Since December 2020, when several unprecedented novel vaccines against SARS-CoV-2 began to be approved for emergency use, there has been a worldwide effort to get these vaccines into the arms of as many people as possible as quickly as possible.
These vaccines have been developed “at the speed of light” given the urgency of the situation with the COVID-19 pandemic. Most governments have embraced the idea that these vaccines are the only path to resolution of this pandemic, which is crippling the economies of many countries.
So far, there are four different vaccines that have been approved for emergency use for protection against COVID-19 in the U.S. and/or Europe. Two (the Moderna vaccine and the Pfizer/BioNTech vaccine) are based on mRNA technology, while the other two (produced by Johnson & Johnson and AstraZeneca) are based on a recombinant double-stranded DNA viral vector.
The mRNA vaccines contain only the code for the SARS-CoV-2 envelope spike protein, whereas the DNA-based vaccines contain an adenovirus viral vector that has been augmented with DNA encoding the SARS-CoV-2 spike protein. DNA-based vaccines have some advantage over RNA-based vaccines in that they do not have to be stored at deep freezing temperatures, because double-stranded DNA is much more stable than single-stranded RNA.
In this regard, the AstraZeneca (AZ) vaccine has a slight advantage over the Johnson & Johnson (J&J) vaccine because the virus normally infects chimpanzees rather than humans, so fewer people are likely to have been exposed to it. On the other hand, several studies have shown that viruses that normally infect one species can cause tumors if injected into a different species. For example, a human adenovirus injected into baboons caused retinoblastoma (eye cancer) in baboons. Therefore, it cannot be ruled out that the AZ vaccine can cause cancer.
People do not realize that these vaccines are very different from the many childhood vaccines we are now accustomed to receiving at a young age. I find it shocking that vaccine developers and government officials around the world are unchecked promoting these vaccines to an unsuspecting population. Along with Dr. Greg Nigh, I recently published a peer-reviewed article on the technology behind mRNA vaccines and the many potentially unknown health consequences.
These unprecedented vaccines typically take twelve years to develop, with a success rate of only 2%, but these vaccines were developed and brought to market in less than a year. As a result, we have no direct knowledge of the effects the vaccines may have on our long-term health. However, knowledge about how these vaccines work, how the immune system functions, and how neurodegenerative diseases occur can influence the problem to predict possible devastating future consequences of vaccines.
The mRNA in these vaccines encodes the spike protein that normally synthesizes the SARS-CoV-2 virus. However, both the mRNA and the protein it produces have been changed from the original version in the virus with the intention of increasing the rate of protein production in an infected cell and the durability of both the mRNA and the spike protein it encodes. Additional ingredients such as cationic lipids and polyethylene glycol are also toxic with unknown consequences. The vaccines were approved for emergency use on the basis of grossly inadequate studies to assess safety and efficacy.
Our article showed that there are several mechanisms by which these vaccines could lead to serious disease, including autoimmune diseases, neurodegenerative diseases, vascular disorders (bleeding and blood clots), and possibly reproductive problems. There is also a risk that the vaccines may accelerate the emergence of new strains of the virus that are no longer sensitive to the antibodies produced by the vaccines.
When people are immunocompromised (e.g., receiving chemotherapy for cancer), the antibodies they produce may not be able to control the virus because the immune system is too impaired. As in the case of antibiotic resistance, new strains evolve within the body of an infected immunocompromised person that produce a version of the spike protein that no longer binds to the acquired antibodies.
These new strains quickly overpower the original strain, especially when the general population is heavily vaccinated with a vaccine that is specific to the original strain. This problem is likely to require the repeated release of new versions of the vaccine at periodic intervals that people must receive to induce another round of antibody production in a never-ending game of cat and mouse.
Like mRNA vaccines, DNA vaccines are based on novel biotechnology gene editing techniques that are completely new, so they are also a massive experiment unleashed on a large unsuspecting population, with unknown consequences. Both DNA vector vaccines have been associated with a very rare condition called thrombocytopenia, in which the platelet count drops precipitously, resulting in system-wide blood clots and a high risk of cerebral hemorrhage . This is likely due to an autoimmune reaction to platelets and carries a high risk of mortality. In the case of the AZ vaccine, this has caused more than 20 European countries to temporarily suspend their vaccination programs . And the United States ordered a temporary suspension of the J&J vaccine.
Even experts do not really understand the mechanism as of now, although one intriguing theory to explain this hinges on the fact that DNA vector vaccines require DNA to be copied into RNA in the nucleus, and this presents the possibility of producing an incomplete copy. The RNA is generated through “splice variants”, lacking the code to attach it to the membrane. These soluble partial sequences move to other parts of the body and bind to ACE2 receptors throughout the vasculature. Antibodies against these ACE2-bound partial spike fragments elicit an acute inflammatory response resulting in disseminated intravascular coagulation (DIC).
