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Researchers examined tissues for spike and nucleocapsid proteins in a patient with COVID-19. Spike proteins are targeted by vaccines, while nucleocapsid proteins are not. In respiratory secretions, spike proteins were found, indicating the virus's presence. In the brain of a vaccinated patient who died, spike proteins were present, but nucleocapsid proteins were not. The absence of nucleocapsid proteins in the brain is puzzling.

Dr. Pretorius and a colleague discuss unusual clotting observed after COVID-19 vaccination, including embalmers reporting back pressure when introducing embalming fluid and the extraction of very long, congealed clots—six inches to several feet—as well as patients with long brachial clots. They note thousands of clotting reports in VAERS across all vaccine types, describing these clots as not normal. Some clots cause major emboli affecting circulation to the lungs, detected by scans and perfusion studies, while others are microclots with a branching pattern visible in imaging. A clinician also shared a photo of a clot with a complete branching pattern into medium and smaller vessels. Dr. Pretorius’ work is cited to explain the mechanism: spike protein can induce immediate clumping of proteins in platelet-poor plasma in the absence of platelets, a highly unusual clotting pathway not relying on the classical coagulation cascade. This is described as a proteinaceous, pseudo-amyloid–like clot. The spike protein is reported to circulate after vaccination, with studies in the Journal of Immunology showing spikes in circulation and exosomes up to four months after shots. Long-haul COVID data (Patterson’s study) reportedly shows S1 protein present in nonclassical monocytes in blood, suggesting persistence of spike protein, whether from infection or the vaccine, which can induce clotting pathways on its own. Dr. Pretorius discusses observations of upregulation of intercellular adhesion molecules (ICAMs) on leukocytes within clots, causing white blood cells to adhere in addition to fibrin, contributing to difficulty in dissolving these clots. Concerning treatment and detection, the speakers describe depletion of plasminogen, reducing the body’s ability to break down clots, and note that standard anticoagulants are less effective against these clots, which are described as amyloid-like and atypical. They emphasize that these are not the classical clotting pathways involving platelet activation and typical thrombin–fibrin cascades. They contrast this with expectations of standard clotting mechanisms and reference the unusual, non-classical pathway highlighted by Pretorius. The discussion also mentions the idea that spike protein in circulation can drive clotting without the usual platelet activation, and that some patients have continued to experience spike-related effects long after vaccination. They assert that vaccines were developed targeting the original Wuhan strain and may not cover Omicron; they suggest the shot’s risk-benefit balance is unfavorable given ongoing clotting, immune suppression, and cancer-inducing pathways, and they claim data indicate those who receive two or three shots may acquire Omicron at a higher rate than those unvaccinated. They conclude that the shot is expired for a virus that is no longer circulating in its original form and argue that vaccination induces dangerous pathologic processes with no protective benefit.

