Originally part of the outer coat of the SARS-CoV2 virus, where it functions as a “key” to “unlock” (infect) cells, spike proteins are also produced in large amounts by the mRNA “vaccines,” triggering a short-lived immune response in the form of antibodies. However, a growing body of evidence has shown that the spike protein is harmful by itself, independent of the rest of the virus.
The following (I. Alphabetical List) collects over 250 peer-reviewed scientific studies confirming that the spike protein is highly pathogenic on its own; most in vitro studies cited here used recombinant spike proteins or spike proteins in pseudoviral vectors, and produced pathological effects not reliant on the SARS-CoV2 viral machinery.
The second section (II. Categories) organizes the research into broad categories including affected tissues and organ systems, mechanisms, and evidence from clinical pathology. Because these areas overlap, many articles appear more than once in the second section.
A short list of research papers that explain the mechanisms of harm caused by the “spike protein.”
Avolio E et al., “The SARS-CoV-2 Spike Protein Disrupts Human Cardiac Pericytes Function through CD147 Receptor-Mediated Signalling: A Potential Non-infective Mechanism of COVID-19 Microvascular Disease,”Clinical Science 135, no. 24. (December 22, 2021): 2667–2689, doi: https://doi.org/10.1042/CS20210735
Boschi C et al., “SARS-CoV-2 Spike Protein Induces Hemagglutination: Implications for COVID-19 Morbidities and Therapeutics and for Vaccine Adverse Effects,”International Journal of Biological Macromolecules 23, no. 24 (2022): 15480, doi: https://doi.org/10.3390/ijms232415480
Idrees D and Vijay Kumar, “SARS-CoV-2 Spike Protein Interactions with Amyloidogenic Proteins: Potential Clues to Neurodegeneration,”Biochemical and Biophysical Research Communications 554 : 94–98, doi: https://doi.org/10.1016/j.bbrc.2021.03.100
Khan S et al., “SARS-CoV-2 Spike Protein Induces Inflammation via TLR2-Dependent Activation of the NF-κB Pathway,”eLife 10 (December 6, 2021): e68563, doi: https://doi.org/10.7554/elife.68563
Lei Y et al., “SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2,”Circulation Research 128, no. 9 (2021): 1323–1326, doi: https://doi.org/10.1161/CIRCRESAHA.121.318902
Nuovo JG et al., “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.”Ann. Diagn. Pathol. 2021, 51, 151682. doi: https://doi.org/10.1016/j.anndiagpath.2020.151682
Parry PL et al., “‘Spikeopathy’: COVID-19 Spike Protein Is Pathogenic, from Both Virus and Vaccine mRNA,”Biomedicine 11, no. 8 (August 17, 2023): 2287, doi: https://doi.org/10.3390/biomedicines11082287
Patra T et al., “SARS-CoV-2 spike protein promotes IL-6 trans-signaling by activation of angiotensin II receptor signaling in epithelial cells.”PLoS Pathog. 2020;16:e1009128. doi: https://doi.org/10.1371/journal.ppat.1009128
Raghavan S et al., “SARS-CoV-2 Spike Protein Induces Degradation of Junctional Proteins That Maintain Endothelial Barrier Integrity.”Front. Cardiovasc. Med. 2021, 8, 687783. doi: https://doi.org/10.3389/fcvm.2021.687783
Robles JP et al., “The Spike Protein of SARS-CoV-2 Induces Endothelial Inflammation through Integrin α5β1 and NF-κB Signaling,”JBC 298, no. 3 (March 2022):3, 101695, https://doi.org.10.1016/j.jbc.2022.101695
Shirato K and Takako Kizaki, “SARS-CoV-2 Spike Protein S1 Subunit Induces Pro- inflammatory Responses via Toll-Like Receptor 4 Signaling in Murine and Human Macrophages,”Heliyon 7, no. 2 (February 2, 2021):e06187, doi: https://doi.org/10.1016/j.heliyon.2021.e06187
Singh N and Anuradha Bharara Singh, “S2 Subunit of SARS-nCoV-2 Interacts with Tumor Suppressor Protein p53 and BRCA: An in Silico Study,”Translational Oncology 13, no. 10 (October 2020): 100814, doi: https://doi.org/10.1016/j.tranon.2020.100814
Sui Y et al., “SARS-CoV-2 Spike Protein Suppresses ACE2 and Type I Interferon Expression in Primary Cells From Macaque Lung Bronchoalveolar Lavage,” Frontiers in Immunology 12 (June 4, 2021), https://doi.org.10.3389/fimmu.2021.658428
Zheng Y et al., “SARS-CoV-2 Spike Protein Causes Blood Coagulation and Thrombosis by Competitive Binding to Heparan Sulfate,”International Journal of Biological Macromolecules 193 (December 15, 2021): 1124– 1129, doi: https://doi.org/10.1016/j.ijbiomac.2021.10.112
The injections contain a variety of components, including their declared ingredients, which are modified mRNA within pegylated lipid nanoparticles (pegLNPs). PegLNPs are tiny nanoparticles with nearly limitless tissue penetration. They deliver their genetic payloads into all tissues, including the brains, ovaries, testicles, and unborn children of any pregnant women injected.