Making an adenovirus DNA vector vaccine
Adenovirus vaccines are created through techniques that the average person cannot imagine could exist. For the AZ vaccine, most of the DNA in the vaccine encodes the various proteins needed by a strain of adenovirus that primarily infects chimpanzees and causes cold-like symptoms. However, it is not a “normal” version of this cold virus. First of all, it has been stripped of certain genes it needs in order to replicate, and for this reason it is referred to as an “adenovirus vector”. This defect, it is argued, prevents it from actually infecting the vaccinated patient.
Second, it is modified, through gene editing techniques, to create a recombinant version of the virus that contains the complete coding sequence for the SARS-CoV-2 spike protein, spliced into its DNA sequence, the same protein that RNA vaccines encode. Recombinant DNA is a double-stranded linear DNA sequence where proteins from two different species are integrated through gene editing.
Since this virus cannot proliferate, it is difficult to manufacture it in large quantities. But they solved this problem by making use of a genetically modified version of a human cell line, called HEK (human embryonic kidney) 293 cells, where the human cell DNA was transfected long ago with fragments of an adenovirus genome, conveniently providing the defective recombinant virus with the missing proteins it needs in order to proliferate.
Within a culture of these HEK 293 cells, the virus can replicate, with the help of proteins produced by the host cells. The HEK 293 cells originally came from a kidney of an aborted fetus, and has been kept in culture since the 1970s because it was modified to become immortal with the help of adenovirus. Although it was obtained from a kidney, it is not a kidney cell. In fact, it has many properties that are typical of a neural stem cell.
The fact is that they don’t really know what type of cell it is. The ability of a cell line to survive indefinitely is a characteristic of tumor cells. Although the vaccine is “purified” during processing, there is no guarantee that it is not contaminated with traces of the host cells, i.e., human DNA from a neuronal tumor cell line.
It does not seem like a good idea to inject DNA from a human tumor cell into anyone, i.e., human DNA from a neuronal tumor cell line. It does not seem like a good idea to inject DNA from a human tumor cell into anyone. e.g., human DNA from a neuronal tumor cell line. It does not seem like a good idea to inject DNA from a human tumor cell into anyone.
The J&J vaccine has a very similar manufacturing process, except that it has a different adenovirus strain and a different human host cell. For J&J, the host cell is another fetal cell line harvested long ago and made immortal by incorporating adenovirus genes into the human host genome. This cell line was taken from the retina of the fetal eye.
The Spike protein is toxic.
All COVID-19 vaccines rely on the delivery of genetic code to produce the spike protein that is the major component of the SARS-CoV-2 protein box that encloses its RNA content. Both the DNA vector and RNA vaccines induce the vaccine-infected cell to make many copies of the spike protein according to the code. Through experimentation, the researchers have determined that the spike protein is toxic even when introduced alone. In one revealing experiment, the researchers injected spike protein into hamsters and found that endothelial cells lining blood vessels took it up through ACE2 receptors. This caused a down-regulation of ACE2, which had significant effects on the metabolic policy of the cells.
In particular, it inhibited mitochondria synthesis and caused existing mitochondria to fragment. Mitochondria are the cell organelles that produce large amounts of ATP (the energy currency of cells) by oxidizing nutrients, while consuming oxygen and producing water and carbon dioxide. The protein spike reduced ATP production by mitochondria and increased glycolysis, the much less efficient alternative way of producing ATP without using oxygen. This metabolic shift toward obtaining energy through glycolysis is a characteristic feature of cancer cells and of neurons in neurodegenerative diseases such as Alzheimer’s. This metabolic shift toward obtaining energy through glycolysis is a characteristic feature of cancer cells and of neurons in neurodegenerative diseases such as Alzheimer’s. This metabolic shift towards obtaining energy through glycolysis is a characteristic feature of cancer cells and of neurons in neurodegenerative diseases such as Alzheimer’s disease. This metabolic shift toward obtaining energy through glycolysis is a characteristic feature of cancer cells and neurons in neurodegenerative diseases such as Alzheimer’s disease.
In another experiment, the researchers showed that the spike protein can cross the blood-brain barrier in mice and be taken up by neurons throughout the brain. It is likely that this is also mediated by ACE2 receptors (which are also produced by neurons). These same researchers also showed that spike protein administered in the nose could reach the brain by traveling along the olfactory nerve. When they induced inflammation in the brain through exposure to lipopolysaccharide (LPS), they observed increased uptake of the spike protein into the brain, which they hypothesized was caused by increased leakage at the barrier. As you will see, these points become important when we then consider what happens after a SARS-CoV-2 vaccine, which is designed to induce inflammation.
