VACUNAS SARS-COV-2 Y ENFERMEDADES NEURODEGENERATIVAS por Stephanie Seneff
Nuestro artículo mostró que existen varios mecanismos por los cuales estas vacunas podrían conducir a una enfermedad grave., incluidas enfermedades autoinmunes, enfermedades neurodegenerativas...
VACUNAS SARS-COV-2 Y ENFERMEDADES NEURODEGENERATIVAS
por Stephanie Seneff
Desde diciembre de 2020, cuando varias vacunas novedosas sin precedentes contra el SARS-CoV-2 comenzaron a aprobarse para uso de emergencia, ha habido un esfuerzo mundial para llevar estas vacunas a los brazos de tantas personas como sea posible lo más rápido posible. Estas vacunas se han desarrollado “a la velocidad de la luz”, dada la urgencia de la situación con la pandemia de COVID-19. La mayoría de los gobiernos han adoptado la idea de que estas vacunas son el único camino hacia la resolución de esta pandemia, que está paralizando las economías de muchos países.
Hasta el momento, hay cuatro vacunas diferentes que han sido aprobadas para uso de emergencia para protección contra COVID-19 en los EE. UU. y/o Europa. Dos (la vacuna Moderna y la vacuna Pfizer/BioNTech) se basan en tecnología de ARNm, mientras que las otras dos (producidas por Johnson & Johnson y AstraZeneca) se basan en un vector viral recombinante de ADN de doble cadena. Las vacunas de ARNm contienen solo el código para la proteína de punta de la envoltura del SARS-CoV-2, mientras que las vacunas basadas en ADN contienen un vector viral de adenovirus que se ha aumentado con ADN que codifica la proteína de punta del SARS-CoV-2. Las vacunas basadas en ADN tienen una cierta ventaja sobre las vacunas basadas en ARN en el sentido de que no tienen que almacenarse a temperaturas de congelación profunda, porque el ADN de doble cadena es mucho más estable que el ARN de cadena sencilla.
En este sentido, la vacuna de AstraZeneca (AZ) tiene una ligera ventaja sobre la vacuna de Johnson & Johnson (J&J) porque el virus normalmente infecta a los chimpancés en lugar de a los humanos, por lo que es probable que menos personas hayan estado expuestas [1, 2]. Por otro lado, varios estudios han demostrado que los virus que normalmente infectan a una especie pueden causar tumores si se inyectan en una especie diferente. Por ejemplo, un adenovirus humano inyectado en babuinos causó retinoblastoma (cáncer de ojo) en los babuinos [3]. Por lo tanto, no se puede descartar que la vacuna AZ pueda provocar cáncer.
La gente no se da cuenta de que estas vacunas son muy diferentes de las muchas vacunas infantiles que ahora estamos acostumbrados a recibir a una edad temprana. Me parece impactante que los desarrolladores de vacunas y los funcionarios gubernamentales de todo el mundo estén promoviendo imprudentemente estas vacunas en una población desprevenida. Junto con el Dr. Greg Nigh, recientemente publiqué un artículo revisado por pares sobre la tecnología detrás de las vacunas de ARNm y las muchas consecuencias potencialmente desconocidas para la salud .[4]. Estas vacunas sin precedentes normalmente tardan doce años en desarrollarse, con una tasa de éxito de solo el 2%, pero estas vacunas se desarrollaron y lanzaron al mercado en menos de un año. Como consecuencia, no tenemos conocimiento directo de los efectos que las vacunas puedan tener sobre nuestra salud a largo plazo. Sin embargo, el conocimiento sobre cómo funcionan estas vacunas, cómo funciona el sistema inmunitario y cómo se producen las enfermedades neurodegenerativas puede influir en el problema para predecir las posibles consecuencias devastadoras futuras de las vacunas.