The mRNA is modified by substituting N1-methylpseudouridine in place of uridine. This gives the RNA an unusually long lifespan of at least half a year, compared to natural mRNA, which typically lasts only a few hours. As a result, the subjects' cells continue producing the foreign coronavirus spike protein for an extended period.
This modification involving N1-methylpseudouridine also introduces errors in reading the RNA, leading to the production of a wide array of unpredictable and random proteins in addition to the spike proteins. The production of these toxic spike proteins and other protein products continues for at least six months and possibly much longer.
The injections also contain various undeclared contents and contaminants, including chemical contaminants and an array of plasmid DNA. The plasmid DNA includes a list of concerning genetic sequences, which are still under investigation. These include the presence of SV40 enhancer and SV40 promoter sequences—genetic engineering tools used to facilitate the incorporation of foreign DNA into the subjects' chromosomes. This raises the serious risk of permanent genetic modification in the human subjects. Research on this issue is ongoing, though we already have laboratory cell culture evidence of genetic integration of this DNA into human chromosomes.
Nanoparticle Toxicity
Lipid nanoparticles have known serious toxic effects, especially if injected repeatedly, which the C-19 injections are.
Polyethylene Glycol
Polyethylene glycol triggers adverse immune responses in many people.
Toxic Spike Proteins
Coronavirus spike proteins (SP) are known toxins. The spike protein of the engineered SARS-CoV-2 virus—whether from the virus itself or produced in subjects' cells following the injections—exhibits enhanced toxicity compared to natural coronavirus spike proteins. These modifications include the incorporation of a furin cleavage site and the elimination of hemagglutinin esterase expression on the surface of the spike protein.
Blood Clotting
The elimination of hemagglutinin esterase contributes to the spike protein's exceptional ability to cause blood clots at both the microscopic and macroscopic levels.
Accelerated Deterioration and Aging of Many Organs
Ongoing microvascular clotting is a contributing mechanism that accelerates organ deterioration, causing the organs of victims to age faster than normal. This can lead to a variety of clinical conditions, including accelerated microvascular dementia and kidney failure.
Reverse ORF, Spider Silk Protein, and “Calamari Clots”
One of the unusual findings in the genetic analysis of the undeclared plasmid DNA content of the C-19 mod-mRNA injections is a reverse open reading frame at the end of the plasmid DNA sequence coding for the spike protein. This causes ribosomes to also read the spike protein genetic sequence in the reverse direction, resulting in a completely different protein. The reverse sequence contains significant sections resembling the highly unusual proteins found in spider silk. This may help explain the unusual white, rubbery proteinaceous 'clots' extracted from the arteries and veins of many deceased injection victims by morticians and pathologists. The nature of these clots and the reverse translation of the spike protein genetic sequence require further study.
unusual rubbery clots found in many victims’ arteries and veins
Quasi-Autoimmune Pathology
Cells that produce the spike protein, as well as cells to which the spike protein adheres via ACE2 receptors, display a foreign protein on their surface. This triggers the subjects’ immune systems to attack these spike-protein-laden cells and tissues as if they were foreign, or 'non-self.' This is one of the major mechanisms of injury observed in the first year following the injections. Autopsy samples from young hearts, testicles, ovaries, kidneys, brains, placentas, and other tissues show affected organs heavily laced with spike protein and under intense autoimmune attack by the subjects' own immune systems. This resembles organ rejection seen in transplants, where the victims’ organs appear foreign to their immune system and are 'rejected.'
