Serial section analyses of the COVID-19 brain shows that the endothelial cells of the microvessels contained the spike glycoprotein (panel (C)), the ACE2 receptor (panel (D)) and IL 6 (panel (F)), but not viral RNA (panel (E)). The fluorescent yellow signal marks co-localisation of the spike protein with IL6 (panel (G)) and caspase 3 (panel (H)), respectively, in these endothelial cells. Each magnification is 800× with DAB (brown) signal (panels (C–F)) or Fast Red (red) (panel D). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.).
1. Does the Vaccine Produced Spike Protein Have Protective Closed RBDs?
- No studies have determined the stability of the vaccine-induced spike protein, but free spike protein has been found circulating up to 19 days post-vaccination in the plasma of young individuals with post-vaccine myocarditis 54.
- Moreover, the detrimental effects of other angiotensinases (POP and PRCP) deficiency on BP, thrombosis and inflammation are well supported”.
- When this surface current flow is static, with efficient separation of the positively charged Stern layer and negative surface membrane charges, the zeta potential is enhanced and the size, shape, proportion, and curvature of the erythrocyte transforms to the optimal shape.
Cell culture in vitro experiment of brain endothelial cells (a component of the BBB) showed the S1 subunit (RBD) bound to ACE-2 of endothelial cells to traverse the BBB. The S1 subunit correlated with mitochondrial impairment and also entered cell nuclei; the authors postulated that it could disrupt gene expression 168. Animal studies demonstrate the accelerated transition from pre-clinical to clinical stages of prion disease in settings of co-infection, with neuroinflammation, elevated pro-inflammatory cytokines, and enhanced activation of A1 reactive astrocytes 214.
- Cosentino and Marino (2022) reviewed the evidence for widespread biodistribution of the mRNA and concluded that “evidence strongly supports the possible link between inappropriate expression of S protein in sensitive tissues and subsequent tissue damage” 86 (p. 2).
- The word ‘spikeopathy’ was coined by French researcher Henrion-Caude 98 at a conference and given the varied and substantial pathological effects of the SARS-CoV-2 spike protein, we suggest the use of the term will have heuristic value.
- The immune response involves the activation of a highly complex network of activator and inhibitor pathways.
- This presence of spike proteins in pathological tissue that has contributed to patients’ demise could be described as analogous to finding a ‘smoking gun’ at the scene of a crime, only the ‘shot’ was delivered in some cases months earlier.
- Of note SARS-CoV-2 viral infection, especially the earlier variants, can cause loss of smell and thus shows neurotoxicity to the olfactory nerve.
Khavinson et al. in a paper titled “Homology between SARS-CoV-2 and human proteins” found more than two dozen heptamers and octamers, homologous with human proteins, some of which fuse to extended lengths along the length of the SARS-CoV-2 spike protein 136. They noted that given the “structural similarity, a part of the immune response will be directed against the proteins of the host organism” (p.1). The spike protein also was found to “competitively inhibit the bindings of antithrombin and heparin cofactor II to heparin/HS, causing abnormal increase in thrombin activity” 122. In another mouse study, the spike protein was also found to “bind to the blood coagulation factor fibrinogen and induces structurally abnormal blood clots with heightened proinflammatory activity” and that “spike delays fibrinolysis” 123 (preprint). Although the public health authorities’ narrative is that myocarditis from COVID-19 vaccines is mild and self-limiting, the evidence is that symptomatically while this might be the case, pathological changes in these young hearts are persistent.
This was based on ethical principles given the fear of COVID-19 17, but the loss to scientific integrity of only having short-term placebo-controlled trials was noted by the WHO Ad Hoc Expert Group on the Next Steps for Covid-19 Evaluation (2020) 18. The vaccine was meant to protect the over age 60 with the greatest risk of mortality from COVID-19 10, yet a risk analysis by Dopp and Seneff (2022) 250 showed that the likelihood of dying from the injection is only 0.13% lower than the risk of dying from the infection in those aged over 80 years. A case report of an autopsy in a previously healthy 22-year-old male military recruit in South Korea revealed extensive myocarditis five days after Pfizer mRNA COVID-19 vaccination. The authors stressed the importance of conducting histopathological investigations during autopsies.
The claim that the COVID-19 vaccines have saved many millions of lives is predicated on modelling based on case fatality rates (CFR) in China in February 2020 published by Verity et al. in The Lancet 11. The authors estimated a CFR of 6.4% (5.7–7.2) in those aged over 60 years and “up to 13.4% (11.2–15.9) in those aged 80 years or older… with an overall infection fatality ratio for China of 0.66% (0.39–1.33)” (abstract). Fortunately, the virus mutated, and these modelling predictions did not materialise as the pandemic unfolded over the next three years. Central to individual informed consent decisions and public health policy is the weighing of the risks of an illness versus the risks and potential benefits of an intervention. Given the risks of novel gene-based COVID-19 vaccines, were they worth it in light of the severity of SARS-CoV-2 infection?
“SARS-CoV-2 and its Spike protein directly stimulated platelets to facilitate the release of coagulation factors, the secretion of inflammatory factors, and the formation of leukocyte-platelet aggregates”. “The highest levels of AZD1222 vector DNA (103 to 107 copies/µg DNA) were observed in the intramuscular administration sites and sciatic nerve (close proximity to the administration sites) on Day 2. Lower levels of AZD1222 vector DNA (4 copies/μg DNA) were observed in the bone marrow, liver, spleen and lung on Day 2.