Bonjour à tous, Anaïs Bloqué, docteur en biologie santé, explique les impacts de la protéine Spike du SARS-CoV-2 sur le système immunitaire inné, basés sur son article récent. La Spike seule n'active pas complètement le TLR 4, un récepteur immunitaire, et ne permet pas la production d'interférons de type 1, essentiels pour lutter contre le virus. Pour une activation complète, la Spike doit s'associer au LPS (des bactéries gram négatifs). L'activation des interférons 1 augmente l'expression d'ACE2, le récepteur du virus, sensibilisant l'organisme à l'infection. Les interférons 1 peuvent aussi être activés par les RLR, notamment MDA5, qui détecte l'ARN messager modifié des vaccins anti-COVID. De plus, la Spike, protéine amyloïde, peut déclencher le TLR 4 en s'associant aux fibres amyloïdes A bêta 42, créant un "double effet amyloïde". L'augmentation de NF-κB par les interférons 1 peut bloquer la p53, un suppresseur de tumeur, et induire l'expression du MIR-29b, qui bloque ACE2. Chez les personnes avec comorbidités, ayant déjà de faibles niveaux d'ACE2, cette interaction Spike-LPS devient dangereuse, créant une boucle d'amplification inflammatoire. La Spike persiste longtemps dans l'organisme, et avec ses propriétés amyloïdes, pourrait entraîner des pathologies dégénératives à long terme. --- Hello everyone, Anaïs Bloqué, Doctor of Philosophy in Health Biology, explains the impacts of the SARS-CoV-2 Spike protein on the innate immune system, based on her recent article. The Spike alone does not fully activate TLR 4, an immune receptor, and does not allow the production of type 1 interferons, which are essential for fighting the virus. For complete activation, the Spike must associate with LPS (from gram-negative bacteria). Activation of interferon 1 increases the expression of ACE2, the virus's receptor, sensitizing the body to infection. Interferons 1 can also be activated by RLRs, in particular MDA5, which detects the modified messenger RNA of anti-COVID vaccines. In addition, Spike, an amyloid protein, can trigger TLR 4 by associating with amyloid A beta 42 fibers, creating a "double amyloid effect". The increase in NF-κB by interferons 1 can block p53, a tumor suppressor, and induce the expression of MIR-29b, which blocks ACE2. In people with comorbidities, who already have low levels of ACE2, this Spike-LPS interaction becomes dangerous, creating an inflammatory amplification loop. Spike persists in the body for a long time, and with its amyloid properties, could lead to long-term degenerative pathologies.

Some research suggests the coronavirus can infect brain cells, impacting memory and cognitive functions. Understanding this could help treat long COVID symptoms like brain fog and fatigue. Early treatment may prevent brain damage.

I contracted SARS in South Korea during the outbreak. It caused neurological symptoms and was different from the flu or norovirus. I couldn't get a proper diagnosis, but I realized it was serious when I saw what was happening in Wuhan. There was an effort to suppress information beyond the official narrative. I believed it came from a lab and published a paper on it. I've been trying to inform people about the role of viruses in chronic neurodegenerative diseases. The spike protein in the virus can misfold and cause amyloidosis. There are safety concerns with gene transfection, and we're seeing excess deaths, especially in dementia cases. Synthetic peptides may be a contributing factor.

As a doctor, the speaker states they have never seen something so injurious to the human body, invading the brain, heart, and bone marrow. It allegedly stimulates antibodies to attack platelets and other cells, causing unprecedented blood clotting and blood vessel damage. The speaker cites data from the University of Pittsburgh suggesting it causes cancer. They question how a single protein can injure the brain, heart, bone marrow, and immune system, cause blood clotting, and potentially cause cancer, calling it a weapon. The speaker references three papers, including one by Farkas in Military Medicine and Tubei Yan in preprint, which reportedly conclude that it is a bioweapon according to strict military criteria.

