important pieces of information:
1) What is the blood/plasma viral load we need in a patient to show signs of endothelial cell damage (we only know these patients died from COVID-19 complications)?
2) How does this viral load compare to the amount of spike protein displayed on [pseudo]viruses, based on the experimental data presented in the study?”
Therefore, Bridle’s claim that the spike protein from SARS-CoV-2 is alone responsible for blood clotting and other vascular symptoms in COVID-19 patients remains unsupported at this point in time. The potential of the spike protein to cause vascular damage in COVID-19 patients requires further investigation.
Vaccine-derived spike proteins differ from the spike protein produced in infection and behave differently in the body
Bridle’s claim rests on the assumption that if the viral spike protein causes cardiovascular toxicity in COVID-19 patients, the spike protein produced in vaccinated people should be toxic as well. However, this assumption is incorrect because there are important differences between the spike protein produced during infection and the spike protein produced by vaccination.
While both mRNA vaccines and viral vector vaccines carry the instructions to produce the entire spike protein, the cells break down much of the protein into small fragments. Furthermore, unlike infection, the spike protein from COVID-19 vaccination doesn’t get assembled into new viral particles. Instead, it contains a component that makes it attach to the cell surface as it would do to the viral surface. Finally, the spike protein produced by the U.S. FDA-authorized COVID-19 vaccines is genetically modified to enhance the immune response and prevent its binding to ACE2 receptors, based on methods developed in an earlier study[7].
Contrary to Bridle’s assumption, these differences suggest that vaccine-derived and infection-derived spike protein « behave very differently » in the body, as the Salk Institute stated in a press release.
Al-Ahmad explained:
“When it comes to COVID19 vaccines, cases of thrombosis (clotting) following COVID19 vaccines have been reported with the Oxford-AstraZeneca and the Johnson & Johnson vaccines [However,] the incidence of thrombosis following immunization is very likely to be below or similar to the background occurrence of such events in the population. The EMA made it clear: the benefits still outweigh the very small perceived risk when it comes to clotting and cerebral venous thrombosis.”
In contrast, COVID-19 makes infected individuals more likely to develop blood clots, which affect up to 50% of hospitalized COVID-19 patients[8].
Most of the spike protein generated by vaccination remains at the injection site; protein levels in the blood are very low
COVID-19 vaccines are injected in the upper arm muscle, where they instruct the muscle cells to produce the spike protein. Most of the vaccine remains around the injection site, either in the muscle cells or in the lymph nodes responsible for the immune response.
Bridle claimed that this assumption is wrong, and the spike protein from COVID-19 enters the bloodstream, accumulating in tissues such as the spleen, bone marrow, liver, adrenal glands, and ovaries. Bridle based this claim on a small study by Ogata et al. that examined blood samples from people who received the Moderna COVID-19 vaccine and detected spike protein in 11 out of 13 vaccinated people[9].
Bettinger explained that the sample size of this study was very small. Besides reporting that part of the vaccine-derived spike protein enters the blood, “nothing about being detrimental is mentioned in the publication,” she added.
Ogata et al. found extremely low levels of the spike protein compared to the harmful levels reported in animal studies, as Uri Manor, one of the authors of the study in hamsters, pointed out on Twitter. The blog Deplatform Disease calculated that the amount of spike protein that the authors found in vaccinated people was about 100,000 times lower than the levels of viral spike protein shown to cause harm. This is “a situation that could hypothetically occur in severe COVID-19 patients, pending studies confirming it, but not achievable in vaccinated people, at least for those who received the Moderna vaccine, and unlikely to occur for the other vaccines”, explained Al-Ahmad.