‘Spiked’ tissues undergoing this autoimmune attack may lead to clinical presentations in the days or months following injection, but can also contribute to progressive damage and the accelerated aging of many organs and tissues.
Quasi-autoimmune pathology
Antigenic Mimicry and Autoimmune Diseases
The spike protein also bears some resemblance to numerous natural proteins in the body, including syncytin-1, an essential protein in both female and male reproductive tissues. The immune response triggered against the spike protein can also target these natural proteins, causing another collection of autoimmune diseases and adverse effects, including miscarriages and infertility.
Ribosome Frame Shifting and More Autoimmune Disease
Due to the modified uridine in the injected mRNA, ribosome frame shifting occurs, which means that many errors are made as our cells' ribosomes read the mRNA. In addition to predominantly producing the spike protein, a large array of random proteins and protein fragments are generated. Each of these has the potential to resemble a natural protein in the body sufficiently to trigger more autoimmune diseases.
Antibody Dependent Enhancement (ADE)
The production of large amounts of spike protein within the subjects' bodies triggers a dramatic production of adaptive antibodies to the spike protein. These antibodies have various toxic effects, including the enhancement of coronavirus infections. This is one of the reasons that we observe increased rates of COVID infection, hospitalization, and death among the “vaccinated” versus the “unvaccinated.” This process is called antibody-dependent enhancement (ADE). Experimental vaccination against coronaviruses, especially against their spike protein, has been associated with a high incidence of ADE. In these experiments, like the current global experiment on humans, the antibodies produced by vaccination end up helping the virus infect the subjects rather than providing protection.
Immune System Damage, Increased Cancer and All Infections
The subjects' dramatic immune response to the spike protein produced following the injections weakens the immune system in various ways, including the suppression of CD4 and CD8 positive T cells. This damage to the subjects' immune systems is one factor accounting for the rise in cancers, particularly aggressive cancers, and a wide variety of infections among the “vaccinated.
Multiple Mechanisms to Cause Cancer
The injections have multiple mechanisms for causing cancer. These include immune system damage and chromosomal DNA damage. The insertion of foreign genetic material into the human genome has many harmful effects that are still being discovered, including the disruption of various tumor suppression genes that normally protect our DNA from damage and defend us against cancer.
Additionally, the spike protein (SP) of SARS-CoV-2 and these injections has many unique characteristics, including the capacity to migrate into our cells’ nuclei and damage the DNA, thereby interrupting tumor suppressor genes. This adds further potential mechanisms for causing cancer.
Antibody Mediated Selection: Driving the Evolution of Variants and Extending the Pandemic
Another reason many of us warned against this genetic “vaccine” program is the issue of Antibody Mediated Selection (AMS). AMS explains that although vaccination may play a role in averting a pandemic before it occurs, it is likely to prolong a pandemic and drive the evolution of one variant after another if administered during an ongoing pandemic. This serves as the foundation for a golden rule of vaccinology: we should never try to vaccinate our way out of a pandemic. Attempting to do so drives the evolution of the virus, creating one variant after another. These variants are particularly dangerous to the “vaccinated” subjects, as opposed to those with natural exposure and immunity. Natural immunity is broad and responds to many aspects of the virus, so the virus cannot simply adapt its spike protein to evade it. However, due to the injection campaigns, we have extended what would naturally have been a few months of active infections to now four years of variants, infections, and more misguided injections. This has been profitable for the vaccine industry but devastating for mankind.