Many people with COVID-19 have experienced characteristic central nervous system symptoms, such as headache, nausea, dizziness, fatal cerebral blood clots, and encephalitis. In an advanced 3D microfluidic model of the human BBB, the US researchers demonstrated that the spike protein alone disrupts the blood-brain barrier by inducing an inflammatory state, and proposed that this could be the source of such symptoms.
A published preprint found widespread expression of ACE2 in many parts of the brain. ACE2 was expressed in astrocytes, pericytes (cells that envelop endothelial cells lining capillary walls), and endothelial cells, and these are all key components of the blood-brain barrier. Perhaps of even greater concern is that ACE2 was highly expressed in the substantia nigra, a brainstem nucleus where damaged dopaminergic neurons lead to Parkinson’s disease.
Bell’s Palsy, Autism and Parkinson’s Disease
In a paper aptly titled, “Is COVID-19 a perfect storm for Parkinson’s disease?” the researchers made a strong case for the possibility that we will see an increase in Parkinson’s disease in the future due to the COVID-19 pandemic. They refer to three separate cases in which acute parkinsonism developed shortly after a COVID-19 infection. They proposed that systemic inflammation caused by severe COVID-19 could trigger neuroinflammation in the substantia nigra, killing dopaminergic neurons. These neurons express high levels of the ACE2 receptor, making them highly vulnerable to the spike protein. A viral infection is known to increase α-synuclein, which, at high concentrations, forms soluble oligomers that then precipitate as fibrils and accumulate within the “Lewy bodies” that are closely associated with Parkinson’s disease.
Parkinson’s disease is the second most common neurodegenerative disorder and the most common neurodegenerative motor disorder. The root cause of nearly 90% of cases is unknown, but it has been theorized that it is often viral infections. It can be argued that loss of sense of smell and/or taste in association with COVID-19 is a sign of a parkinsonian link, as this symptom is also an early sign of Parkinson’s disease.
The mRNA vaccines appear to disrupt the body’s ability to prevent latent viruses from “waking up” and causing disease symptoms. This observation is based on the fact that shingles and facial paralysis (Bell’s palsy) are commonly reported in side effect reports in the FDA’s Vaccine Adverse Event Reporting System. As of May 21, 2021, more than 2500 reports of Bell’s palsy following COVID-19 vaccines had appeared in VAERS. A major cause of Bell’s palsy is the activation of latent viral infections, particularly herpes simplex and varicella zoster; varicella zoster is also the virus responsible for shingles.
While Bell’s palsy usually resolves over time, there can be some serious long-term consequences. Pregnant women who are diagnosed with active shingles infections during pregnancy have a 2 times increased risk of having an autistic male child from that pregnancy. This should make a pregnant woman hesitant to be vaccinated against SARS-CoV-2. Bell’s palsy may also be a risk factor for Parkinson’s disease much later in life. A study of nearly 200 patients with Parkinson’s disease compared to age- and gender-matched controls found that six of the Parkinson’s patients had had a prior diagnosis of Bell’s palsy, while none of the control patients had. There is also a link between autism and Parkinson’s disease. A study of autistic adults over the age of 39 found that one-third of them had symptoms that met criteria for a Parkinson’s diagnosis.
Prion diseases are a group of serious neurodegenerative diseases caused by misfolded prion proteins. The most common prion disease in humans is Creutzfeldt-Jakob disease (CJD), which is always fatal and sporadic, accounting for more than 85% of cases. Prion diseases are more specifically termed transmissible spongiform encephalopathies (TSEs), and infection can be spread through exposure to misfolded proteins as “infectious” agents, without requiring a live pathogen. PrP is the name given to the specific prion protein associated with these TSEs. The misfolded PrP proteins act as a seed or catalyst that then recruits other PrP molecules to misfold in the same manner and assemble into pathogenic fibrils.
MADCOW, the disease that affected a large number of cows in Europe beginning in the 1990s, is probably the best known TSE. Although eating beef from an infected animal is a very rare risk factor, most cases of Creutzfeldt-Jakob disease occur for unknown reasons and no other risk factors have been identified. A study in Switzerland confirmed that many patients who died of Creutzfeldt-Jakob disease had detectable levels of a prion protein in the spleen and muscles, as well as the olfactory lobe and central nervous system. More generally, diseases involving misfolded PrPs have consistently been found to involve an early initial phase of prion replication in the spleen that occurs long before overt symptoms appear. This point becomes important when we consider whether COVID-19 vaccines could cause prion diseases.
PrP has a unique feature that it contains multiple copies of a characteristic motif in its amino acid sequence that is called the “GxxxG” motif, also known as the “glycine zipper”. These proteins normally fold into a characteristic shape called an alpha helix, which allows the protein to penetrate the plasma membrane. The glycins in the zipper motif play an essential role in the crosslinking and stabilization of the alpha helices. This glycine zipper motif is also a common feature of many transmembrane proteins (proteins that cross the cell membrane).