El ARNm de estas vacunas codifica la proteína espiga que normalmente sintetiza el virus SARS-CoV-2. Sin embargo, tanto el ARNm como la proteína que produce se han cambiado de la versión original en el virus con la intención de aumentar la tasa de producción de la proteína en una célula infectada y la durabilidad tanto del ARNm como de la proteína de pico que codifica. Los ingredientes adicionales como los lípidos catiónicos y el polietilenglicol también son tóxicos con consecuencias desconocidas. Las vacunas fueron aprobadas para uso de emergencia sobre la base de estudios sumamente inadecuados para evaluar la seguridad y la eficacia.
Nuestro artículo mostró que existen varios mecanismos por los cuales estas vacunas podrían conducir a una enfermedad grave., incluidas enfermedades autoinmunes, enfermedades neurodegenerativas, trastornos vasculares (hemorragia y coágulos de sangre) y posiblemente problemas reproductivos. También existe el riesgo de que las vacunas aceleren la aparición de nuevas cepas del virus que ya no sean sensibles a los anticuerpos producidos por las vacunas. Cuando las personas están inmunocomprometidas (p. ej., reciben quimioterapia para el cáncer), es posible que los anticuerpos que producen no puedan controlar el virus porque el sistema inmunológico está demasiado deteriorado. Al igual que en el caso de la resistencia a los antibióticos, nuevas cepas evolucionan dentro del cuerpo de una persona inmunocomprometida infectada que produce una versión de la proteína espiga que ya no se une a los anticuerpos adquiridos. Estas nuevas cepas dominan rápidamente a la cepa original, especialmente cuando la población general está fuertemente vacunada con una vacuna que es específica de la cepa original. Es probable que este problema requiera el lanzamiento repetido de nuevas versiones de la vacuna a intervalos periódicos que las personas deberán recibir para inducir otra ronda de producción de anticuerpos en un juego interminable del gato y el ratón.
Al igual que las vacunas de ARNm, las vacunas de ADN se basan en técnicas novedosas de edición de genes de biotecnología que son completamente nuevas, por lo que también son un experimento masivo desatado en una gran población desprevenida, con consecuencias desconocidas. Ambas vacunas de vector de ADN se han asociado con una condición muy rara llamada trombocitopenia, en la que el recuento de plaquetas cae precipitadamente, lo que da como resultado coágulos de sangre en todo el sistema y un alto riesgo de hemorragia cerebral [5]. Esto probablemente se deba a una reacción autoinmune a las plaquetas y conlleva un alto riesgo de mortalidad. En el caso de la vacuna AZ, esto ha provocado que más de 20 países europeos suspendan temporalmente sus programas de vacunación [6]. Y Estados Unidos ordenó una suspensión temporal de la vacuna J&J.
Incluso los expertos no entienden realmente el mecanismo a partir de ahora, aunque una teoría fascinante para explicar esto depende del hecho de que las vacunas de vectores de ADN requieren que el ADN se copie en ARN en el núcleo, y esto presenta la posibilidad de producir una copia incompleta. , generado mediante “variantes de empalme”, al que le falta el código para adherirse a la membrana [7]. Estas secuencias parciales solubles se desplazan a otras partes del cuerpo y se unen a los receptores ACE2 en toda la vasculatura. Los anticuerpos contra estos fragmentos de pico parciales unidos a ACE2 provocan una respuesta inflamatoria aguda que da como resultado una coagulación intravascular diseminada (CID).
Cómo hacer una vacuna de vector de ADN de adenovirus
Las vacunas de adenovirus se crean a través de técnicas que el ciudadano medio no puede imaginar que puedan existir. Para la vacuna AZ, la mayor parte del ADN en la vacuna codifica las diversas proteínas que necesita una cepa de adenovirus que infecta principalmente a los chimpancés y causa síntomas similares a los del resfriado [1]. Sin embargo, no es una versión “normal” de este virus del resfriado. En primer lugar, se le ha despojado de ciertos genes que necesita para poder replicarse, y por esta razón se lo denomina “vector de adenovirus”. Este defecto, se argumenta, evita que infecte realmente al paciente vacunado. En segundo lugar, se modifica, a través de técnicas de edición de genes, para crear una versión recombinante del virus que contiene la secuencia de codificación completa para la proteína del pico del SARS-CoV-2, empalmado en su secuencia de ADN, la misma proteína que codifican las vacunas de ARN. El ADN recombinante es una secuencia de ADN lineal de doble cadena donde las proteínas de dos especies diferentes se integran a través de la edición de genes.
