COVID-19 Vaccine Harms

By Len Duggan 16 / Apr / 2025
Len Duggan's picture

COVID-19 Vaccine Harms

 

Introduction

This article explores the significant and growing body of scientific evidence pointing to serious health risks associated with COVID-19 mRNA vaccines. It investigates the complex immune responses triggered by these injections, focusing especially on the troubling shift toward the production of IgG4 antibodies after repeated doses. This class switch undermines the immune system’s ability to clear infection and leads to chronic illness, autoimmune dysfunction, and even cancer.

One of the most pressing dangers is the potential for cardiovascular damage, particularly myocarditis in young, otherwise healthy individuals. Frequently underdiagnosed, this heart inflammation can present with few symptoms until triggered by physical exertion — potentially leading to sudden cardiac events or death.

Also examined is the alarming possibility of genomic integration. The mRNA vaccines contain SV40 promoter sequences and residual DNA fragments, which — under certain conditions — may trigger reverse transcription, embedding the spike gene into human DNA. This would mean indefinite production of the spike protein, potentially for the rest of the recipient’s life.

The pathogenicity of the spike protein itself is another central concern. Originally thought to be a harmless antigen, the spike protein is now understood to be biologically active and toxic in its own right. It binds to ACE2 receptors, penetrates vital organs, disrupts cardiovascular function, and triggers immune and inflammatory responses. It also interferes with red blood cells, impairing oxygen delivery and promoting clot formation. This phenomenon — now known as spikeopathy — has been implicated in long-COVID, post-vaccination syndromes, and a range of chronic diseases.

The article also outlines mounting evidence of prion-like neurological disease. Conditions resembling Alzheimer’s and Creutzfeldt-Jakob disease (mad cow disease) have been reported in individuals — including young adults — shortly after vaccination. These observations align with experimental data showing that the spike protein contains prion-like domains and may induce protein misfolding in the brain.

Further, the article revisits Antibody-Dependent Enhancement (ADE) — a well-documented problem in coronavirus vaccine development long before COVID-19. ADE has now been confirmed in autopsy studies, where vaccine recipients failed to mount effective responses against the wild virus and instead suffered from overwhelming infections marked by immune dysfunction and tissue destruction.

Finally, this article highlights the persistent spike expression observed in vaccine recipients. Without a built-in regulatory mechanism, the mRNA continues to generate spike protein for months — and possibly years — after the injection. In some cases, spike protein has been detected in circulation or tissues up to 700 days after vaccination, raising profound concerns about the long-term burden this imposes on the immune system.

1/ Persistent Spike Expression after COVID-19 Vaccine

The prolonged expression of the SARS-CoV-2 spike protein following mRNA vaccination is a significant concern, with studies showing its persistence for up to 700 days in some cases. This extended expression can result in continuous immune activation, preventing the immune system from adequately handling other viruses such as Epstein-Barr (EBV) or latent infections, thereby contributing to immune dysfunction. The ongoing presence of the spike protein also drives the immune system toward a class switch to IgG4, a response associated with immune tolerance and reduced immune activity. This class switch further exacerbates the body’s inability to properly defend against new or reactivated pathogens.

The spike protein infiltrates various body systems, triggering persistent inflammation and immune responses. These inflammatory effects can last far beyond the typical duration of an infection, leading to chronic tissue damage and ongoing health issues. This prolonged-expression is not without risks, for instance, research has documented the persistence of the S1 subunit of the spike protein in CD16+ monocytes up to 245 days in individuals with post-vaccination symptoms resembling Post-Acute Sequelae of COVID-19 (PASC) (Patterson 2024). This suggests that even in individuals who are SARS-CoV-2 negative, the spike protein remains a source of immune system disturbance.

In addition, there are indications that the spike protein could integrate into the host’s genome, raising concerns that it may be expressed for the lifetime of the vaccine recipient. Boros et al. (2024) found that biochemically modified mRNA and frameshifted spike proteins persist in human tissues and circulation long after vaccination, reinforcing the potential for long-term implications. This persistent expression could be due to spike proteins either being released in exosomes, which might escape immune clearance, or through integration into the host genome, making their expression potentially lifelong.

Furthermore, the spike protein's ability to infiltrate various tissues has been documented in several studies, with notable findings such as the expression of the spike protein in the vascular endothelial cells and eccrine glands of the skin (Sano 2023). This expression was linked to persistent dermatological symptoms, including erythema following vaccination. Studies have also revealed the presence of spike protein in cerebral arteries, suggesting potential links to neurological disorders such as haemorrhagic strokes post-vaccination (Ota 2025).

The persistence of spike protein in circulation also raises alarms regarding cardiovascular health. Research by Yonker (2023) detected circulating spike proteins in individuals suffering from myocarditis following mRNA vaccination, providing evidence of ongoing cardiovascular involvement long after the initial vaccination. Additionally, other studies have explored how persistent viral proteins, including the spike, contribute to the reactivation of latent infections such as varicella-zoster virus, further compounding the risks associated with long-term immune activation (Yamamoto 2023).

In conclusion, the spike protein presents multiple, complex health risks including, continuous immune activation, potential for chronic inflammation, and the possibility of genomic integration demands further investigation to understand the full scope of the vaccine’s long-term impact on human health.

2/ Pathogenicity of the Spike Protein (spikopathy)

The spike protein, whether originating from natural SARS-CoV-2 infection or produced in the body following mRNA vaccination, is increasingly recognised as intrinsically pathogenic. This concept, referred to in emerging literature as “spikeopathy,” underlines a growing understanding that the spike protein is not merely an inert target for antibodies, but an active contributor to tissue damage, inflammation, and long-term disease.

Several peer-reviewed and preprint studies now confirm that the spike protein alone is sufficient to trigger endothelial damage, inflammation, coagulation disturbances, and immune dysregulation. Importantly, the spike protein encoded by the mRNA vaccines is not identical to the natural SARS-CoV-2 spike. It has been intentionally stabilized in a prefusion conformation to enhance immunogenicity, but this modification appears to come at a cost: it is more resistant to degradation and induces stronger inflammatory responses (Robles 2022; Perico 2022; Villacampa 2024; Parry 2023).

Evidence is mounting that the vaccine-derived spike protein is more toxic than its viral counterpart, particularly in cardiac tissue. A UK-based study by the British Heart Foundation demonstrated that spike protein alone can bind to heart cells and alter their function (BHF, 2021). While myocarditis cases after mRNA vaccination are common, especially among young males, suggesting a unique pathogenic role of the vaccine spike (Truong 2021). However, Tuvali (2022) found no significant increase in myocarditis or pericarditis in individuals infected with SARS-CoV-2 without vaccination.