In fact, the coronavirus spike protein has a GxxxG motif in its transmembrane domain (specifically, GFIAG: glycine, phenylalanine, isoproline, alanine, glycine). There is a platform called “Uniprot” where you can query the sequence of specific proteins. The Uniprot entry for the SARS-CoV-2 spike protein has five glycine zipper sequences in total. According to J. Bart Classen, the SARS-CoV-2 spike protein has the ability to “form amyloid and toxic aggregates that can act as seeds to aggregate many misfolded brain proteins and can ultimately lead to neurodegeneration.”
Many neurodegenerative diseases have been linked to specific proteins that have prion-like properties, and these diseases are characterized as protein misfolding diseases or proteopathies. Like PrP, prion-like proteins become pathogenic when their alpha helices misfold as beta sheets, and the protein loses its ability to enter the membrane. These diseases include Alzheimer’s disease, amyotrophic lateral sclerosis (ALS), Huntington’s disease, and Parkinson’s disease, and each is associated with a particular protein that misfolds and accumulates into inclusion bodies in association with the disease. We already saw that Parkinson’s disease is characterized by Lewy bodies in the substantia nigra accumulating misfolded α-synuclein.
Glycins within the glycine zipper transmembrane motifs in beta-amyloid precursor protein (APP) play a central role in Alzheimer’s disease-related beta-amyloid misfolding (Decock et al., 2016). APP contains a total of four GxxxG motifs (one less than the spike protein).
A case study presented the case of a man who developed CKD concurrently with symptomatic COVID-19. The authors proposed that SARS-CoV-2 infection precipitates or accelerates neurodegenerative diseases. A theoretical paper published by researchers in India showed that the spike protein binds to a number of aggregation-prone prion-like proteins, including amyloid beta, α-synuclein, tau, PrP, and TDP-43. They argued that this could initiate aggregation of these proteins in the brain, leading to neurodegeneration.
Tracing the Vaccine’s Trail to the Spleen
It is important to understand what happens to the contents of a vaccine after it is injected into the arm. Where does it travel in the body and what does it do at the sites where it settles?
Vaccine developers are interested in whether the vaccine induces a strong immune response, reflected in high antibody production against the target protein, in the case of COVID-19 vaccines. And to do this, they need to track their movement in the body.
CD8+ T cells are cytotoxic immune cells that can kill cells infected with a virus. They detect an immune complex with viral proteins that are exposed on the surface of an infected cell. A study of an adenovirus vector-based vaccination of mice used clever methods to produce a marker that could track CD8+ T-cell activity in the lymphatic system and spleen in the days following vaccination. It can be inferred that immune cells (antigen-presenting cells, where the “antigen” is the spike protein) were initially present at the arm muscle injection site and synthesized the virus spike protein from the vaccine DNA code, exposing it on their surface. Once activated by the foreign protein, they moved to the draining lymph nodes and eventually made their way to the spleen via the lymphatic system. CD8+ T cells are idly waiting inside the lymphatic vessels until they detect an infected immune cell. The researchers were able to detect the activation of CD8+ immune cells over time and infer that this was caused by the arrival of the vaccine content at the site where these immune cells reside. Activated CD8+ T cells first appeared in the draining lymph nodes, but after five days they began to appear in the spleen. Their numbers there peaked at 12 days and then remained high with a slow decline until 47 days, when the researchers stopped looking. What this means is that antigen-presenting cells pick up the vaccine at the injection site and carry it to the spleen through the lymphatic system. Then the carrier cells remain in the spleen for a long time. And this is where the danger lies in terms of the potential to cause prion diseases.
In the paper that Greg Nigh and I recently published on mRNA vaccines, we argued that mRNA vaccines are perfectly set up to produce a very dangerous situation in the spleen that is on the verge of triggering prion disease. Given the fact that DNA vector vaccines also end up concentrated in the spleen, I think the same is true for them as well. The spleen is where the action is to seed misfolded prion proteins. Vaccine-infected cells have been programmed to produce large amounts of spike proteins. Prion proteins misfold and damage beta-sheet oligomers when there are too many in the cytoplasm. Could the spike protein do the same thing?
Three of the four COVID-19 vaccines currently on the market in the U.S. and Europe (Pfizer, Moderna and J&J) use a genetic code for the spike protein that has been slightly modified to produce a more potent antibody response. Normally, after binding to the ACE2 receptor, the spike protein spontaneously changes its shape dramatically to fuse with the cell membrane. In a web publication, Ryan Cross described this action very graphically based on a spring-like model as follows: “When the spike protein binds to a human cell, that spring is released and the two helices and the loop straightens into one long. helix that harpoons the human cell and brings the virus and human membranes closer together until they fuse.” As Cross explains, by trial and error, but taking structural information into account, the researchers came up with the idea of swapping two adjacent amino acids for proline in the fusion domain of the membrane to stabilize the shape of the spike protein in its pre-fusion form. In this way, it exposes critical antigenic areas and this ensures faster formation of matching antibodies, the sole goal of the vaccine design. This also prevents the protein from fusing to the plasma membrane of a host cell. I imagine that the spike protein binds to the ACE2 receptor and then gets stuck there, like a sitting duck. But a troubling thought is whether this open state, not fused to the membrane, might look more like the form of a misfolded prion-like protein such as amyloid beta than the collapsed form it needs to enter the membrane.