While some of the vaccine might end up in the bloodstream, the body breaks it down over time. The European Medicines Agency (EMA) explained in a 23 March 2021 letter that the proportion of vaccine that enters the bloodstream is very small and almost all of that ends up in the liver:
“The uptake of the mRNA in the vaccine occurs mainly in macrophages and dendritic cells of the immune system at the site of injection and draining lymph nodes […] It was found that the vaccine’s mRNA, formulated inside lipid nanoparticles, remains mainly at the injection site and only small amounts can reach other tissues, such as the liver. »
Regarding the COVID-19 AstraZeneca vaccine, upon administration of the same vector carrying another virus protein, it was found that most of the injected viral vector remained at the injection site, and only low amounts were detected in other tissues.
The non-clinical studies performed with the three COVID-19 vaccines did not identify any safety concerns linked to their tissue distribution in the animal model under the experimental conditions used.”
Al-Ahmad debunked in his blog Bridle’s claim that mRNA vaccines cross the blood-brain barrier causing damage to the brain and other organs. The claim is based on a purportedly leaked report from Pfizer about the distribution of lipid nanoparticles, like those carrying the COVID-19 vaccine, in mice. Al-Ahmad explains that, despite the extremely high doses injected, the levels observed in the brain and other organs were very low.
In addition to repeating Bridle’s allegations, the LifeSiteNews’ article misused the U.S. Vaccine Adverse Event Reporting System to make other misleading and unsupported claims. One example is the implication that the spike protein produced by COVID-19 vaccines caused thousands of adverse events “including the 4,000 deaths, and nearly 15,000 hospitalizations”. It also stated that mRNA COVID-19 vaccines caused hundreds of cases of blood clots. Such claims are unsubstantiated.
Besides the lack of evidence for any harmful effect of the spike protein produced by COVID-19 vaccines, VAERS reports alone don’t provide evidence that COVID-19 vaccines caused an adverse event, as Health Feedback explained in previous reviews here, here, and here. Therefore, VAERS reports of blood clotting don’t prove that any component of the COVID-19 vaccines, including the spike protein derived from them, damage blood vessels.
Conclusion
The claim that the spike protein from COVID-19 vaccination can cause vascular damage in vaccinated people is unsupported and misleading. While the potential effect of the spike protein produced during infection on blood vessels deserves further investigation, the claim that COVID-19 vaccines will cause similar problems is unsubstantiated. In fact, the available evidence contradicts this claim, instead suggesting that COVID-19 vaccines targeting the spike protein might not only protect against viral infection but also against vascular damage. Al-Ahmad concluded:
“COVID-19 vaccines have been given to over 100 million Americans and have been shown to be extremely safe, associated with a dramatic decrease in fatal COVID-19 cases, hospitalization, and probably contribute to the overall decrease in transmission within the community. These are undeniable facts that contradict any claims made until now of vaccines causing blood clots […], infertility […], or brain/heart damage.”
The study by Ogata et al. published in Clinical Infectious Diseases reports that part of the spike protein enters the blood[9]. However, nothing about being detrimental is mentioned in the publication. These findings are also based on a small sample size.
SCIENTISTS’ FEEDBACK
The study by Lei et al. published in Circulation Research, done in hamsters, actually concludes by stating that “vaccination-generated antibody and/or exogenous antibody against S protein not only protects the host from SARS-CoV-2 infectivity but also inhibits S protein-imposed endothelial injury”[6]. That is, COVID-19 vaccines may actually prevent vascular damage.
So the problem here is linking two completely unrelated studies. And the fact that the clots have only been found with viral vector vaccines. There is a massive leap between the two studies, and the LifeSiteNews article is cherry-picking what is presented.
Is the spike protein toxic to endothelial cells, causing blood clots, heart, and brain damage?
An interesting pattern with the anti-vaccine crowd is the inappropriate use of scientific literature or the cherry-picking of poor studies to make bold claims in an attempt to vilify vaccines, as seen in this latest instance citing a rapid communication from Lei and colleagues published in Circulation Research[6].
The latest trend amongst anti-vaccine groups is the claim that the spike (S) protein produced by COVID-19 vaccines is a toxin, and it damages various tissues, including endothelial cells. What is the science behind the claim, and how does it hold up under scrutiny? In this rebuttal, I will specifically address the claim with regards to the endothelial cell perspective.