Additional Mechanisms of Injury
There are additional mechanisms of injury, including prion diseases, and more research is needed regarding the injury mechanisms associated with these injections. The details of the immune system disturbances caused by these injections are extensive. This presentation serves as just a brief introduction.
Daily Clout Report #2: Pfizer – 136 Deaths and 1625 Serious Cases of ‘Ineffectiveness’ Revealed
April 8, 2022 • by Vicki F. Goldstein, RN, JD, Team 1
Introduction
In the first paragraph of Pfizer document 2.4 NONCLINICAL OVERVIEW, Pfizer states that “BNT162b2 is a nucleoside modified mRNA (modRNA) expressing full-length S [spike] with two proline mutations (P2) to lock the transmembrane protein in an antigenically optimal prefusion conformation” (p. 6, https://phmpt.org/wp-content/uploads/2022/03/125742_S1_M2_24_nonclinical-overview.pdf).
They list two references (Pallesen et al., 2017; Wrapp et al., 2020) as their justification for this design. That is the end of Pfizer’s discussion on why that particular design was selected, and it appears that Pfizer conducted no further research before selecting this design (or construct) and proceeding with vaccine development. This, as it turns out, is quite important.
Concerns Regarding the Pfizer mRNA Construct
There are three primary concerns regarding the Pfizer approach used to design their mRNA vaccine.
The basic Pfizer construct utilizing two proline substitutions to stabilize the spike protein molecule is flawed, and the protein molecule as well as the mRNA itself, remain unstable.
The spike protein has been shown to cause disease; therefore, a vaccine based on the spike protein will promote pathogenesis, not prevent it.
The S1 subunit of the spike protein has been shown to shed into the circulatory system, thereby furthering disease.
The following discussion expands on these three concerns.
Concern 1: Pfizer selected the Pallesen et al. (2017) construct as the basis for the Pfizer vaccine.
The work described by Pallesen et al. (2017) was performed on the MERS-CoV virus. Pallesen selected proline substitutions based on the work of others (Qiao et al., 1998; Sanders et al., 2002; Krarup, et al., 2015).
Pfizer also references a paper in the journal Science authored by Daniel Wrapp (Wrapp et al., 2020). Wrapp cites Pallesen et al. (2017) and the work of Robert Kirchdoerfer et al. (2018) who evaluated the Pallesen-style double proline substitutions (S2P) in the spike protein of SARS-CoV. Wrapp et al. (March 2020) assessed the 2P substitution in the spike protein of SARS-CoV-2, evaluating the construct for its affinity for the host cell receptor ACE2. Wrapp did not evaluate the SARS-CoV-2 S2P antigenicity nor the fate of the S1 subunit that is shed when the spike protein binds to the cell.
Wrapp et al. (March 2020) states that “Knowing the atomic level structure of the SARS-CoV-2 spike will allow for additional protein engineering efforts that could [emphasis added] improve antigenicity and protein expression for vaccine development.” It appears that Pfizer took this article and used it as is to create a vaccine without “additional protein engineering efforts” as suggested by Wrapp et al. (2020).
Moreover, the purpose of introducing two proline substitutions into the spike protein as described by Pallesen and Wrapp (Pallesen et al., 2017; Wrapp et al., 2020; Pfizer, p. 6, https://phmpt.org/wp-content/uploads/2022/03/125742_S1_M2_24_nonclinical-overview.pdf) was to stabilize the spike protein to improve its thermal stability, conformation and antigenicity. But, as stated by Hsieh et al. (2020) with co-author Daniel Wrapp, “even with these (2P) substitutions the SARS-CoV-2 S-protein remains unstable and difficult to produce reliably in mammalian cells, hampering R&D of subunit vaccines.”
Hsieh and Wrapp (Hsieh et al., July 2020) found that 26 of 100 variants that they created and tested had higher expression than the S-2P substitution that Pfizer selected. One of their variants, labeled Hexa-Pro, contained four proline substitutions in addition to the S-2P substitutions and had nearly 10X greater expression, had improved thermal stability and retained the desired conformation.