The speaker discusses a long-running claim from the pandemic era: that they could smell when someone had COVID or had been recently vaccinated, and that many others reported a distinctive odor associated with COVID. They acknowledge that some people can barely smell it while others experience headaches, nausea, or sickness, and note that many people's sense of smell has been altered during and after illness. The video focuses on the scent profile and the chemistry behind spike protein exposure, rather than virology, arguing that spike protein alone can drive COVID-related injury and long COVID, with no need for viral components. The speaker references research from 2024–2025 examining sweat and breath to identify chemicals that change in COVID and post-COVID vaccine states, noting that the research looks at both long-haul and long COVID profiles as well as post-vaccine chemistry in terms of odor. According to the presented science, spike protein flips the body’s chemistry, turning sweat into a distinct odor described as a strange, sour, greasy signal with a metallic twist. The speaker recalls smelling a mixture of metal and formaldehyde and explains that compounds such as fatty acids and ketones surge, along with pheromones that could subtly influence behavior. The description asserts that during spike protein exposure, cells are in chaos, and the protein binds to receptors like ACE2, triggering a biochemical storm that alters volatile organic compounds (VOCs), which are the gaseous clues the body releases. VOCs are said to create an odor that is subtle yet disturbing, detectable within about one to two feet indoors, with outdoors and humidity affecting detectability. Key chemical changes cited include: oxidative stress leading to reactive oxygen species and the production of nonanol (a greasy, rancid compound) that quadruples in sweat in long COVID; methyl oleate rising to at least twice the usual amount, adding a soapy, earthy layer; a shift to ketone production (two-butanone) giving a faint acetone-like sweetness; iron release from ferritin forming an iron pentacarbonyl, contributing a metallic, rusty penny smell; malondialdehyde (MDA), a burnt fat aldehyde, increasing two to three times in long-haul cases and sharpening the scent with a rancid sting; benzaldehyde increasing due to tryptophan breakdown, giving a sharp formaldehyde-like bite; two ethyl hexanol from skin ester hydrolysis adding a plasticky soapiness (some respondents reported soapiness). Ethyl octanoate is mentioned as mimicking an alarm pheromone in bees, contributing a pear-like scent and signaling danger. The speaker links VOCs to behavioral and social effects, noting heightened pheromonal signals: cortisol spike with a 40% rise in androstanone (giving a musky scent and potentially calming or influencing competitive behavior), drostanone rising by about 50% adding an animalic, sweaty edge that can trigger avoidance or aggression, and ethyl octanoate resembling an alarm pheromone. They describe hive-like social effects, cognitive rigidity, conformity, and a perceived protective or suppressive social response, including references to depopulation theories and population sterilization, interpreted as social control mechanisms embedded in the bioweapon narrative. The speaker, a former clinical psychologist with a background in mass-killing prevention and biowarfare response, signals intent to delve deeper in future videos and invites comments on topics to cover next.

This substance is extremely harmful to the human body, affecting the brain, heart, and bone marrow. It triggers the immune system to attack our own cells, leading to blood clotting and damage to blood vessels. Research from the University of Pittsburgh suggests it may even cause cancer. The ability of a single protein to invade critical organs and systems raises serious concerns. Three studies, including one by Farkas in military medicine, have classified it as a bioweapon based on strict military criteria.

The clots being formed, we've run mass spectrometry on these clots. They don't look like normal clots. They don't have the same composition. They don't have fibrin. They don't have thrombin, which are normal things you would see in a normal coagulation cascade. They have, instead, all the fibrinogen chains—alpha, beta, and gamma. They have them in a strange differential where it's not one-to-one-to-one; it's about 36 to 16 to 4 by ratios. They're aberrantly cross-linked by sulfide bonds. There's a ton of tin for some reason. I don't know why there's tin in there, but there's a ton of tin in there and a ton of phosphorus. And the spike protein is actually coated in GLIKNAK, which is a phosphate donor. So that might explain all the phosphorus if it's providing the energetics or in some way by cleaving or creating phosphate bonds. So I think that that's a big problem because that's a slow progression of coagulopathy that's, I think, narrowing the lumens of the vascular system, which is contributing to some of the organ failure that we're seeing, some of the neurological symptomatology that we're seeing, some of the fatigue, and things of that nature. And then finally, the spike protein is shown to produce—it’s shown to induce misfolding of proteins and actually

Using more c and g in biotechnology translates proteins quicker, evading the immune system. However, altering the folding structure by increasing GC content in Pfizer's and Moderna's drugs poses risks. Computer models show significant differences in folding between the drugs and the natural virus, potentially leading to prion disease concerns. These modifications make the drugs more hazardous than the original virus.

In a deceased patient, spike protein was found in the heart but not nucleocapsid protein. The autopsy revealed bronchopneumonia, Parkinson's disease, necrotic encephalitis, and myocarditis. The author suggests that the spike protein in affected tissues was likely from gene-based COVID-19 vaccines, not a SARS CoV-2 infection, as nucleocapsid protein was absent. Spike protein was found in areas with brain and heart inflammation, possibly contributing to the disease.