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. “The pathogenic mechanisms by which mRNA vaccination triggers the development of autoimmune disease remains unclear. MRNA vaccination beldex coin price today inr triggers potential cross-reactivity between antibodies against the spike protein and self-antigens and may also activate immune responses, leading to the production of interferon I and other pro-inflammatory cytokines and chemokines”. In 2020, prior to the launch of the vaccines, Lyons-Weiler suggested that more than one-third of COVID-19 proteins, the spike protein included, show problematic homology with key proteins in the human immune system. Vojdani et al. 9 cited Lyons-Weiler and went further in their testing, performing epitope mapping and applied monoclonal anti-SARS-CoV-2 spike protein and nucleoprotein antibodies to 55 human tissue antigens in vitro.
4. Carcinogenic Effects
TNF and C1q from activated microglia further activate A1 astrocytes 215 that are thought to be neurotoxic by mediating neuronal damage and serving as foci for prion propagation 216. Non-neutralising antibodies after vaccination against spike protein peptides in mice have also been demonstrated to activate glial cells and astrocytes 217, consistent with this proposed mechanism of activated astrocytes, prion formation and cognitive dysfunction. Avolio et al. 101 found the free SARS-CoV-2 spike protein, separated from the virus, could cause microvascular disease via several mechanisms, which include stimulation of cardiac pericytes to engage in pro-inflammatory cytokine production via CD147 receptor binding. Further evidence for the pathogenicity of spike protein is from mouse studies where spike protein-induced cardiac fibrosis and myocardial contractile impairment may underlie COVID-19-related cardiomyopathy 102. Yonker et al. 54 found free spike proteins in the blood of 16 adolescents and young adults who developed post-vaccination myocarditis, but not in 45 post-vaccination age-matched controls without myocarditis.
After interaction with the receptor, the spike protein undergoes a conformational rearrangement leading to exposure of the S2 subunit, insertion of the fusion peptide into the membrane of the target cell, and refolding of S2. This refolding pulls the fusion peptide and transmembrane domain of the spike protein together, drawing the target cell and viral membranes together and causing their fusion. Secure platform using trusted brokers, strong encryption and EU compliance Fundspire Axivon Belgium As an analogy, imagine a bottle opener pulling the cork up from the bottle neck—but the cork is connected to a cell membrane that gets pulled up along with it 28. The SARS-CoV-2 virion carries spike protein in the form of trimers, predominantly in prefusion form. Prefusion spike protein trimers on each virus are found in various conformations, either closed with all three RBDs lying down at the top of the spike—or open, in which one or more of the RBDs protrude from the top of the spike.
2. Autoimmune Disease
The amount of possible mechanisms of spike-mediated damage in the brain is matched in real life by the prevalence of neurological and neurodegenerative adverse effects and urgently requires further research. A. Evidence of SARS-CoV-2 spike protein in cardiac tissue after COVID-19 vaccination. (A–C) Representative immunohistochemical stainings of SARS-CoV-2 spike protein in EMBs from patients diagnosed with DCMi after receiving Comirnaty® (panel (A,B), patients 5 and 10) or Vaxzevria® (panel (C), patient 13). “Activation of BV-2 microglia by S1 resulted in the increased release of TNF-α, IL-6 and IL-1β, which are hallmarks of neuroinflammation.
1.1. Myocarditis and Pericarditis
Finally, we reviewed the best autopsy case series currently available, performed in Germany, that establish the connections between spikeopathy and multiple organ failures, neuropathies and death. “Yes, that is the finding that we have now been able to collect using special methods. This means that we are actually certain that in this case, we can still detect this toxin in the vessel walls 122 days after the vaccination. Neurological symptoms are commonly noted post-COVID-19, in ‘long Covid’ and post mRNA vaccination, raising the possibility of prion involvement.
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Though speculative, these considerations are supported by a case report of prion disease due to vaccination 193. In an in vitro experiment, spike protein was proteolyzed into smaller segments by neutrophil elastase, some of which exhibited amyloidogenic properties 185. Another study looked at the toxin-like domain of the RBG on S1, which binds to α7 nAChR, increasing levels of IL-1b and TNFα in the brain and impaired episodic memory in mice 178.
COVID-19 Modelling Versus Real-World Data
The accumulation of spike protein inside cells could have toxic and apoptotic effects 29. The virus uses the spike protein to bind with ACE-2 receptors on cell surfaces to enter the cells. For this to happen, the receptor binding domain (RBD) on the S1 subunit undergoes hinge-like extension from the ‘down’ to ‘up’ position to interact with the ACE-2 receptor. Controversy has surrounded the use of the gene-based vaccines and this article explores the reason for this. To meet the widespread desire for ‘safe and effective’ vaccines, gene-based technology offers rapid speed of production. Hope has perhaps influenced much of the published literature as well as media narrative.
Pharmacovigilance databases, like its own FAERS and the CDC’s VAERS, are acknowledged to have large under-reporting factors. “The biodistribution of AZD1222 following intramuscular administration is expected to be similar to that of AdCh63, confined to the site of injection and draining lymph nodes”. According to your profile you’re still using MacOS 10, the new graphics engine requires al least macOS 12, your gpu may not be supported as well. Just saying… I am a novice when it comes to this sorta thing so any help you can provide would be appreciated. Then I spent some months where I was doing all my SU on the v18 beta, so of course that was a parallel, vanilla installation and didn’t have those shortcut changes.