Numerous articles since then state that the 2P substitution used by Pallesen/Pfizer is unstable (McCallum et al., 2020, posted online Aug. 2020; Xiong et al., 2020; Brun et al., 2020; Juraszek et al., 2021). Brun et al. (posted November 2020) even made suggestions for improving the Pfizer BNT162b2 vaccine after describing why it was a suboptimal design.
Why did Pfizer select the Pallesen construct requiring storage in ultra-low-temperature freezers when the HexaPro construct is more stable, can be stored at room temperature and has much greater expression?
Concern 2: Pfizer did not address the well-documented pathogenesis caused by the coronavirus spike protein before release of their vaccine and before FDA approval.
In a 2005 article, Kuba demonstrated that SARS-CoV spike protein injected into mice worsened their lung disease (Kuba, 2005).
In 2008, Wang et al. demonstrated that the receptor binding domain (RBD) of the spike protein of SARS-CoV leads to internalization of ACE2, resulting in downregulation and subsequent lung injury (Wang et al., 2008). The authors concluded that “because the RBD spike binding to ACE2 contributes to SARS pathogenesis, the use of subunit vaccines based on RBD spike should be considered carefully.”
Wang et al. (2020) and Semimukai et al. (2020) noted that recombinant spike protein induced antibodies in mice and protected against SARS-CoV infection, but lung eosinophilic immunopathology was observed in the immunized mice after SARS infection.
Elizabeth M. Rhea and her co-authors reported on-line in December 2020 and published in March 2021 (Rhea et al., 2021) that S1 subunit labeled with radioiodine (I-S1) readily crosses the mouse blood-brainbarrier (BBB) and could explain the adverse effects of S1 and/or SARS-CoV-2 such as encephalitis, respiratory difficulties and reduced ability to smell. I-S1 was also detected in kidney, liver and spleen.
In January 2021, Letarov et al. published an article in the journal Biochemistry (Moscow), titled Free Sars-CoV-2 Spike Protein S1 Particles May Play a Role in the Pathogenesis of COVID-19 Infection (Letarov et al., 2021). They noted that the upregulation of cell surface expression of ACE1 and/or downregulation of ACE2 can lead to pulmonary damage. This occurs during SARS infection and by recombinant SARS-CoV spike protein. They hypothesize that S1 molecules carry intact RBDs, and their binding to ACE2 may induce ACE2 downregulation and deleterious downstream effects such as increased inflammation, thrombosis, and pulmonary damage.
Letarov et al. (2021) also reference the work of Zhang et al. (2020) who elucidated a spike protein mutation in SARS-CoV-2 (the D614G variant) that is associated with increased infectivity but reduced S1 shedding and mild symptoms. This is further evidence that the spike protein is responsible for pathogenesis.
Nuovo et al. (2021, posted online Dec. 2020) reported on the endothelial cell damage caused by the S1 subunit of the spike protein. They reported two main findings: 1) Human COVID-19 cases demonstrated microvessel endothelial damage in the brain and other organs, including the skin, due to circulating spike protein that induces cytokine production resulting in microencephalopathy; and 2) injection of the S1 full-length spike subunit into mice (but not the S2 subunit) induced an equivalent microvascular encephalopathy as seen in human COVID-19 cases. The authors further note that although their study “focused on the brain, it should be stressed that there are other sites where there is a rich bed of microvessels with the ACE2 receptor, including skin/subcutaneous fat and the liver. As has been documented in human patients, microvessels at these sites can also display an endothelialitis that, in the skin/fat can induce complement activation/hypercoagulable state and the so-called cytokine storm typical of fatal COVID-19.”
“In sum, the data presented indicates that the full length S1 subunit of the spike protein of SARS-CoV-2 alone is capable, without the infectious virus, of inducing systemic microendothelial cell damage in mice with a cognate pattern of complement activation and increased cytokine expression and the concomitant thrombosis/hypercoagulable state. This disease pattern strongly parallels the extra-pulmonary manifestation of severe human COVID-19 and suggests that the latter may not represent systemic infectious virus. Thus, prevention of the CNS disease so common in severe COVID-19 may require neutralization/removal of the circulating pseudovirus.”