**French Summary:** Anaïs Bloqué explique l'impact de la protéine Spike du SARS-CoV-2 sur le système immunitaire inné, en se concentrant sur le TLR 4. La Spike seule n'active pas complètement le TLR 4 pour induire une réponse antivirale complète (interférons de type 1). L'association Spike-LPS (lipopolysaccharide bactérien) est nécessaire. L'activation des interférons 1 augmente l'expression d'ACE2, récepteur du virus, via les ISG, sensibilisant l'organisme à l'infection. Les ARN messagers des vaccins peuvent aussi activer les interférons 1 via MDA5. La Spike, protéine amyloïde, peut induire la production de fibres A bêta 42, aggravant l'inflammation. L'augmentation de NF-κB par les ISG peut bloquer p53 (suppresseur de tumeur) et induire le micro-ARN MIR-200c, diminuant l'expression d'ACE2. Chez les personnes avec comorbidités (diabète, obésité), une boucle d'amplification inflammatoire Spike-LPS-TLR4 réduit l'ACE2 disponible, menant à une suractivation de l'angiotensine 2. La Spike persistante pourrait causer des pathologies dégénératives à long terme. **English Translation:** Anaïs Bloqué explains the impact of the SARS-CoV-2 Spike protein on the innate immune system, focusing on TLR 4. Spike alone does not fully activate TLR 4 to induce a complete antiviral response (type 1 interferons). The Spike-LPS (bacterial lipopolysaccharide) association is necessary. Activation of interferon 1 increases ACE2 expression, the virus receptor, via ISGs, sensitizing the body to infection. Vaccine mRNAs can also activate interferon 1 via MDA5. Spike, an amyloid protein, can induce the production of A beta 42 fibers, worsening inflammation. Increased NF-κB by ISGs can block p53 (tumor suppressor) and induce microRNA MIR-200c, decreasing ACE2 expression. In people with comorbidities (diabetes, obesity), a Spike-LPS-TLR4 inflammatory amplification loop reduces available ACE2, leading to overactivation of angiotensin 2. Persistent Spike could cause long-term degenerative pathologies.

Our study investigates the impact of the SARS-CoV-2 spike protein on blood hypercoagulation. We used microscopy and mass spectrometry to examine the spike protein's interaction with platelets and fibrinogen. Results using platelet-poor plasma showed the spike protein may disrupt blood flow. Mass spectrometry revealed structural changes in beta and gamma fibrinogen, complement, and prothrombin after adding spike protein S1. These changes, similar to those observed in COVID-19 patient blood clots, showed resistance to trypsinization. We propose that the spike protein's presence in the bloodstream contributes to hypercoagulation in COVID-19 patients, potentially causing impaired fibrinolysis and persistent microclots. This finding has significant clinical implications. Our goal was to determine the spike protein's effects, as its interaction with these blood components warrants further investigation.

Spike is a toxin that can cross the blood-brain barrier, causing disruption to the brain's blood vessels and leading to inflammation. This inflammation is responsible for the brain fog experienced by both COVID patients and those who have been vaccinated. Despite claims that there have been no deaths or injuries from the vaccine, this is not true. The image shown reveals the presence of inflammation in the brain, indicated by the blue color. This inflammation is a result of the spike toxin.

The speaker discusses the inflammatory and amyloidogenic effects of small sequences called epitopes, which can cause memory dysfunction in mice. They also mention a study that found the introduction of gene transfection technologies containing the spike protein can induce amyloidogenic cascades. The speaker highlights a 200% increase in the diagnosis of CJD in France after the rollout of vaccination programs, suggesting a potential link. They discuss the loss of cognitive function associated with exposure to the spike protein and propose that amyloidogenic disease processes may underlie long-haul COVID-19 symptoms. The speaker mentions the role of viral infections in facilitating intercellular aggregate dissemination and shares examples of misfolding prion amyloidogenic diseases.