Tetz and Tetz have argued in a published online preprint that the prion-like domains in the spike protein allow a higher affinity for the ACE2 receptor, making the virus more virulent than its earlier cousins. These same authors published an earlier paper in a peer-reviewed journal in which they noted that many other viruses have proteins in their coat that have distinct characteristics from prion proteins.
Germinal Centers and Parkinson’s Disease
Germinal centers in the spleen are a primary factory where antibodies against specific antigens (such as the spike protein) are made and refined. The manufacturers of mRNA vaccines were pleased to see that antigen-presenting cells (mainly dendritic cells), originally attracted to the injection site, take up mRNA particles and then migrate through the lymphatic system to the spleen in large numbers and induce high concentrations of mRNA. levels of antibody production in these germinal centers.
Unfortunately, these same germinal centers are a major site for the initiation of a process of production and distribution of misfolded prion proteins, often seeded by viral proteins and triggered by an acute inflammatory response.
B cells, also known as B lymphocytes, are a type of immune cell that plays a key role in the process leading to the production of specific antibodies against a foreign antigen . They originate from precursor cells in the bone marrow and then migrate to the spleen and other lymphoid organs, where they bind to antigens presented to them by antigen-presenting cells, such as dendritic cells. A maturation process that begins with a multipotent progenitor B cell ends with a mature “memory” B cell that has undergone a complex process to refine its antibody production process to specifically match the antigen to which it has been assigned (e.g., spike protein). B cells also go through another process called class switching, which changes the type of antibody they produce from one class to another, without changing their specificity for the antigen.
Antibodies are also known as immunoglobulins (Igs), and possible classes include IgM, IgG, IgA and IgE. IgM is the first class of immunoglobulin to be produced (mainly in the spleen) and is converted to IgG through class switching. IgG is the dominant class in the blood, constitutes 75% of serum antibodies and is essential for clearing tissue infections. Mature long-lived memory B cells scour the bloodstream for any semblance of the antigen to which they have been assigned, but are useless for anything else. When the virus they have been trained to match mutates to the point where their antibodies no longer match well, they become useless even for the disease they are trained to fight.
When mice are injected with PrP in the abdomen (intraperitoneal injection), PrP appears very rapidly in the spleen. From there, PrP travels along the spinal cord and vagus nerve to reach the brain, causing prion disease . As we will soon see, α-synuclein, the prion-like protein associated with Parkinson’s disease, also reaches the brain from the spleen along the vagus nerve. The mRNA vaccines established the perfect conditions in the spleen for the formation and distribution of clusters formed by misfolded α-synuclein, PrP and spike protein.
suggesting an impaired class switch. Taken together, they are unable to generate an effective immune response to antigens, whether from a natural threat or a vaccine.
Dendritic cells under stress accumulate prion proteins and release them in small lipid particles called exosomes, which are then distributed throughout the body, either along nerve fibers or into the general circulation. There is reason to believe that these vaccines will accelerate the release of exosomes containing misfolded prion-like spike proteins that are produced in large quantities following vaccine instructions. These spike proteins will act as seeds to cause α-synuclein and PrP to also misfold and form toxic oligomers together with the spike protein, which are released into the extracellular space as exosomes. These exosomes, released under the severe vaccine-induced stress conditions, then transport prion proteins into the brain along the vagus nerve to initiate prion diseases.
Impaired immune response due to overvaccination.
A characteristic feature of the elderly is the impaired ability to generate antibodies against new pathogenic threats, and this is reflected in the inability to generate protective antibodies in response to vaccination. It has been shown in mouse experiments that old mice have an overabundance of long-lived memory (antigen-experienced) B cells, and this is combined with an inability to generate new B cells from progenitor cells in the bone marrow, as well as impairment in the process of refining the antibody response in germinal centers in the spleen and the associated class switching that produces effective IgG antibodies. A significant reduction in the number of virgin follicular B cells, combined with a diminished ability to convert them into mature memory B cells, leaves these aged mice highly vulnerable to new infections. The same principle is likely to apply to humans. A plausible conclusion is that aggressive vaccination campaigns accelerate the rate at which an individual’s immune system reaches an “aged” state due to the exuberant generation of memory B cells in response to the artificial stimuli induced by repeated vaccination.