Lei et al. (April 2021) created a pseudovirus exhibiting spike protein but containing no virus inside and concluded that the spike protein alone is sufficient to cause damage to the vascular endothelial cells.
With so much evidence demonstrating a direct link between the presence of the spike protein S1 subunit in the circulatory system and pathogenesis, why would Pfizer create a vaccine that not only injects spike protein into the patient, but converts the cells of the patient into “spike protein factories” that turn out the spike protein S1 subunit, the very molecule that causes illness?
Concern 3: Pfizer did not address the well-documented shedding of the coronavirus spike protein into the circulatory system, where it crosses over to multiple organ systems to cause pathogenesis, before release of their vaccine.
It was shown as early as 1994 (Bullough et al., 1994) that the surface spike protein of an enveloped virus (Influenza) would release a subunit after proteolytic cleavage of the structure upon binding to the host cell surface. Work by Alexandra Walls (2017) demonstrated that the proteolytic processing of coronavirus spike proteins allows shedding of the S1 subunit.
Brun et al. (posted on-line November 2020) reported the process by which spike protein is processed within the host cell and soluble S1 subunit was secreted into the extracellular space via lysosomes. Their work indicated that the production of spike vaccine antigen protein without a virus to incorporate the protein into the viral envelope created an overexpression system and secretion of the protein by the cell (shedding). They suggest that the secreted spike proteins do not mimic the spike glycoproteins as they are presented on the actual virus and may effectively act as a decoy, eliciting more of the unwanted sub-optimal, non-neutralizing antibodies that are incapable of neutralizing the virus.
The authors state that the Pfizer BNT162b vaccines (and other similar type vaccines) rely on the supplied RNA sequence to use the host cell machinery to faithfully produce the spike protein in its fully folded, glycosylated and assembled state, resembling a natural infection, and they trigger a robust innate and humoral response; however, this does not happen. They go on to suggest a better vaccine design, one that abolishes the furin cleavage site (which is intact in the Pfizer construct) and introduces mutations that lock the spike protein in the prefusion conformation to prevent shedding and elicit a more potent antibody response.
Rhea et al. (2021, posted on-line December 2020) noted that coronavirus spike proteins are often cleaved; therefore, S1 could be shed and shed S1 may cross the BBB. Shedding of the S1 subunit of the spike protein was also noted by Liu et al. (2020), Letarov et al. (2021), Rhea et al. (2020), Zhang et al. (2020) and Henderson et al. (2020).
Given that the Pfizer mRNA construct design is sub-optimal; given that it has been well established (since 2005 to 2008) that spike proteins cause disease; and given that the spike protein S1 subunit is shed during binding of the virus or pseudovirus with the host cell, as well as secreted by host cells producing spike protein following injection with an mRNA-derived spike protein vaccine, why would Pfizer develop and release an mRNA vaccine that demonstrates all three of these deleterious qualities? Why would Pfizer develop and release an mRNA vaccine that demonstrates poor design with limited immunogenicity, requires storage at very low temperatures, and results in the production of a spike protein that readily sheds into the circulatory system to cause pathogenesis in multiple organ systems? And why would the FDA approve it?