Spike protein has also been shown to:

  • Infiltrate vital organs, including the brain, heart, liver, and kidneys.
  • Attach to red blood cells, impairing oxygen delivery and promoting clot formation (Parry 2022).
  • Trigger autoimmune responses, including molecular mimicry with human proteins and aberrant immune activation (Brawer 2024).

According to Hulscher (2023), the spike protein plays a direct role in cardiovascular and thrombotic injury post-vaccination. The persistence of spike protein in patients suffering from long-COVID and vaccine-related adverse events has been documented up to 15 months post-injection.

Lataster (2024) echoes these concerns, highlighting the possibility that spike-driven class switching to IgG4 could lead to immune suppression, autoimmunity, and even cancer — all of which indicate that the vaccine-induced spike is not just immunogenic but potentially chronically pathogenic.

In conclusion, the spike protein — particularly the stabilized version encoded by COVID-19 mRNA vaccines — is not a harmless antigen. It is a biologically active molecule capable of interfering with multiple physiological systems, with documented implications in cardiovascular disease, neurodegeneration, immune dysregulation, and systemic inflammation. Ongoing expression of this protein from prolonged mRNA persistence or potential genomic integration presents a serious long-term health concern that warrants immediate and transparent scientific investigation.

3/ SV40 Sequences and the Risk of Genome Integration

One of the most serious concerns surrounding the safety of mRNA-based COVID-19 vaccines is the presence of simian virus 40 (SV40) sequences within the residual plasmid DNA. SV40 is a known oncogenic virus historically associated with cancer risk due to its ability to activate dormant genetic elements and interfere with cellular control mechanisms.

A 1992 study by Feuchter demonstrated that SV40 large T antigen can activate a wide range of human endogenous retrovirus-like sequences (HERVs), which are normally silent within the genome. This activation may initiate gene expression in regions of the DNA that are typically inactive, potentially leading to oncogenesis or other forms of dysregulation.

More recently, a 2024 study by Kammerer et al. analysed the contents of BioNTech's mRNA-based COVID-19 vaccines and found significant amounts of residual plasmid DNA, including the SV40 promoter/enhancer and an antibiotic-resistance gene. The authors issued a clear warning:

“Our results raise grave concerns regarding the safety of the BNT162b2 vaccine and call for an immediate halt of all RNA biologicals unless these concerns can be dispelled.”
(Kammerer, 2024)

This is not an isolated finding. Speicher (2023) confirmed the presence of the SV40 promoter-enhancer-ori specifically in Pfizer vials, with a preliminary correlation between higher DNA content and the frequency of serious adverse events (SAEs) (Speicher, 2023). These findings raise the possibility that the inclusion of SV40 sequences — known to activate retroelements — could contribute to long-term genomic instability.

Genome Integration via Reverse Transcriptase

There is also growing evidence that components of the vaccine may be reverse-transcribed and integrated into the human genome. A 2022 study by Aldén et al. showed that in human liver cells, the Pfizer vaccine’s mRNA was reverse-transcribed and integrated into host DNA within six hours of exposure. The authors identified endogenous reverse transcriptase activity — potentially upregulated by the presence of SV40 — as the likely mechanism for this process.

Earlier studies support this concern. Noutsopoulos (2006) found that SV40 infection increases the retro-transposition frequency of VL30 elements — viral-like retrotransposons similar to human HERVs. Tzavaras (2003) showed that SV40 transformation of cells could enable non-autonomous retrotransposons to move through trans-complementation by inducing endogenous reverse transcriptases.

Kowarz et al. (2022) also highlighted that SV40 poly(A) signal sequences can be involved in splice events that lead to unexpected production of secreted spike protein — a potentially dangerous outcome, as it could bind to ACE2 receptors throughout the body and provoke systemic effects.

Oncogenic Transformation

The potential for SV40 sequences to participate in malignant transformation is well-established. MacKenzie (2002) showed that SV40 T antigen, when combined with telomerase and oncogenic N-Ras, could model multiple stages of cancer in human endothelial cells. SV40’s long-documented role in oncogenesis raises serious concerns about its presence in a widely distributed pharmaceutical product.

4/ The Spike Protein and Prion-Like Disease: A Growing Concern

One of the lesser-known but potentially serious concerns surrounding the COVID-19 mRNA vaccines is the prion-like activity of the spike protein. This possibility has been raised by several researchers and has implications for long-term neurological health, especially given the persistence of spike protein in the body after vaccination.

What Are Prions?

Prions are misfolded proteins that can induce nearby proteins—especially in the brain—to also misfold. Once this begins, it creates a domino effect, leading to toxic aggregates that damage neural tissue. This misfolding mechanism is what underlies Creutzfeldt-Jakob disease (CJD), kuru, and other deadly neurodegenerative conditions Classen, 2021.

Unlike viruses or bacteria, prions do not carry genetic material. Instead, they cause disease through structural corruption—a unique mechanism that is impossible for the immune system to detect or stop once it begins.

Spike Protein: A Prion-Like Candidate?

Multiple studies suggest that the SARS-CoV-2 spike protein, especially the S1 subunit used in COVID-19 mRNA vaccines, contains prion-like domains—sections of the protein with the potential to misfold or induce misfolding in other proteins.

  • A 2022 paper identified prion-like domains in the spike protein that differ between variants, influencing both transmissibility and disease severity (Tetz 2022).
  • Computational models suggest that the receptor-binding domain (RBD) of the spike protein may be amyloidogenic, especially in the Omicron variant, meaning it could form toxic aggregates similar to those seen in Alzheimer’s disease (Aksenova 2022).
  • Other studies have linked spike protein exposure to neuroinflammation and protein misfolding processes (Seneff 2022).

Clinical Cases: Prion Disease After Vaccination

Though rare, there have now been multiple case reports and observational studies describing the onset of prion disease-like symptoms, sometimes within days or weeks of COVID-19 vaccination:

  • A series of 26 CJD cases following vaccination were reported by Perez (2023), suggesting a potential pattern worth investigating.
  • A 2023 case report in The American Journal of Case Reports documented the rapid onset of prion disease in a patient shortly after vaccination (Makhoul 2023).
  • Other studies raise similar alarms, pointing to a potential link between spike exposure and early-onset neurodegeneration, including Alzheimer’s and ALS-like syndromes (Zhao 2022; Seneff 2023).