The speaker claims HIV exists in the spike protein, citing Luc Montagnier, who won a Nobel Prize for identifying HIV. Montagnier identified 18 RNA fragments matching HIV and SIV. The speaker questions how the PRRA insert, requiring 12 nucleotides, could be a mutation, and points to a larger HIV insert of 1,770 nucleotide bases. The speaker details the four steps required for the virus to enter the body: ACE2 receptor, TMPRSS2, furin cleavage site (PRRA), and neuropilin NRP1. They claim black people are more infected because they have more TMPRSS2 receptors. The speaker notes only SARS CoV-2 has the PRRA insert, and the NIH owns the patent for the insertion of enzymes related to the furin cleavage site, useful for HIV glycoprotein and tumor progression. Animal studies in humanized mice showed 95% died after two weeks, exhibiting spongiform encephalopathy (mad cow disease). Rhesus macaque monkeys developed inflammatory cells and Lewy bodies (Alzheimer's) in their brains, suggesting the spike protein crosses the blood-brain barrier. The speaker claims Kevin W. McCarran has warned of these neurological effects. The speaker alleges the U.S. government, through various agencies and individuals, is responsible for the virus's creation at the Wuhan Institute of Virology and that it was intentionally released in the wet market.

White fibrous clots found in the living and dead recipients of mRNA vaccines are being ignored, but research reveals their composition and cause. The spike protein mutates fibrin into jagged, misfolded, insoluble amyloid, similar to prionic infections. Microclots form and align into large white clots, initiated by spike protein fragments like spike 601. Prolene, a "kinker protein" added to the spike protein, causes misfolding, with proline being prevalent in the clots. A 2021 paper showed the SARS CoV-2 spike induces abnormal blood clots due to the fibrinogen beta chain. Plasma exposed to the spike protein is imbalanced, with the fibrinogen beta chain being dominant. These clots contain four times the normal amount of phosphorus, released from lipid nanoparticles. Similar clots in 1988 were caused by sulfur-based heparin, which was resolved by reducing sulfur content. A 2017 paper showed altered phosphorus levels cause cancer. Thomas Havilland, who shares this information, is being ignored by mainstream and alternative media. Undertakers are seeing massive white fibrous clots at record levels.

Arrhythmias are common in COVID-19, and there are auto antibodies in this pathway that may be causing them. Additionally, there is a connection between t1r receptors and depression and dementia, which can lead to brain fog and fatigue. The challenge is to find something in COVID-19 that cannot be explained using these four substances.

The comparison to HIV is important because both viruses can be asymptomatic. HIV taught us a lot about immunology and changed cancer therapy. Similarly, we are now learning about the impact of the virus on mitochondria, brain fog, and our neurons through long COVID. Mild and moderate COVID can cause destruction, just like HIV did to our immune system. However, the brilliant science that came out of HIV research transformed how we treat the virus, allowing people to live normal lives. We need to do the same for long COVID, so that those affected can not only survive but also thrive.

The video discusses the potential adverse effects of the spike protein in SARS-CoV-2 on human prion protein and amyloid fibril formation. The speaker highlights a study showing that spike amyloid fibrils can accelerate the formation of amyloid fibrils associated with prion diseases and Alzheimer's. They also mention recent research suggesting that other viruses, like H5N1 influenza, may impact and misfold prion protein. The speaker emphasizes the importance of understanding these interactions and their potential implications. They briefly mention the symptoms and diagnostic challenges of prion diseases like Creutzfeldt-Jakob disease. Overall, the video explores the role of the spike protein in amyloidosis and its potential impact on neurological tissues.

The spike protein from the COVID-19 virus circulates in the body and can land in multiple organs, causing various diseases. Lab studies have shown that even without the virus, just injecting the spike protein can induce the same lung, vascular, heart, and brain diseases as COVID-19. The spike protein is considered the toxin responsible for causing the disease. This raises questions about why we are injecting something that is essentially a toxin into the human body, as it is not a traditional vaccine.