Juraszek, J., et al., Nature Communications, 2021; 12, Article number 244. Stabilizing the closed SARS-CoV-2 spike trimer. https://pubmed.ncbi.nlm.nih.gov/33431842/
Kirchdoerfer, R., et al., Scientific Reports, 2018; 8:15701; DOI:10.1038/s41598-018-34171-7. Stabilized coronavirus spikes are resistant to conformational changes induced by receptor recognition or proteolysis. https://pubmed.ncbi.nlm.nih.gov/30356097/
Krarup, A., et al., Nat Commun, 2015; 6:8143. A highly stable prefusion RSV F vaccine derived from structural analysis of the fusion mechanism. https://pubmed.ncbi.nlm.nih.gov/26333350/
Kuba, K., et al., Nature Medicine, 2005; 11(8):875-879. A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury. https://pubmed.ncbi.nlm.nih.gov/16007097/
Lei, Y., et al., Circulation Research. 2021; 128:1323-1326. SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2. https://pubmed.ncbi.nlm.nih.gov/33784827/
Letarov, A., et al., Biochemistry (Moscow), 2021; 86(3):257-261. Free SARS-CoV-2 Spike Protein S1 Particles May Play a Role in the Pathogenesis of COVID-19 Infection. https://pubmed.ncbi.nlm.nih.gov/33838638/
Liu, C., et al., Structure, 2020; 28(11):1218-1224. The Architecture of Inactivated SARS-CoV-2 with Postfusion Spikes Revealed by Cryo-EM and Cryo-ET. https://pubmed.ncbi.nlm.nih.gov/33058760/
McCallum, M., et al., Nature Structural & Molecular Biology, October 2020; 27:942–949. Structure-guided covalent stabilization of coronavirus spike glycoprotein trimers in the closed conformation. https://pubmed.ncbi.nlm.nih.gov/32753755/
Nuovo, G., et al. Annals of Diagnostic Pathology 51, 2021; 151682. 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. https://pubmed.ncbi.nlm.nih.gov/33360731/
Pallesen, J., et al., Proc Natl Acad Sci, 2017; 114:E7348-E7357. Immunogenicity and structures of a rationally designed prefusion MERSCoV spike antigen. https://pubmed.ncbi.nlm.nih.gov/28807998/
Qiao, H., et al., Journal Cell Biol, 1998; 141:1335-1347. Specific single or double proline substitutions in the “spring-loaded” coiled-coil region of the influenza hemagglutinin. https://pubmed.ncbi.nlm.nih.gov/9628890/
Rhea, E., et al., Nature Neuroscience, March 2021; 24:368-378. The S1 protein of SARS-CoV-2 crosses the blood–brain barrier in mice. https://pubmed.ncbi.nlm.nih.gov/33328624/
Sanders, R., et al., Journal Virology, 2002; 76:8875-8889. Stabilization of the soluble, cleaved, trimeric form of the envelope glycoprotein complex of human immunodeficiency virus type1. https://pubmed.ncbi.nlm.nih.gov/12163607/
Semimukai et al., Microbiol Immunol, 2020; 64:33-51. Gold nanoparticle-adjuvanted S protein induces a strong antigen-specific IgG response against severe acute respiratory syndrome-related coronavirus infection, but fails to induce protective antibodies and limit eosinophilic infiltration in lungs. https://pubmed.ncbi.nlm.nih.gov/31692019/
Walls, A., et al., PNAS, October 17, 2017; 114(42):11157-11162. Tectonic conformational changes of a coronavirus spike glycoprotein promote membrane fusion. https://pubmed.ncbi.nlm.nih.gov/29073020/
Wang, S., et al., Virus Research, 2008; 136:8-15. Endocytosis of the receptor-binding domain of SARS-CoV spike protein together with virus receptor ACE2. https://pubmed.ncbi.nlm.nih.gov/18554741/
Wang, Y., et al., J Med Virol, 2020; 93:892-898. SARS-CoV-2 S1 is superior to the RBD as a COVID-19 subunit vaccine antigen. https://pubmed.ncbi.nlm.nih.gov/32691875/
Xiong, X., et al., Nat Struct Mol Biol, October 1, 2020; 27(10):934-941. A thermostable, closed SARS-CoV-2 spike protein trimer. https://pubmed.ncbi.nlm.nih.gov/32737467/
Zhang, L., et al., bioRxiv. Preprint. June 12, 2020. The D614G mutation in the SARS-CoV-2 spike protein reduces S1 shedding and increases infectivity. https://pubmed.ncbi.nlm.nih.gov/32587973/
The published articles listed below clearly show that the “spike protein” is toxic to human life in many, many ways. Introducing the genetic blueprint to enable the cells throughout the body to manufacture such a potent toxin is ABSURD.