1. COVID-19 and vasculitis/endothelial cells damage: still a work-in-progress situation
Endothelial cells are a type of cells lining the inside of our blood vessels, from big caliber arteries to fine microvessels deep inside our tissues. It is a type of cell that emerges early during development from a mesoderm lineage (the same embryonic lineage that will give rise to connective tissues, including muscles and bones).
Endothelial cells play important roles as a physical and chemical filter between the circulating blood and the peripheral tissues. As a mesh, they retain blood cells and plasma proteins inside the blood vessels and participate in the regulation of blood pressure by secreting relaxing factors (e.g., nitric oxide, endothelium-derived hyperpolarizing factor) for the muscle cells lining blood vessels. In certain tissues (e.g., brain, eyes, or testis), such endothelial cells can be further specialized, resulting in a much more tightened barrier phenotype that acts as a strict barrier, such as the blood-brain barrier (BBB) observed in the brain.
However, endothelial cells are very fragile cells that can be damaged by various agents. One of these potential hazardous agents may be SARS-CoV-2 itself, the virus responsible for the COVID-19 pandemic.
The first high-impact study that documented possible vascular endothelial damage in patients was the study from Varga and colleagues, published last year in The Lancet journal[4], which reported the presence of endothelial lesions in both classical histological (stained tissues with chemicals) and electron microscopy preparations of two deceased COVID-19 patients. However, such studies have limitations, as reported in a letter to the editor a few weeks following its publication[10], highlighting a few limitations and caveats of such observations.
Another study by Nuovo and colleagues also reported endothelial cell damage[5] before the Circulation Research study by Lei and colleagues[6]. Nuovo and colleagues reported similar observations in post-mortem tissues of 13 deceased COVID-19 patients, as well as neurological alterations in mice infected with spike protein via IV infusion (full-length or S1 fraction) at a dose considered very high (3 micrograms/150 microliters or 20 micrograms/milliliter per mouse).
This study also reported endothelial cell damage in the blood vessels of the brain on post-mortem tissues, but fell short of indicating the presence of fully functional virions (the authors reported the presence of pseudovirions, lacking the presence of SARS-CoV-2 RNA in most preparations).
At this point, we have some indications that SARS-CoV-2 can be detrimental to endothelial cells, but we are lacking two important pieces of information:
1) What is the blood/plasma viral load we need in a patient to show signs of endothelial cell damage (we only know these patients died from COVID-19 complications)?
2) How does this viral load compare to the amount of spike protein displayed on [pseudo]viruses, based on the experimental data presented in the study?
We must consider whether any studies showing the transport and/or toxicity of spike protein reflect an amount that can be achieved realistically in COVID-19 patients.
2. The Lei et al. rapid communication in Circulation Research
Rapid/short communications are a type of scientific article commonly encountered in the literature when you have a discovery that is so important that it needs to be shared, but you have not been able to conduct a significant number of experiments to have a study as a whole.
Short communications are essential to break important findings, but they also come with the peril encountered by preliminary studies: we are lacking confirmatory experiments, we are often having a limited number of experiments done that can show similar outcomes with different approaches, and more dangerously, they can be interpreted by non-scientists as irrefutable evidence. Quite often, these short communications provide more questions than answers, and due to their limited word count, often leave important information out.
One of the problems of working with the SARS-CoV-2 virus is the high risk associated with manipulating such a virus. It is highly infectious and easily spread via aerosols and droplets, making its manipulation in cell culture a high-risk activity for the researcher. As of now, any work involving the culture and maintenance of infectious SARS-CoV-2 requires the use of a Biosafety Level 3 (BSL-3) research facility to conduct such experiments, including the culture of functional viruses. As a comparison, HIV only requires a BSL-2+ laboratory. Bacteria such as Mycobacterium tuberculosis (which is the causative agent of tuberculosis) requires a BSL-3 facility. These laboratories require special facilities and engineering controls to avoid biological agents escaping outside the lab, in addition to trained personnel for manipulating these agents.