Though these findings are not conclusive, they highlight a worrying pattern and justify further investigation. The rare nature of these diseases—especially in younger individuals—makes their appearance in temporal proximity to vaccination hard to ignore.

The Role of Persistent Spike Protein

The persistence of spike protein in the body long after vaccination may also play a role. A 2024 study published in Cell Host & Microbe detected spike protein at the skull-brain interface, even in individuals long after acute infection (Rong 2024). If spike protein continues to be expressed in sensitive neurological tissues, it could provide a chronic trigger for prion-like misfolding and neuroinflammation.

This may be further compounded by reverse transcription mechanisms or immune tolerance due to IgG4 class switching, allowing spike to evade clearance—a perfect storm for long-term neurological risk.

In Summary: A Potential Health Warning

  • The spike protein encoded by COVID-19 mRNA vaccines has structural features associated with prion-like behaviour.
  • Reports of early-onset neurodegenerative conditions, including CJD, in close temporal proximity to vaccination are now appearing in medical literature.
  • Long-term persistence of spike protein in neurological tissues may further increase risk.
  • While causality has not yet been established, the mechanisms involved are biologically plausible, and the evidence base is growing.

Given the severity of prion disease and its resistance to treatment, this subject demands urgent, transparent scientific scrutiny—not dismissal.

 

5/ Heart Damage and Myocarditis Following COVID-19 Vaccination

Myocarditis, inflammation of the heart muscle, has been recognised as a serious adverse effect of COVID-19 mRNA vaccines, particularly among young and otherwise healthy individuals. The risk is particularly high among males aged 12 to 39 years, with vaccine-related myocarditis occurring more frequently after the second dose. While the clinical course of vaccine-associated myocarditis is generally considered mild, there is an undeniable concern that many cases go undiagnosed or untreated, leaving affected individuals vulnerable to sudden cardiac events and sudden death syndrome—especially during strenuous physical activity.

Incidence and Underdiagnosis

Multiple studies confirm that myocarditis is a known side effect of mRNA vaccines. A study by Heidecker (2022) published by the European Society of Cardiology notes that the rates of myocarditis vary by age and sex, with the highest incidence observed in males between the ages of 12 and 39 years. While the clinical course is often mild, with rare cases of left ventricular dysfunction, heart failure, and arrhythmias, it is likely that many mild cases remain undiagnosed because cardiac magnetic resonance imaging (CMR), which is crucial for diagnosis, is not commonly performed in mild or asymptomatic cases.

In fact, Takada (2024) observed that in the Japanese population, vaccination with the SARS-CoV-2 mRNA vaccines was significantly associated with myocarditis and pericarditis, particularly in individuals under the age of 30, with male patients being disproportionately affected. These findings highlight the ongoing concern regarding myocarditis risk and underscore the importance of proper diagnostic protocols, especially in young individuals who may not immediately associate chest pain with a heart condition.

The Risk of Sudden Cardiac Events

One of the greatest concerns surrounding vaccine-induced myocarditis is the risk of sudden death, particularly during vigorous physical exertion. The myocardium, when inflamed, is more prone to arrhythmias, which can be fatal under stress. After a diagnosis of myocarditis, it is imperative for any athlete or highly active individual to refrain from physical exercise to prevent exacerbating heart dysfunction, as recommended by the CDC and other medical authorities (CDC.gov).

Many young, fit individuals may overlook symptoms of myocarditis, such as chest pain, believing it to be something as innocuous as "trapped wind"—a common misconception. Unfortunately, this kind of underestimation could be putting countless young people at risk. The full extent of myocarditis cases following vaccination may be far greater than those that have been formally documented. As young people remain unaware of the risk, many are walking time bombs, their heart condition unknown to them and undiagnosed, waiting to crash during physical activity.

Clinical and Laboratory Findings

Several studies provide strong evidence that the mRNA vaccines can induce myocarditis and related cardiac dysfunction. In a 2022 case study, two intern doctors developed vaccine-induced myocarditis shortly after receiving the BNT162b2 COVID-19 vaccine, both of whom were otherwise healthy and had no family history of cardiac disease (Canakci 2022). These individuals had to be hospitalized and treated, though their recovery was relatively swift. This supports the assertion that many individuals, particularly younger adults, may experience heart damage that goes unrecognised unless specifically investigated.

A 2022 study by Schreckenberg revealed that the spike protein of the mRNA vaccines is capable of entering cardiac cells, potentially causing arrhythmias and disrupting normal heart function. In laboratory settings, both the Moderna (mRNA-1273) and Pfizer-BioNTech (BNT162b2) vaccines induced irregular heart contractions, raising concerns about the long-term risks of these vaccines, especially in those with predisposing factors or who engage in intense physical activity.

Myocarditis vs. Natural Infection

Interestingly, research suggests that natural infection with SARS-CoV-2 does not seem to increase the risk of myocarditis to the same extent as the vaccine. Tuvali (2022) analysed data from over 750,000 individuals and found no significant association between COVID-19 infection and the development of myocarditis or pericarditis, further emphasizing that the vaccine—rather than the virus itself—poses a much greater risk of heart complications.

Conclusion: The Importance of Awareness and Testing

Given the severe risks posed by myocarditis, it is imperative that any individual who has received the COVID-19 vaccine, especially those who are young and active, be tested for myocarditis if they experience any chest pain or other cardiac symptoms. Early diagnosis and intervention are crucial to preventing potentially fatal outcomes. Furthermore, it is essential for healthcare providers to raise awareness of this risk, especially among fit young people who may not otherwise consider heart conditions in the event of chest discomfort.

In conclusion, the mRNA vaccine’s potential for heart damage—particularly myocarditis—should not be underestimated. It is vital that we take these risks seriously and ensure proper monitoring, diagnosis, and prevention strategies are in place to protect the health of individuals, particularly those in high-risk groups.

 

6/ Class Switch and Chronic Disease: The Role of IgG4

The immune response is a tightly regulated process involving a complex network of cells and signalling molecules. In viral infections, the immune system typically produces IgG1 and lesser amounts of IgG3 antibodies, which are effective at activating immune pathways that neutralise and clear viruses. However, under conditions of chronic antigen exposure—such as long-term infections or cancer—the body may shift toward producing IgG4 antibodies instead. This antibody class switch can profoundly alter immune function, with significant implications for long-term health.

IgG4 and Its Role in Immunity

Unlike other subclasses of IgG, IgG4 is associated with immune tolerance rather than immune activation. It is most commonly elevated in response to chronic antigenic stimulation, such as persistent infections or parasitic infestations. In these contexts, IgG4 acts to dampen immune reactions and reduce inflammation. While this may prevent immune overreaction, it also risks suppressing the body’s ability to effectively respond to genuine threats.