Bonjour à tous, Anaïs Bloqué, docteur en biologie santé, explique les impacts de la protéine Spike du SARS-CoV-2 sur le système immunitaire inné, basés sur son article récent. La Spike seule n'active pas complètement le TLR 4, un récepteur immunitaire, et ne produit pas d'interférons de type 1, essentiels pour la réponse antivirale. Pour une activation complète, la Spike doit s'associer au LPS (des bactéries Gram négatif). L'activation des interférons 1 augmente l'expression d'ACE2, le récepteur du virus, via les ISG, sensibilisant l'organisme à l'infection. Les ARN messagers des vaccins peuvent aussi lancer la production d'interférons 1 via MDA5. La Spike, protéine amyloïde, peut aussi déclencher le TLR 4 avec des fibres amyloïdes, entraînant un "double effet amyloïde". L'augmentation de NF-κB par les ISG peut bloquer la p53, potentiellement cancérigène. De plus, NF-κB induit le MIR-200c, qui bloque l'ACE2. Chez les individus avec comorbidités, une boucle d'amplification inflammatoire se crée : Spike-LPS-TLR4 induit interférons 1, ISG, surexpression d'ACE2, augmentation de NF-κB, MIR-200c, diminution d'ACE2 et augmentation d'angiotensine 2. La Spike persiste longtemps, et ses propriétés amyloïdes font craindre des pathologies dégénératives à long terme. --- Hello everyone, Anaïs Bloqué, PhD in health biology, explains the impacts of the SARS-CoV-2 Spike protein on the innate immune system, based on her recent article. Spike alone does not fully activate TLR 4, an immune receptor, and does not produce type 1 interferons, which are essential for the antiviral response. For complete activation, Spike must associate with LPS (from Gram-negative bacteria). Activation of interferon 1 increases the expression of ACE2, the virus's receptor, via ISGs, sensitizing the body to infection. Vaccine mRNAs can also trigger the production of interferon 1 via MDA5. Spike, an amyloid protein, can also trigger TLR 4 with amyloid fibers, leading to a "double amyloid effect." The increase in NF-κB by ISGs can block p53, which is potentially carcinogenic. In addition, NF-κB induces MIR-200c, which blocks ACE2. In individuals with comorbidities, an inflammatory amplification loop is created: Spike-LPS-TLR4 induces interferon 1, ISG, ACE2 overexpression, increased NF-κB, MIR-200c, decreased ACE2 and increased angiotensin 2. Spike persists for a long time, and its amyloid properties raise concerns about long-term degenerative pathologies.

They examined tissues for spike and nucleocapsid proteins. Spike proteins are targeted by vaccines, while nucleocapsid proteins are not. In a patient positive for SARS-CoV-2, spike proteins were found in respiratory secretions, but nucleocapsid proteins were not. In an autopsy of a vaccinated patient who was not tested for SARS-CoV-2, spike proteins were present in the brain, but no nucleocapsid proteins were detected. The absence of nucleocapsid proteins in the brain is unexplained.

The speaker believes mRNA vaccines are producing an abnormal spike protein that doesn't enter the membrane, potentially leading to prion problems. Prion proteins misfold into beta sheets in the cytoplasm, forming crystals that attract other proteins and create fibrils like Alzheimer's plaque. The speaker claims the vaccines produce many spike proteins that cannot enter the membrane, increasing the likelihood of becoming problematic prion proteins. This is described as a setup for Parkinson's disease, potentially causing earlier onset or new cases in vaccinated individuals. The speaker suggests annual boosters may accelerate the development of Parkinson's.

COVID-19 did happen, but it was caused by lipid nanoparticle technology, not a virus. These nanoparticles hijack the human immune and neurological systems, leading to mild to severe disease. The so-called spike proteins are actually lipid nanoparticles, not a virus. When a magnetic hydrogel infects a biological cell, it becomes covered in spikes, which are the spike proteins. This technology reprograms the cell to release synthetic toxins in the body, causing COVID-19. James Giordano, who advised the US military and intelligence community in 2008, discussed the use of lipid nanoparticle technology as neuro weapons.