In this short communication, Lei and colleagues circumvented the issue by creating pseudoviruses that express spike protein on their viral shell. Here is the first caveat: we don’t have any information about the type of pseudoviruses used. Are these aggregates of spike proteins like the Novavax vaccine candidates? Are these adenoviruses encoding for the spike protein? Are these Syrian hamster-specific viruses used for that purpose since the animals infected are Syrian hamsters?
The second caveat is we don’t know what the viral load given to the animals is. Furthermore, is the expression of spike protein by these pseudoviruses comparable to SARS-CoV-2 virions?
And the third, the use of Syrian hamsters. It is always dangerous to jump from animals to humans assuming it will be comparable. Translation from the bench to the bedside remains an extremely dangerous and risky procedure, as most interventions and drug candidates fail to translate efficacy observed on the bench into clinically relevant therapy.
It is important to note that the authors reported an inoculum of 108 PFU [acronym for “Plaque-Formation Unit”, which represents the number of infectious or live viruses in a preparation] per mL (100 million/mL), using only a very small size (N=3 animals per experiment) for in vivo studies. Usually, a minimum number of N=8 per group is not unheard of for animal studies to achieve a minimal statistical significance. We don’t have any idea how this inoculum compares to clinical information. Is that viral load comparable to humans? If yes, at which clinical stage?
We also know that the in vitro studies were conducted in the presence of recombinant S1 protein, a genetically-produced viral protein, not the natural and full-form of the protein present in viral particles. This is important because it also means that the use of recombinant proteins may miss the sugar-branching or glycosylation found in the natural form of the protein as found in SARS-CoV-2 viruses[11].
The amount used was 4 microgram [one millionth of a gram]/mL, which also appears pretty excessive. To put this into perspective, Buzhdygan and colleagues[12] used 10 nanomolar [10 nanomoles per liter, which equals 1015 molecules of protein, per liter] of the recombinant spike protein S1 domain in cultured human brain endothelial cells, a concentration considered sufficient to observe statistically significant damage in brain endothelial cells. If we assume a molecular weight of ~76 kDa, it would result in a concentration of 760 microgram per liter (or 760 nanograms/mL).
A recent study by Ogata and colleagues[9] reported the detection of spike protein in the plasma of patients following immunization with the Moderna vaccine, which was barely over the limit of detection. The authors noted values up to 6812 picograms [one thousand billionth of a gram] per mL (peak concentration) during the first week after the first injection. No subsequent peak and detection above detection levels were observed after the second injection. No full-length spike protein was detected at any time, and no nucleocapsid protein was detected in either of the patients, which allows us to rule out any shedding from COVID-19 naturally.
It is important to compare the values: we indicate possible damage if you expose cells and animals to 4-760 micrograms/mL (with a study injecting 20 micrograms/mL in mice). These values have yet to be compared to values observed in patients’ plasma/serum, but they are at least 59 times higher than the plasma concentration observed in Moderna-vaccinated patients and may require 1,000 times that concentration to see actual damage in humans (in vitro on cultured brain endothelial cells). A situation that could hypothetically occur in severe COVID-19 patients, pending studies confirming it, but not achievable in vaccinated people, at least for those who received the Moderna vaccine, and unlikely to occur for the other vaccines.
3. What about the clotting?
In the article, Bridle makes the following statement: “when that happens it can do one of two things: it can either cause platelets to clump, and that can lead to clotting. That’s exactly why we’ve been seeing clotting disorders associated with these vaccines. It can also lead to bleeding.”