Elevated IgG4 levels have been linked to a range of chronic conditions. These include autoimmune diseases, cancers, and a unique condition known as IgG4-related disease (IgG4-RD)—a fibroinflammatory disorder in which IgG4-positive plasma cells infiltrate tissues, leading to chronic inflammation, fibrosis, and organ dysfunction. This disease can affect any organ system, with common manifestations including autoimmune pancreatitis, kidney inflammation, interstitial lung disease, and even neurological issues (Detlefsen 2018; Giliani 2024; Saitakis 2021; Wallace 2019). 

Vaccine-Induced IgG4 Class Switch

Recent studies have raised concerns about the impact of repeated COVID-19 mRNA vaccinations on the immune system’s antibody profile. Evidence now shows that after multiple doses, especially three or more, many individuals exhibit a marked shift toward producing IgG4 antibodies. Unlike the early vaccine response, which is dominated by pro-inflammatory IgG1 and IgG3, the late-stage response shows a dominance of non-inflammatory IgG4.

This change is not just a shift in numbers—it has functional consequences. IgG4 antibodies are far less effective at virus neutralisation and cannot efficiently mediate important immune responses like antibody-dependent cellular phagocytosis or complement activation.

  • Espino (2024) reported that after three doses of an mRNA vaccine, individuals developed high levels of IgG4 that persisted long-term and failed to neutralize the virus.
  • Irrgang (2022) similarly found that IgG4 levels rose months after the second dose and were further boosted after a third vaccination or breakthrough infection.
  • Perez (2025) linked this IgG4 class switch to an increased risk of breakthrough infections, suggesting reduced overall immunity.

These findings raise serious concerns about long-term vaccine efficacy and the possibility of immune tolerance toward SARS-CoV-2.

The Risks of IgG4 in Chronic Disease

Raised IgG4 levels are consistently associated with immune dysfunction and chronic illness. In IgG4-related disease, the antibody promotes tissue damage and scarring across multiple organs. In autoimmune disorders such as rheumatoid arthritis and systemic lupus erythematosus, elevated IgG4 may reflect a failed attempt by the body to control autoimmune inflammation—an attempt that ultimately adds to disease complexity (Sakthiswary 2021;  Naramala 2019).

Importantly, IgG4 has also been implicated in cancer. Because it promotes immune tolerance, IgG4 may enable tumour cells to escape immune surveillance. High IgG4 expression has been reported in cancers such as breast cancer, non-Hodgkin lymphoma, and others, where it is thought to assist tumour growth and spread (Hirano 2014; Takahashi 2009).

Conclusion

While IgG4 can play a regulatory role in limiting inflammation, its involvement in chronic antigen exposure and its ability to suppress immune responses pose serious threats to long-term health. The growing body of research linking IgG4 to immune exhaustion, autoimmunity, and cancer cannot be ignored—especially in light of its persistent elevation following repeated mRNA vaccination.

This antibody class switch should be regarded as a warning sign of vaccine-induced immune dysfunction with serious implications for long-term health. As the scientific community continues to explore the long-term effects of chronic antigen exposure and vaccine-driven class switching, it is vital to re-evaluate current vaccine recommendations and prioritise further investigation into the health implications of elevated IgG4.

7/ Antibody-Dependent Enhancement and COVID-19 Vaccination

Antibody-dependent enhancement (ADE) is a phenomenon in which antibodies generated during an immune response—rather than neutralising the pathogen—enhance its entry into host cells and worsen the disease. This process has long been a known risk in vaccine development for coronaviruses. In multiple preclinical studies, attempts to create SARS and MERS vaccines were abandoned because of ADE and immune-mediated pathology upon viral challenge, particularly in the lungs (Agrawai 2016; Bottazzi 2020).

One of the most compelling early warnings came from a 2012 study by Tseng which evaluated four different SARS-CoV vaccine candidates. All vaccinated animals developed lung immunopathology upon viral challenge—even in the absence of detectable virus—suggesting that the vaccines induced an aberrant immune response that made the disease worse, not better. Similarly, a 2008 study by Yasui found that immunisation with SARS-CoV nucleocapsid protein led to severe pneumonia upon viral exposure, pointing to a potential role for vaccine-induced immune priming in disease enhancement. Bolles (2011) and other animal studies further confirmed that even double-inactivated virus vaccines could provoke heightened eosinophilic inflammation in the lungs following viral exposure.

A broader pattern of vaccine-associated enhanced respiratory disease (VAERD) has been observed in both human and veterinary settings, as noted by Khurana (2013). In pigs and children vaccinated with certain respiratory virus vaccines, subsequent exposure to the wild-type virus resulted in worsened lung pathology, not protection. These findings were echoed in influenza vaccine research by Rajao (2016), reinforcing that immune priming gone awry can be a dangerous and recurring issue in respiratory vaccine development.

ADE Confirmed in Human Autopsies

The theoretical concerns raised by these preclinical studies are no longer hypothetical. Autopsy findings in humans have provided compelling evidence that COVID-19 vaccination can, in some cases, result in fatal immune dysfunction consistent with ADE or VAED.

In one well-documented case, Hansen (2021) reported on an 86-year-old man who died shortly after receiving the BNT162b2 vaccine and subsequently contracting SARS-CoV-2. Despite showing antibodies against the spike protein (indicating the vaccine "worked" as intended), he developed a systemic viral infection and died of acute respiratory and renal failure. Autopsy revealed no signs of typical COVID-19 pneumonia, but rather the widespread presence of the virus and signs of immune failure. Notably, no antibodies were found against the nucleocapsid protein—meaning his immune system had been trained to respond only to the spike, and not the full virus. The body failed to recognize and fight the infection.

This pattern was also observed at the Second Pathology Conference held in Berlin by Prof. Dr. Arne Burkhardt (2021), where 15 post-mortem examinations were presented. In 12 of the 15 cases, pathologists concluded that the vaccine was the probable cause of death. Immune cell infiltration and autoimmune-like tissue destruction were seen in multiple organs, including the heart, lungs, kidneys, ovaries, and spleen. Unusual foreign materials were also found in blood vessels, and micro-embolisms were documented. This pattern of pathology was consistent with an overactive or misdirected immune response, raising serious concerns about vaccine-induced immune dysregulation. These findings are further supported by reports from embalmers by Haviland (2024) who have observed unusual fibrinous clots in deceased individuals who had recently been vaccinated. The presence of amyloid-like material in the vessels and tissues of the deceased has raised alarm, with some embalmers documenting a notable increase in these unusual formations since the widespread administration of COVID-19 vaccines. In a survey conducted by embalmers, many reported the presence of abnormally thick, fibrous clots that appear to be linked to immune system dysfunction. These observations add to the growing body of evidence suggesting that the immune responses triggered by COVID-19 vaccines may have unforeseen consequences, including abnormal clotting and tissue damage.