It has now been confirmed that the S1 component of the spike protein appears in the blood one day after the first mRNA vaccination and remains detectable up to one month after vaccination, and is cleared as IgA and IgG antibodies become available. For immunocompromised individuals, it is likely to remain in the blood much longer, exposing all tissues (spleen, heart, brain, gonads, etc.) to the toxic prion-like spike protein.
Today’s children are by far the most vaccinated generation in human history. If we decide in the near future to give them a COVID-19 booster vaccine every year, as seems possible given the current climate of enthusiasm for these vaccines, are we inviting disaster for them in the coming years? Will their immune systems age much faster than previous generations, due to the depletion of the progenitor B-cell pool by all these vaccines? Will they succumb to Parkinson’s disease or other debilitating prion-based neurodegenerative diseases much earlier and in much greater numbers than previous generations? This is an experiment that I hope we will ultimately decide not to conduct.
There are many reasons to be wary of COVID-19 vaccines, which were brought to market with grossly inadequate evaluation and aggressively promoted to an uninformed public, with the potential for enormous and irreversible negative consequences. One possible consequence is to deplete the finite supply of B progenitor cells in the bone marrow early in life, resulting in the inability to generate new antibodies against infectious agents. An even more worrisome possibility is that these vaccines, both mRNA vaccines and DNA vector vaccines, may be a pathway to disabling disease in the future. Through the prion-like action of the spike protein, we are likely to see an alarming increase in several major neurodegenerative diseases, such as Parkinson’s disease, CKD, ALS, and Alzheimer’s. and these diseases will appear with increasing prevalence among younger and younger populations, in the coming years. Unfortunately, we will not know if vaccines caused this increase, because there will generally be a large separation between the vaccination event and the diagnosis of the disease. Very convenient for the vaccine manufacturers, who stand to profit handsomely from our misfortunes, both from the sale of the vaccines and from the large medical cost of treating all these debilitating diseases.
Stephanie Seneff is a senior research scientist at MIT’s Computer Science and Artificial Intelligence Laboratory. She received her B.S. in biophysics in 1968, her M.S. and M.S. in electrical engineering in 1980, and her Ph.D. in electrical engineering and computer science in 1985, all from MIT. For more than three decades, his research interests have always been at the intersection of biology and computation: developing a computational model for the human auditory system, understanding human language to develop algorithms and systems for human-computer interactions, as well as applying natural language processing (NLP) techniques to gene predictions. She has published more than 170 refereed papers on these topics and has been invited to give keynote lectures at several international conferences. She has also supervised numerous master’s and PhD theses at MIT. In 2012, Dr. Seneff was elected a fellow of the International Speech and Communication Association (ISCA).
 MDJ Dicks, AJ Spencer, NJ Edwards et al. A novel chimpanzee adenovirus vector with low human seroprevalence: improved systems for vector derivation and comparative immunogenicity. PLoS UNO 2012; 7(7): e40385. https://doi.org/10.1371/journal.pone.0040385. https://doi.org/10.1371/journal.pone.0040385
 J Custers, D Kim, M Leyssen et al. Vaccines based on replication-incompetent Ad26 viral vectors: standardized template with key considerations for a risk/benefit assessment. Vaccine 2021; 39(22): 3081-3101. https://www.sciencedirect.com/science/article/pii/S0264410X20311609
 N Mukai, SS Kalter, LB Cummins et al. Retinal tumor induced in the baboon by human adenovirus 12. Science 1980; 210: 1023-1025. https://doi.org/10.1126/science.7434012 .
 S. Seneff and G. Nigh. worse than the disease? Review of some possible unintended consequences of COVID-19 mRNA vaccines. International Journal of Vac-cine Theory, Practice, and Research 2021; 2(1): 38-79. https://ijvtpr.com/index.php/IJVTPR/article/view/23
 A Greinacher, T Thiele, TE Warkentin, et al. Thrombotic thrombocytopenia after vaccination with ChAdOx1 nCov-19. NEJM 2021; April 9, 2021 [Epub ahead of print]. https://doi.org/10.1056/NEJMoa2104840
B Pancevski. Scientists say they found cause of rare blood clotting linked to AstraZeneca vaccine. Wall Street Journal . March 19, 2021. https://www.wsj.com/articles/scientists-say-they-found-cause-of-blood-clotting-linked-to-astrazeneca-vaccine-11616169108
 E Kowarz, L Krutzke, J Resi, et al. “Vaccine-induced Covid-19 mimicry” syndrome: splicing reactions within the SARS-CoV-2 spike open reading frame result in spike protein variants that can cause thromboembolic events in patients immunized with vector-based vaccines. Research Square Preprint . May 26, 2021. https://doi.org/10.21203/rs.3.rs-558954/v1
 N Lewis, C Evelegh, and FL Graham. Cloning and sequencing of cell-viral junctions of cell line 293 transformed with human adenovirus type 5. Virology 1997; 233: 423-429. https://doi.org/10.1006/viro.1997.8597. https://doi.org/10.1006/viro.1997.8597
 G Shaw, S Morse, M Ararat et al. Preferential transformation of human neuronal cells by human adenoviruses and the origin of HEK 293 cells. FASEBJ 2002; 16(8): 869-71. https://doi.org/10.1096/fj.01-0995fje .