Here is a conundrum of the statement: you cannot be the coagulopathic agent that is prothrombotic (generate blood clots and stop blood flow in a vessel) and be antithrombotic (which results in bleeding) at the same time. The ACE2 receptor appears to exert an antithrombotic activity under normal conditions, therefore we can assume tampering with such a receptor can contribute to clot formation[13].
What we know for now is that there is a high incidence of clotting events in COVID-19 cases. There are various reports which indicate that up to 50% (50 out 100) of hospitalized COVID-19 patients present signs of coagulation (clotting issues)[8].
When it comes to COVID-19 vaccines, cases of thrombosis (clotting) following COVID-19 vaccination have been reported with the Oxford-AstraZeneca and Johnson & Johnson vaccines. By early spring 2021, several cases of coagulopathy resulting in cerebral venous thrombosis (CVT) were documented in various countries utilizing such vaccines (both of which are non-mRNA vaccines).
CVT accounts for 0.5% of all stroke admissions, according to Bousser and Ferro[14]. To put these into perspective, the European Union (EU) experienced 1.12 million stroke events in 2017[15], which would give us an estimate of 509 stroke events per 100,000 people. Hence, the number of CVTs occurring in the EU population could be estimated by 2.5 per 100,000 persons.
According to the European Medicines Agency, 18 cases of CVT were reported following the immunization of 20 million people with the Oxford-AstraZeneca COVID-19 vaccine. This number brings us to an estimate of 0.09 per 100,000 people. In other words, the incidence of CVT following immunization is very likely to be below or similar to the background occurrence of such events in the population. The EMA made it clear: the benefits still outweigh the very small perceived risk when it comes to clotting and CVT.
4. What about the heart and brain? What about the distribution of the vaccine in the body?
Earlier reports commented on heart anomalies in young patients, around 12 to16 years old, following immunization with the Pfizer-BioNTech COVID-19 vaccine. So far, the reports of this myocarditis (heart damage) are rare, mostly mild, and still under monitoring. However, the incidence of these cases doesn’t seem to be above the baseline rate.
When it comes to the distribution of the COVID-19 vaccines in the body (and damage to the brain and other organs), the LifeSiteNews article goes even further into fear-mongering, giving a platform to Stephanie Seneff, a computer scientist at the Massachusetts Institute of Technology, who is a well-known anti-genetically modified organisms (GMO) activist. Seneff is known for her questionable claim that “half of all children will be autistic by 2025” (spoiler alert: the incidence of autism in the general population in 2020 was 1 in 54 people, based on 2016 data), citing the use of glyphosate, a common herbicide used in agriculture for the past 50 years, as the main culprit.
Such a bold and unsubstantiated claim has even been denounced by certain GMO skeptics, questioning the credibility of Seneff as an authority figure on that topic[16]. In the LifeSiteNews article, Seneff went as far as to claim that “the results of this leaked Pfizer study tracing the biodistribution of the vaccine mRNA are not surprising, but the implications are terrifying”.
I have personally discussed these biodistribution data (as obtained by Bridle and colleagues) on my blog, as I teach pharmacokinetics to pharmacy students. The data is pretty clear: the number of vaccines needed to be injected in a 12-year old to reproduce the findings observed in rats and reported as “terrifying” would be equivalent to 60,000 doses given at once, to reproduce the number of nanoparticles used in that study.
At this point, neurological damage from COVID-19 vaccines remains to be documented, but neurological damage from COVID-19 itself is common. Such damage can be multifactorial, and it remains unclear what the contributing factors are. The high expression of ACE2 in the nasal cavity could be one point of entry for the virus to invade the brain[17], the hypoxemia (decreased oxygen saturation in the blood) that is a major issue encountered in COVID-19 patients (since neurons are extremely susceptible to hypoxic injury), and the systemic inflammation associated with COVID-19 that can activate the brain endothelium and possibly drive some neuroinflammation.
5. Concluding remarks
Here is the great peril of anti-vaccine and fear-mongering disinformation spreaders: twist and exaggerate claims. These studies are reflecting a near-impossible scenario that requires a ridiculous amount of spike protein that has yet to match clinically relevant concentrations, yet much higher than values observed in small studies.