These findings were further supported by a 2024 autopsy review from Hulscher, which confirmed vaccine-induced myocarditis as a cause of death. Using internal and external consistency, biological plausibility, and the Bradford Hill criteria, the authors concluded that there was a high likelihood of a causal link between mRNA vaccination and sudden cardiac death.

 

 

Real-World Evidence of Immune Misdirection

Taken together, these autopsy findings provide strong real-world evidence that vaccine-induced immune responses may not always align with the demands of natural infection. A critical takeaway is the potential mismatch between vaccine-generated immunity and the body's need to mount a broad, multi-epitope defence against the wild virus. This mismatch—a hallmark of both ADE and VAED—may lead to inadequate neutralisation, increased viral replication, and immune-mediated tissue damage upon next exposure to SARS-CoV-2.

The consistent pattern of lymphocytic infiltration, organ damage, and fatal outcomes seen in autopsy cases echoes what was seen in earlier animal studies. Far from being a theoretical risk, ADE in the context of COVID-19 vaccination has been observed, documented, and pathologically confirmed in humans.

 

Conclusion

The mRNA COVID-19 vaccines were launched as a solution, but growing scientific evidence suggests they are often a source of long-term harm. The risks documented throughout this article are not speculative — they are supported by peer-reviewed research, autopsy findings, and biological plausibility grounded in immunology and molecular biology.

The pathogenicity of the spike protein, its prolonged presence in the body, and its potential integration into the host genome raise alarm bells that cannot be ignored. When combined with the class switch to IgG4, the data suggest a vaccine-induced environment of immune exhaustion and tolerance, where the body becomes less able to clear infections, suppresses inflammation too early, and may fail to prevent or detect cancer and promote autoimmunity.

Cardiovascular injury — particularly myocarditis in young men — is no longer rare, but rather systemically underreported and underdiagnosed. Prion-like neurodegeneration and antibody-dependent enhancement are no longer theoretical — they are occurring, documented in case reports, and seen in pathology.

These findings demand urgent attention. To continue vaccination campaigns without addressing these risks is not just negligent — it is dangerous. Science must not be silenced, and medicine must return to its core ethic: first, do no harm.

The precautionary principle must now take precedence. Until these mechanisms are fully understood and independently investigated, further use of these products should be suspended. Only through transparent inquiry, honest risk-benefit reassessment, and the protection of informed consent can trust in medicine be restored — and lives be safeguarded.

 

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Gilani, S.I., Buglioni, A. and Cornell, L.D., 2024, March. IgG4-related kidney disease: clinicopathologic features, differential diagnosis, and mimics. In Seminars in Diagnostic Pathology(Vol. 41, No. 2, pp. 88-94). WB Saunders. https://pubmed.ncbi.nlm.nih.gov/38246802/

Halma, M.T.J., Plothe, C., Marik, P., Lawrie, T.A., 2023. Strategies for the management of spike protein-related pathology. Microorganisms, 11(5), p.1308. https://doi.org/10.3390/microorganisms11051308

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Haviland 2024 WORLDWIDE EMBALMER BLOOD CLOT SURVEY (United States, Canada, United Kingdom, Australia) (Conducted 11 Nov – 14 Dec 2024) https://www.howbadismybatch.com/amyloidsurvey.pdf

Hirano, K., Tada, M., Sasahira, N., Isayama, H., Mizuno, S., Takagi, K., Watanabe, T., Saito, T., Kawahata, S., Uchino, R. and Hamada, T., 2014. Incidence of malignancies in patients with IgG4-related disease. Internal medicine (Tokyo, Japan), 53(3), pp.171-176. https://pubmed.ncbi.nlm.nih.gov/24492683/

Heidecker, B., 2022. Myocarditis following COVID-19 vaccination. European Heart Journal – Cardiovascular Pharmacotherapy, 8(9), pp.805–807. https://pubmed.ncbi.nlm.nih.gov/36065751/

Hulscher, F., 2024. Clinical approach to post-acute sequelae after COVID-19 infection and vaccination. Cureus, 16(1), e54736. https://pubmed.ncbi.nlm.nih.gov/37626783/

Hulscher, N., Hodkinson, R., Makis, W. and McCullough, P.A., Autopsy findings in cases of fatal COVID-19 vaccine-induced myocarditis. ESC Heart Fail. 2024. https://pubmed.ncbi.nlm.nih.gov/38221509/

Irrgang, P., Gerling, J., Kocher, K., Lapuente, D., Steininger, P., Habenicht, K., Wytopil, M., Beileke, S., Schäfer, S., Zhong, J. and Ssebyatika, G., 2022. Class switch toward noninflammatory, spike-specific IgG4 antibodies after repeated SARS-CoV-2 mRNA vaccination. Science immunology, 8(79), p.eade2798. https://pmc.ncbi.nlm.nih.gov/articles/PMC9847566/

Kalkeri, R., Zhu, M., Cloney-Clark, S., Plested, J.S., Parekh, A., Gorinson, D., Cai, R., Mahato, S., Ramanathan, P., Aurelia, L.C. and Selva, K.J., 2024. Altered IgG4 antibody response to repeated mRNA versus recombinant protein SARS-CoV-2 vaccines. The Journal of infection, 88(3), p.106119. https://pubmed.ncbi.nlm.nih.gov/38360356/

Kammerer, T., Fiechtner, B., et al., 2024. Plasmid DNA impurities in mRNA COVID-19 vaccines. Science, Public Health Policy & the Law, 5, pp.1-24. https://publichealthpolicyjournal.com/wp-content/uploads/2025/02/KammererEtAl_SciencePublicHealthPolicyAndTheLaw_v5.2019-2024.Dec_2024.pdf

Khurana, S., Loving, C.L., Manischewitz, J., King, L.R., Gauger, P.C., Henningson, J., Vincent, A.L. and Golding, H., 2013. Vaccine-induced anti-HA2 antibodies promote virus fusion and enhance influenza virus respiratory disease. Science translational medicine, 5(200), p.200ra114. https://pubmed.ncbi.nlm.nih.gov/23986398/