Abdi A et al., “Biomed Interaction of SARS-CoV-2 with cardiomyocytes: Insight into the underlying molecular mechanisms of cardiac injury and pharmacotherapy.”Pharmacother. 2022;146:112518. doi: 10.1016/j.biopha.2021.112518
Aboudounya MM and RJ Heads, “COVID-19 and Toll-Like Receptor 4 (TLR4): SARS-CoV-2 May Bind and Activate TLR4 to Increase ACE2 Expression, Facilitating Entry and Causing Hyperinflammation.”Mediators Inflamm. 2021;2021:8874339. doi: https://doi.org/0.1155/2021/8874339
Al-Kuraishy HM et al., “Changes in the Blood Viscosity in Patients With SARS-CoV-2 Infection.” Front. Med. 2022;9:876017. doi: 10.3389/fmed.2022.876017
Avolio E et al., “The SARS-CoV-2 Spike Protein Disrupts Human Cardiac Pericytes Function through CD147 Receptor-Mediated Signalling: A Potential Non-infective Mechanism of COVID-19 Microvascular Disease,”Clinical Science 135, no. 24. (December 22, 2021): 2667–2689, doi: https://doi.org/10.1042/CS20210735
Baldari CT et al., “Emerging Roles of SARS-CoV-2 Spike-ACE2 in Immune Evasion and Pathogenesis,” Trends in Immunology 44 no. 6 (June 2023), doi: https://doi.org/10.1016/j.it.2023.04.001
Biering SB et al., “SARS-CoV-2 Spike Triggers Barrier Dysfunction and Vascular Leak via Integrins and TGF-β Signaling,” Nature Communications 13 (2022): 7630, https://doi.org.10.1038/s41467-022-34910-5
Boschi C et al., “SARS-CoV-2 Spike Protein Induces Hemagglutination: Implications for COVID-19 Morbidities and Therapeutics and for Vaccine Adverse Efects,”International Journal of Biological Macromolecules 23, no. 24 (2022): 15480, doi: https://doi.org/10.3390/ijms232415480
Buzhdygan TP et al., “The SARS-CoV-2 Spike Protein Alters Barrier Function in 2D Static and 3D Microfluidic in-Vitro Models of the Human Blood-Brain Barrier.”Neurobiol. Dis. 2020, 146, 105131. doi: https://doi.org/10.1016/j.nbd.2020.105131
Clough E et al., “Mitochondrial Dynamics in SARS-COV2 Spike Protein Treated Human Microglia: Implications for Neuro-COVID,”Journal of Neuroimmune Pharmacology 16, no. 4 (December 2021): 770–784, doi: https://doi.org/10.1007/s11481-021-10015-6
De Michele M et al., “Evidence of SARS-CoV-2 Spike Protein on Retrieved Thrombi from COVID-19 Patients,”Journal of Hematology Oncology 15, no. 108 (2022), doi: https://doi.org/10.1186/s13045-022-01329-w
Gao X et al., “Spike-Mediated ACE2 Down-Regulation Was Involved in the Pathogenesis of SARS-CoV-2 Infection,”Journal of Infection 85, no. 4 (October 2022), 418–427, doi: 10.1016/j.jinf.2022.06.030
Greenberger LM et al., “Anti-Spike T-cell and Antibody Responses to SARS-CoV-2 mRNA Vaccines in Patients with Hematologic Malignancies,”Blood Cancer Discovery 3, no. 6 (November 2, 2022): 481–489, doi:
Idrees D and Vijay Kumar, “SARS-CoV-2 Spike Protein Interactions with Amyloidogenic Proteins: Potential Clues to Neurodegeneration,”Biochemical and Biophysical Research Communications 554 : 94–98, doi: https://doi.org/10.1016/j.bbrc.2021.03.100
Khan S et al., “SARS-CoV-2 Spike Protein Induces Inflammation via TLR2-Dependent Activation of the NF-κB Pathway,” eLife 10 (December 6, 2021): e68563, doi: https://doi.org/10.7554/elife.68563
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Slow kill to hide the effects
Spike protein is a red herring...
The LNPs were toxic way before that...
https://robc137.substack.com/p/years-before-mrna-and-spike-protein