COVID-19 vaccines have been given to over 100 million Americans and have been shown to be extremely safe, associated with a dramatic decrease in fatal COVID-19 cases, hospitalization, and probably contribute to the overall decrease in transmission within the community. These are undeniable facts that contradict any claims made up to now of vaccines causing blood clots (coagulopathy occurs in a much higher number of COVID-19 patients than COVID-19 vaccinated patients and seems limited to the use of adenovirus-based vaccines such as the Oxford-AstraZeneca vaccine), infertility (several cases of pregnancies occurred in volunteers enrolled in the Pfizer-BioNTech and Moderna clinical trials, no detrimental effects were observed in pregnant women vaccinated) or brain/heart damage (such damage has yet to be reported in the vaccinated population, at a rate above baseline, whereas damage from COVID-19 is well-documented).
READ MORE
Derek Lowe, a chemist and specialist in drug discovery, discussed in his blog in Science Translational Medicine the lack of evidence supporting that COVID-19 vaccines cause vascular damage.
David Gorski, a professor of surgery at Wayne State University and an editor at Science-Based Medicine, addressed in his blog Respectful Insolence many of the alleged dangers attributed to the spike protein produced by COVID-19 vaccination.
REFERENCES
- 1 – Hoffmann et al. (2020) SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor. Cell.
- 2 – Malik et al. (2021) Targets and strategies for vaccine development against SARS-CoV-2. Biomedicine and Pharmacotherapy.
- 3 – Pellicori et al. (2021) COVID‐19 and its cardiovascular effects: a systematic review of prevalence studies. Cochrane Database of Systematic Reviews.
- 4 – Varga et al. (2020) Endothelial cell infection and endotheliitis in COVID-19. The Lancet.
- 5 – Nuovo et al. (2021) Endothelial cell damage is the central part of COVID-19 and a mouse model induced by injection of the S1 subunit of the spike protein. Annals of Diagnostic Pathology.
- 6 – Lei et al. (2021) SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2. Circulation Research.
- 7 – Kirchdoerfer et al. (2018) Stabilized coronavirus spikes are resistant to conformational changes induced by receptor recognition or proteolysis. Scientific Reports.
- 8 – Gómez-Mesa et al. (2021) Thrombosis and Coagulopathy in COVID-19. Current Problems in Cardiology.
- 9 – Ogata et al. (2021) Circulating SARS-CoV-2 Vaccine Antigen Detected in the Plasma of mRNA-1273 Vaccine Recipients. Clinical Infectious Diseases.
- 10 – Goldsmith et al. (2020) Electron microscopy of SARS-CoV-2: a challenging task. The Lancet.
- 11 – Ramírez Hernández et al. (2021) The Role of the SARS-CoV-2 S-Protein Glycosylation in the Interaction of SARS-CoV-2/ACE2 and Immunological Responses. Viral Immunology.
- 12 – Buzhdygan et al. (2020) The SARS-CoV-2 spike protein alters barrier function in 2D static and 3D microfluidic in-vitro models of the human blood–brain barrier. Neurobiology of Disease.
- 13 – Fraga-Silva et al. ACE2 Activation Promotes Antithrombotic Activity. Molecular Medicine.
- 14 – Ferro et al. (2007) Cerebral venous thrombosis: an update. Lancet Neurology.
- 15 – Wafa et al. (2020) Burden of Stroke in Europe: Thirty-Year Projections of Incidence, Prevalence, Deaths, and Disability-Adjusted Life Years. Stroke.
- 16 – Mesnage et al. (2017) Facts and Fallacies in the Debate on Glyphosate Toxicity. Frontiers in Public Health.
- 17 – Sungnak et al. (2020) SARS-CoV-2 entry factors are highly expressed in nasal epithelial cells together with innate immune genes. Nature Medicine.