Kowarz, E., Krutzke, L., Reis, J. and Marschalek, R., 2022. Vaccine-induced COVID-19 mimicry syndrome. Signal Transduction and Targeted Therapy, 7(1), pp.1–3. https://pubmed.ncbi.nlm.nih.gov/35084333/

Lataster, M., 2024. Should we now discuss possible COVID-19 vaccine negative effectiveness? Australian Journal of General Practice, April 2024. https://www1.racgp.org.au/getattachment/abf6c70e-c2db-4035-8cf2-a60e3ae8d2c6/Letters.aspx

Lei, Y., Zhang, J., Schiavon, C.R., He, M., Chen, L., Shen, H., Zhang, Y., Yin, Q., Cho, S.Y., Ballinger, M.N. and Liu, Y., 2021. SARS-CoV-2 spike protein impairs endothelial function via downregulation of ACE2. Circulation Research, 128(9), pp.1323-1326. https://pubmed.ncbi.nlm.nih.gov/33300001/

MacKenzie KL, Franco S, Naiyer AJ, May C, Sadelain M, Rafii S, Moore MA. Multiple stages of malignant transformation of human endothelial cells modelled by co-expression of telomerase reverse transcriptase, SV40 T antigen and oncogenic N-ras. Oncogene. 2002 Jun 20;21(27):4200-11 https://pubmed.ncbi.nlm.nih.gov/12082607/

Makhoul, K., Beeber, T., Cordero, R., Khan, A. and Saliaj, M., 2023. Prion Disease After COVID-19: A Case Report. The American Journal of Case Reports, 24, pp.e940564-1. https://pmc.ncbi.nlm.nih.gov/articles/PMC10519638/

Marchese, A., Lapuente, D., et al., 2024. Mechanisms and implications of IgG4 responses to SARS-CoV-2 and other repeatedly administered vaccines. Nature Reviews Immunology, 24, pp.122–132. https://pubmed.ncbi.nlm.nih.gov/39419185/

Naramala, S., Biswas, S., Adapa, S., Gayam, V., Konala, V.M. and Bose, S., 2019. An Overlapping Case of IgG4-Related Disease and Systemic Lupus Erythematosus. Journal of Investigative Medicine High Impact Case Reports, 7, p.2324709619862297. https://pmc.ncbi.nlm.nih.gov/articles/PMC6643167/

Noutsopoulos D, Vartholomatos G, Kolaitis N, Tzavaras T. SV40 large T antigen up-regulates the retrotransposition frequency of viral-like 30 elements. J Mol Biol. 2006 Aug 18;361(3):450-61. https://pubmed.ncbi.nlm.nih.gov/16859708/

Ota, N., Itani, M., Aoki, T., Sakurai, A., Fujisawa, T., Okada, Y., Noda, K., Arakawa, Y., Tokuda, S. and Tanikawa, R., 2025. Expression of SARS-CoV-2 spike protein in cerebral Arteries: Implications for hemorrhagic stroke Post-mRNA vaccination. Journal of Clinical Neuroscience, 136, p.111223. https://pubmed.ncbi.nlm.nih.gov/40184822/

Parry PI, Lefringhausen A, Turni C, Neil CJ, Cosford R, Hudson NJ, Gillespie J. 'Spikeopathy': COVID-19 Spike Protein Is Pathogenic, from Both Virus and Vaccine mRNA. Biomedicines. 2023 Aug 17;11(8):2287. https://pubmed.ncbi.nlm.nih.gov/37626783/

Perez, J.C., Moret-Chalmin, C. and Montagnier, L., 2023. Emergence of a new Creutzfeldt-Jakob disease: 26 cases of the human version of mad-cow disease, days after a COVID-19 injection. International Journal of Vaccine Theory, Practice, and Research, 3(1), pp.727–770. https://www.ijvtpr.com/index.php/IJVTPR/article/view/66

Perez, J.C., 2025. Post-vaccination IgG4 and IgG2 class switch associates with increased risk of SARS-CoV-2 infections. Clinical and Translational Immunology, 14(1), p.73. https://pubmed.ncbi.nlm.nih.gov/40113142/

Perico L, Morigi M, Galbusera M, Pezzotta A, Gastoldi S, Imberti B, Perna A, Ruggenenti P, Donadelli R, Benigni A, Remuzzi G. SARS-CoV-2 Spike Protein 1 Activates Microvascular Endothelial Cells and Complement System Leading to Platelet Aggregation. Front Immunol. 2022 Mar 7;13:827146. https://pubmed.ncbi.nlm.nih.gov/35320941/

Patterson, B.K., Yogendra, R., et al., 2024. Persistence of S1 spike protein in CD16+ monocytes up to 245 days in SARS-CoV-2 negative post COVID-19 vaccination individuals. medRxiv, 2024-03. https://europepmc.org/article/ppr/ppr826769

Rajão, D.S., Chen, H., Perez, D.R., Sandbulte, M.R., Gauger, P.C., Loving, C.L., Shanks, G.D. and Vincent, A., 2016. Vaccine-associated enhanced respiratory disease is influenced by haemagglutinin and neuraminidase in whole inactivated influenza virus vaccines. The Journal of general virology, 97(7), pp.1489-1499. https://pubmed.ncbi.nlm.nih.gov/27031847/

Robles JP, Zamora M, Adan-Castro E, Siqueiros-Marquez L, Martinez de la Escalera G, Clapp C. The spike protein of SARS-CoV-2 induces endothelial inflammation through integrin α5β1 and NF-κB signaling. J Biol Chem. 2022 Mar;298(3):101695. https://pubmed.ncbi.nlm.nih.gov/35143839/

Rong, Z., Mai, H., Ebert, G., Kapoor, S., Puelles, V.G., Czogalla, J., Hu, S., Su, J., Prtvar, D., Singh, I. and Schädler, J., 2024. Persistence of spike protein at the skull-meninges-brain axis may contribute to the neurological sequelae of COVID-19. Cell host & microbe, 32(12), pp.2112-2130. https://pubmed.ncbi.nlm.nih.gov/39615487/

Saitakis, G. and Chwalisz, B.K., 2021. The neurology of IGG4-related disease. Journal of the Neurological Sciences, 424, p.117420. https://pubmed.ncbi.nlm.nih.gov/33845982/

Sakthiswary, R., Shaharir, S.S. and Wahab, A.A., 2022. Frequency and Clinical Significance of Elevated IgG4 in Rheumatoid Arthritis: A Systematic Review. Biomedicines, 10(3), p.558. https://pubmed.ncbi.nlm.nih.gov/35327360/