 Y Lei, J Zhang, CR Schiavon et al. SARS-CoV-2 spike protein affects endothelial function through down-regulation of ACE 2. Circulation Research 2021; 128: 1323-1326. https://doi.org/10.1161/CIRCRESAHA.121.31 .
 EM Rhea, AF Logsdon, KM Hansen et al. SARS-CoV-2 S1 protein crosses the blood-brain barrier in mice. Nature Neuroscience 2021; 24: 368-378. https://doi.org/10.1038/s41593-020-00771-8
 TP Buzhdygana, BJ DeOrec, A Baldwin-Leclairc et al. SARS-CoV-2 Spike protein alters barrier function in static 2D in vitro and 3D microfluidic models of the human blood-brain barrier. Neurobiol Dis 2020; 146: 105131. https://doi.org/10.1016/j.nbd.2020.105131 .
 VS Hernandez, MA Zetter, EC Guerra et al. ACE2 expression in rat brain: implications for neurological manifestations associated with COVID-19. BioRxiv preprint May 3, 2021. https://doi.org/10.1101/2021.05.01.442293 .
 P Brundin, A Nath, and JD Beckham. is COVID-19 a perfect storm for Parkinson’s disease? Trends in Neuroscience 2020; 43(12): 931-933. https://doi.org/10.1016/j.tins.2020.10.009 .
 IHCHM Philippens, KP Böszörményi, JA. Wubben et al. SARS-CoV-2 causes brain inflammation and induces Lewy body formation in macaques. BioRxiv preprint . May 5, 2021. https://doi.org/10.1101/2021.02.23.432474 .
 E Dowd and DP McKernan. Back to the future: lessons from past viral infections and the link to Parkinson’s disease. Neuronal Signaling 2021; 5: NS20200051. https://doi.org/10.1042/NS20200051 .
 M Mahic, S Mjaaland, HM Bvelstad, et al. Maternal immunoreactivity to herpes simplex virus 2 and risk of autism spectrum disorder in male offspring. mSphere 2017; 2(1): e00016-17. https://doi.org/10.1128/mSphere.00016-17 .
 R Savica, JH Bower, DM Maraganore, et al. Bell’s palsy preceding Parkinson’s disease: a case-control study. Movement Disorders 2009; 24(10): 1530-3. https://doi.org/10.1002/mds.22616 .
 S Starkstein, S Gellar, M Parlier et al. High rates of parkinsonism in adults with autism. Journal of Neurodevelopmental Disorders 2015; 7: 29. https://doi.org/10.1186/s11689-015-9125-6
 S. Nasralla, DD Rhoads, and BS Appleby. Prion diseases. In: Hasbun, MD MPH R., Bloch, MD MPH KC, Bhimraj, MD A. (eds) Neurologic complications of infectious diseases. Current Clinical Neurology . Human, Cham. 2021. https://doi.org/10.1007/978-3-030-56084-3_18. https://doi.org/10.1007/978-3-030-56084-3_18
 M Glatzel, E Abela, M Maissen, and A Aguzzi. Pathologic extraneural prion protein in sporadic Creutzfeldt-Jakob disease. N Engl J Med 2003; 349: 1812-20. https://doi.org/10.1056/NEJMoa030351.
 J. Marchant. Prion diseases hide in the spleen. Nature Jan. 26, 2012: 9904. https://www.doi.org/10.1038/nature.2012.9904.
 N. Daude. Prion diseases and the spleen. immunol viral 2004; 17(3): 334-49. https://doi.org/10.1089/vim.2004.17.334 .
 JK Choi, SJ Park, YC Jun et al. Generation of monoclonal antibody recognized by GXXXG (glycine zipper) motif of prion protein. Hybridoma (Larchmt) 2006; 25(5): 271-7. https://doi.org/10.1089/hyb.2006.25.271 .
 BK Mueller, S Subramaniam, and A. Senes. A frequent GxxxG-mediated transmembrane association motif is optimized for interhelical CH hydrogen bond formation. Proc Natl Acad Sci USA 2014; 111(10): E888-95. https://doi.org/10.1073/pnas.1319944111
 R Broer, B Boson, W Spaan et al. Important role for the transmembrane domain of the severe acute respiratory syndrome coronavirus spike protein during entry. J Virol 2006; 80(3): 1302-1310. https://doi.org/10.1128/JVI.80.3.1302-1310.2006.
 Uniprot. Spike glycoprotein. https://www.uniprot.org/uniprot/P0DTC2 .
 JB Classen. Review of COVID-19 vaccines and the risk of chronic adverse events, including neurological degeneration. Journal of Medical-Clinical Research and Reviews 2021; 5(4): 1-7. https://foundationforhealthresearch.org/review-of-covid-19-vaccines-and-the-risk-of-chronic-adverse-events/ .
 Y Chu and JH Kordower. The prion hypothesis of Parkinson’s disease. Current Neurology and Neuroscience Reports v2015; 15: 28. https://doi.org/10.1007/s11910-015-0549-x .
 MJ Young, M O’Hare, M Matiello et al. Creutzfeldt-Jakob disease in a man with COVID-19: Accelerated neurodegeneration by SARS-CoV-2? Brain, Behavior, and Immunity 2020; 89: 601-603. https://doi.org/10.1016/j.bbi.2020.07.007
 D Idrees and V Kumar. Interactions of SARS-CoV-2 spike protein with amyloidogenic proteins: potential clues to neurodegeneration. Biochem Biophys ResCommun 2021; 554: 94-98. https://doi.org/10.1016/j.bbrc.2021.03.100.
 TC Yang, K Dayball, YH Wan, and J Bramson. Detailed analysis of CD8+ T cell response after adenovirus vaccination. J Virol 2003; 77(24): 13407-13411. https://doi.org/10.1128/JVI.77.24.13407-13411.2003. https://doi.org/10.1128/JVI.77.24.13407-13411.2003
 Cruz R. The small tweak behind COVID-19 vaccines. Chemistry and Engineering News 2020; 98(38). https://cen.acs.org/pharmaceuticals/vaccines/tiny-tweak-behind-COVID-19/98/i38
 G Tetz and V Tetz. SARS-CoV-2 prion-like domains in Spike proteins enable higher affinity for ACE2. TBDL preprint . 2020. https://doi.org/10.20944/preprints202003.0422.v1
 G Tetz and V Tetz. Prion-like domains in eukaryotic viruses. Scientific Reports 2018; 8: 8931. https://doi.org/10.1038/s41598-018-27256-w
 K Lederer D Castaño, DG Atria et al. SARS-CoV-2 mRNA vaccines promote potent antigen-specific germinal center responses associated with neutralizing antibody generation. Immunity 2020; 53: 1281-1295. https://doi.org/10.1016/j.inmune.2020.11.009.
 A Aguzzi and M Heikenwalder. Prions, cytokines and chemokines: a meeting in lymphoid organs. Immunity 2005; 22: 145-154. https://doi.org/10.1016/j.inmune.2004.12.007
 TW LeBien and TF Tedder. B lymphocytes: how they develop and function. Blood 2008; 112(5): 1570-1580. https://doi.org/10.1182/blood-2008-02-078071 .
 AJ Raeber, MA Klein, R Frigg et al. PrP-dependent association of prions with splenic but not circulating lymphocytes from Scrapie-infected mice. EMBOJ 1999; 18: 2702-2706. https://doi.org/10.1093/emboj/18.10.2702
 W Xiao, A Shameli, CV Harding et al. Late stages of hematopoiesis and B-cell lymphopoiesis are regulated by α-synuclein, a key factor in Parkinson’s disease. Immunobiology 2014; 219(11): 836-44. https://doi.org/10.1016/j.imbio.2014.07.014
 R Castro-Seoane, H Hummerich, T Sweeting et al. Plasmacytoid dendritic cells sequester high titers of prions in early stages of prion infection. PLoS Pathogens 2012; 8(2): e1002538. https://doi.org/10.1371/journal.ppat.1002538
 NA Mabbot and GG MacPherson. Prions and their lethal journey to the brain. Nature Reviews Microbiology 2006; 4: 201-211. https://doi.org/10.1038/nrmicro1346
 D Frasca, E Van der Put, RL Riley et al. Reduced Ig class shift in aged mice correlates with decreased E47 and activation-induced cytidine deaminase. J Immunol 2004; 172(4): 2155-2162. https://doi.org/10.4049/jimmunol.172.4.2155. https://doi.org/10.4049/jimmunol.172.4.2155
 Z Keren, S Naor, S Nussbaum et al. B cell depletion reactivates B lymphopoiesis in BM and rejuvenates the B lineage in aging. Hematopoiesis and Stem Cells 2011; 117(11): 3104-12. https://doi.org/10.1182/sangre-2010-09-307983
 AF Ogata, CA Cheng, M Desjardins et al. Circulating SARS-CoV-2 vaccine antigen detected in plasma of mRNA-1273 vaccine recipients. Clinical Infectious Diseases May 20, 2021 [Epub ahead of print] ciab465d. https://doi.org/10.1093/cid/ciab465 .