Sano, H., Kase, M., Aoyama, Y. and Sano, S., 2023. A case of persistent, confluent maculopapular erythema following a COVID‐19 mRNA vaccination is possibly associated with the intralesional spike protein expressed by vascular endothelial cells and eccrine glands in the deep dermis. The Journal of Dermatology, 50(9), pp.1208-1212. https://pubmed.ncbi.nlm.nih.gov/37154426/

Seneff, S., Kyriakopoulos, A.M., Nigh, G. and Mccullough, P.A., 2022. SARS-CoV-2 spike protein in the pathogenesis of prion-like diseases. Authorea Preprints. https://www.authorea.com/doi/full/10.22541/au.166069342.27133443

Seneff, S., Kyriakopoulos, A.M., Nigh, G., McCullough, P.A. and Kyriakopoulos, A., 2023. A potential role of the spike protein in neurodegenerative diseases: a narrative review. Cureus, 15(2). https://pmc.ncbi.nlm.nih.gov/articles/PMC9922164/

Schreckenberg, R., Woitasky, N., Itani, N., Czech, L., Ferdinandy, P. and Schulz, R., 2024. Cardiac side effects of RNA‐based SARS‐CoV‐2 vaccines: hidden cardiotoxic effects of mRNA‐1273 and BNT162b2 on ventricular myocyte function and structure. British Journal of Pharmacology, 181(3), pp.345-361. https://pubmed.ncbi.nlm.nih.gov/37828636/

Speicher, A., et al., 2023. DNA fragments detected in monovalent and bivalent mRNA COVID-19 vaccines: exploratory dose response relationship. OSF Preprints. https://osf.io/preprints/osf/mjc97

Takada, K., Taguchi, K., Samura, M., Igarashi, Y., Okamoto, Y., Enoki, Y., Tanikawa, K. and Matsumoto, K., 2025. SARS-CoV-2 mRNA vaccine-related myocarditis and pericarditis: An analysis of the Japanese Adverse Drug Event Report database. Journal of Infection and Chemotherapy, 31(1), p.102485. https://pubmed.ncbi.nlm.nih.gov/39103148/

Takahashi, N., Ghazale, A.H., Smyrk, T.C., Mandrekar, J.N. and Chari, S.T., 2009. Possible association between IgG4-associated systemic disease with or without autoimmune pancreatitis and non-Hodgkin lymphoma. Pancreas, 38(5), pp.523-526. https://pubmed.ncbi.nlm.nih.gov/19258916/

Tetz G, Tetz V. Prion-like Domains in Spike Protein of SARS-CoV-2 Differ across Its Variants and Enable Changes in Affinity to ACE2. Microorganisms. 2022 Jan 25;10(2):280. doi: 10.3390/microorganisms10020280.  https://pubmed.ncbi.nlm.nih.gov/35208734/

Truong DT, Dionne A, Muniz JC, McHugh KE, Portman MA, Lambert LM, Thacker D, Elias MD, Li JS, Toro-Salazar OH, Anderson BR, Atz AM, Bohun CM, Campbell MJ, Chrisant M, D'Addese L, Dummer KB, Forsha D, Frank LH, Frosch OH, Gelehrter SK, Giglia TM, Hebson C, Jain SS, Johnston P, Krishnan A, Lombardi KC, McCrindle BW, Mitchell EC, Miyata K, Mizzi T, Parker RM, Patel JK, Ronai C, Sabati AA, Schauer J, Sexson Tejtel SK, Shea JR, Shekerdemian LS, Srivastava S, Votava-Smith JK, White S, Newburger JW. Clinically Suspected Myocarditis Temporally Related to COVID-19 Vaccination in Adolescents and Young Adults: Suspected Myocarditis After COVID-19 Vaccination. Circulation. 2022 Feb;145(5):345-356. https://pubmed.ncbi.nlm.nih.gov/34865500/

Tseng, C.T., Sbrana, E., Iwata-Yoshikawa, N., Newman, P.C., Garron, T., Atmar, R.L., Peters, C.J. and Couch, R.B., 2012. Immunization with SARS coronavirus vaccines leads to pulmonary immunopathology on challenge with the SARS virus. PloS one, 7(4), p.e35421. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0035421&f

Tuvali, O., Tshori, S., Derazne, E., Hannuna, R.R., Afek, A., Haberman, D., Sella, G. and George, J., 2022. The incidence of myocarditis and pericarditis in post COVID-19 unvaccinated patients—a large population-based study. Journal of clinical medicine, 11(8), p.2219. https://pubmed.ncbi.nlm.nih.gov/35456309/

Tzavaras T, Eftaxia S, Tavoulari S, Hatzi P, Angelidis C. Factors influencing the expression of endogenous reverse transcriptases and viral-like 30 elements in mouse NIH3T3 cells. Int J Oncol. 2003 Oct;23(4):1237-43. https://pubmed.ncbi.nlm.nih.gov/12964010/

Villacampa, A., Alfaro, E., Morales, C., Díaz-García, E., López-Fernández, C., Bartha, J.L., López-Sánchez, F., Lorenzo, Ó., Moncada, S., Sánchez-Ferrer, C.F. and García-Río, F., 2024. SARS-CoV-2 S protein activates NLRP3 inflammasome and deregulates coagulation factors in endothelial and immune cells. Cell Communication and Signaling, 22(1), p.38. https://pubmed.ncbi.nlm.nih.gov/38225643/

Wallace, Z.S., Perugino, C., Matza, M., Deshpande, V., Sharma, A. and Stone, J.H., 2019. IgG4-related disease. Clinics in chest medicine, 40(3), p.583. https://pmc.ncbi.nlm.nih.gov/articles/PMC7133392/

Yamamoto, M., et al., 2023. Persistent varicella zoster virus infection after COVID-19 vaccination linked to spike protein in skin lesions. Journal of Cutaneous Immunology and Allergy, 6(1), pp.18-23.https://pmc.ncbi.nlm.nih.gov/articles/PMC9537775/

Yasui, F., Kai, C., Kitabatake, M., Inoue, S., Yoneda, M., Yokochi, S., Kase, R., Sekiguchi, S., Morita, K., Hishima, T. and Suzuki, H., 2008. Prior immunization with severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV) nucleocapsid protein causes severe pneumonia in mice infected with SARS-CoV. Journal of immunology (Baltimore, Md.: 1950), 181(9), pp.6337-6348. https://pubmed.ncbi.nlm.nih.gov/18941225/

Yonker, L.M., Swank, Z., et al., 2023. Circulating spike protein detected in post–COVID-19 mRNA vaccine myocarditis. Circulation, 147(11), pp.867-876. https://pubmed.ncbi.nlm.nih.gov/36597886/

Zhao, Y., Jaber, V.R. and Lukiw, W.J., 2022. SARS-CoV-2, long COVID, prion disease and neurodegeneration. Frontiers in Neuroscience, 16, p.1002770. https://pubmed.ncbi.nlm.nih.gov/36238082/

2. Further Reading

Akiyama, M., Yasuoka, H., Yamaoka, K., Suzuki, K., Kaneko, Y., Kondo, H., Kassai, Y., Koga, K., Miyazaki, T., Morita, R. and Yoshimura, A., 2016. Enhanced IgG4 production by follicular helper 2 T cells and the involvement of follicular helper 1 T cells in the pathogenesis of IgG4-related disease. Arthritis Research & Therapy, 18, pp.1-14.348. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4944254/

Bhattacharjee, B., Lu, P., Monteiro, V.S., Tabachnikova, A., Wang, K., Hooper, W.B., Bastos, V., Greene, K., Sawano, M., Guirgis, C. and Tzeng, T.J., 2025. Immunological and Antigenic Signatures Associated with Chronic Illnesses after COVID-19 Vaccination. medRxiv, pp.2025-02.

Cardozo, T. and Veazey, R., 2021. Informed consent disclosure to vaccine trial subjects of risk of COVID-19 vaccines worsening clinical disease. International Journal of Clinical Practice, 75(3), e13795. https://onlinelibrary.wiley.com/doi/full/10.1111/ijcp.13795

Freiberger, S. N., M. Zehnder, G. Gafvelin, H. Grönlund, T. M. Kündig, and P. Johansen. "IgG4 but no IgG1 antibody production after intralymphatic immunotherapy with recombinant MAT-Feld1 in human." Allergy 71, no. 9 (2016): 1366-1370. https://pubmed.ncbi.nlm.nih.gov/27253988/

Gelderloos, A., et al., 2024. Repeated COVID-19 mRNA vaccination increases IgG4/IgG1 ratio in older adults. Vaccine, 42(15), pp.2204–2215. https://pubmed.ncbi.nlm.nih.gov/39272189/

Heeringa, J.J., Karim, A.F., van Laar, J.A., Verdijk, R.M., Paridaens, D., van Hagen, P.M. and van Zelm, M.C., 2018. Expansion of blood IgG4+ B, TH2, and regulatory T cells in patients with IgG4-related disease. The Journal of allergy and clinical immunology, 141(5), pp.1831-1843. https://pubmed.ncbi.nlm.nih.gov/28830675/

Kalkeri, R., et al., 2024. Altered IgG4 antibody response to repeated mRNA versus recombinant protein SARS-CoV-2 vaccines. Vaccine, 42(3), pp.392–400.

Karabudak, S., et al., 2023. A Case Report of Creutzfeldt-Jakob Disease after mRNA COVID-19 Vaccine. Annals of Clinical Case Reports, 8, p.2408.

Kiszel, P.S., et al., 2023. Class switch towards spike protein-specific IgG4 antibodies after SARS-CoV-2 mRNA vaccination depends on prior infection history. Frontiers in Immunology, 14, p.1214596. https://pubmed.ncbi.nlm.nih.gov/37574522/

Klimek, L., et al., 2021. Safety of COVID-19 vaccines in patients with allergies. Allergy, 76(4), pp.1061–1064.

Koneczny, I., 2018. A new classification system for IgG4 autoantibodies. Frontiers in Immunology, 9, p.97. https://pubmed.ncbi.nlm.nih.gov/29483905/

Liu, L., et al., 2021. IgG4-related autoimmune diseases and beyond. International Journal of Molecular Sciences, 22(17), p.9362.

Liu, J., Yin, W., Westerberg, L.S., Lee, P., Gong, Q., Chen, Y., Dong, L. and Liu, C., 2021. Immune Dysregulation in IgG4-Related Disease. Frontiers in Immunology, 12, p.738540. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8440903/

Mevorach, D., et al., 2021. Myocarditis after BNT162b2 mRNA vaccine against Covid-19 in Israel. New England Journal of Medicine, 385(23), pp.2140–2149.

Menezes, F., et al., 2024. Unraveling the SARS-CoV-2 spike protein long-term effect on neuro-PASC. Frontiers in Cellular Neuroscience, 18, p.1481963.

Ohyama, K., Koike, H., Iijima, M., Hashimoto, R., Tomita, M., Kawagashira, Y., Satou, A., Nakamura, S. and Sobue, G., 2013. IgG4-related neuropathy: a case report. JAMA neurology, 70(4), pp.502-505. https://pubmed.ncbi.nlm.nih.gov/23440288/

Perez, J.C., Moret-Chalmin, C. and Montagnier, L., 2022. Towards the emergence of a new form of the neurodegenerative Creutzfeldt-Jakob disease. ScienceOpen.

Regev, K., Nussbaum, T., Cagnano, E., Giladi, N. and Karni, A., 2014. Central nervous system manifestation of IgG4-related disease. JAMA neurology, 71(6), pp.767-770.

Seneff, S., et al., 2023. A potential role of the spike protein in neurodegenerative diseases: A narrative review. Cureus, 15(2).

Tonnerre, P., Wolski, D., Subudhi, S., Al-Jabban, J., Hoogeveen, R.C., Damasio, M., Drescher, H.K., Bartsch, L.M., Tully, D.C., Sen, D.R. and Bean, D.J., 2021. Differentiation of exhausted CD8 T cells after termination of chronic antigen stimulation stops short of achieving functional T cell memory. Nature immunology, 22(8), p.1030. https://pmc.ncbi.nlm.nih.gov/articles/PMC8323980/

Topchyan, H., et al., 2023. The role of CD4 T cell help in CD8 T cell differentiation and function. Nature Reviews Immunology, 23(1), pp.43–59. https://pubmed.ncbi.nlm.nih.gov/37970230/

Utzschneider, D.T., et al., 2020. Early precursor T cells establish and propagate T cell exhaustion. Nature Immunology, 21(10), pp.1256–1266.

Uversky, V.N., Redwan, E.M., Makis, W. and Rubio-Casillas, A., 2023. IgG4 Antibodies Induced by Repeated Vaccination May Generate Immune Tolerance to the SARS-CoV-2 Spike Protein. Vaccines, 11(5), p.991. https://pmc.ncbi.nlm.nih.gov/articles/PMC10222767/

 

 

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