Dado que este virus no puede proliferar, es difícil fabricarlo en grandes cantidades. Pero resolvieron este problema haciendo uso de una versión genéticamente modificada de una línea celular humana, llamada células HEK (riñón embrionario humano) 293, donde el ADN de la célula humana fue transfectado hace mucho tiempo con fragmentos del genoma de un adenovirus, proporcionando convenientemente la virus recombinante defectuoso con las proteínas faltantes que necesita para poder proliferar [8]. Dentro de un cultivo de estas células HEK 293, el virus puede replicarse, con la ayuda de las proteínas que producen las células huésped. Las células HEK 293 provenían originalmente de un riñón de un feto abortado, y se mantiene en cultivo desde la década de 1970, porque fue modificada para volverse inmortal, con la ayuda del adenovirus. Aunque se obtuvo de un riñón, no es una célula renal. De hecho, tiene muchas propiedades que son propias de una célula madre neuronal [9]. El hecho es que en realidad no saben qué tipo de célula es. La capacidad de una línea celular para sobrevivir indefinidamente es una característica de las células tumorales. Aunque la vacuna se “purifica” durante el procesamiento, no hay garantía de que no esté contaminada con restos de las células huésped, es decir, ADN humano de una línea de células tumorales neuronales. No parece una buena idea inyectar el ADN de una célula tumoral humana a nadie. no hay garantía de que no esté contaminado con restos de las células huésped, es decir, ADN humano de una línea de células tumorales neuronales. No parece una buena idea inyectar el ADN de una célula tumoral humana a nadie. no hay garantía de que no esté contaminado con restos de las células huésped, es decir, ADN humano de una línea de células tumorales neuronales. No parece una buena idea inyectar el ADN de una célula tumoral humana a nadie.
La vacuna J&J tiene un proceso de fabricación muy similar, excepto que tiene una cepa de adenovirus diferente y una célula huésped humana diferente. Para J&J, la célula huésped es otra línea celular fetal recolectada hace mucho tiempo y que se hizo inmortal mediante la incorporación de genes de adenovirus en el genoma humano huésped. Esta línea celular se tomó de la retina del ojo del feto.
La proteína Spike es tóxica
Todas las vacunas contra la COVID-19 se basan en el suministro de código genético para producir la proteína espiga que es el componente principal de la caja de proteínas del SARS-CoV-2 que encierra su contenido de ARN. Tanto el vector de ADN como las vacunas de ARN inducen a la célula infectada por la vacuna a fabricar muchas copias de la proteína espiga según el código. A través de la experimentación, los investigadores han determinado que la proteína espiga es tóxica incluso cuando se introduce sola. En un experimento revelador, los investigadores inyectaron proteína espiga en hámsteres y descubrieron que las células endoteliales que recubren los vasos sanguíneos la absorbían a través de los receptores ACE2 [10]. Esto provocó una regulación a la baja de ACE2, que tuvo efectos significativos en la política metabólica de las células. En particular, inhibió la síntesis de mitocondrias y provocó que las mitocondrias existentes se fragmentaran. Las mitocondrias son los orgánulos de la célula que producen grandes cantidades de ATP (la moneda energética de las células) al oxidar los nutrientes, mientras consumen oxígeno y producen agua y dióxido de carbono. La proteína espiga redujo la producción de ATP por parte de las mitocondrias y aumentó la glucólisis, la forma alternativa, mucho menos eficiente, de producir ATP sin usar oxígeno. Este cambio metabólico hacia la obtención de energía a través de la glucólisis es un rasgo característico de las células cancerosas y de las neuronas en enfermedades neurodegenerativas como el Alzheimer. manera de producir ATP sin usar oxígeno. Este cambio metabólico hacia la obtención de energía a través de la glucólisis es un rasgo característico de las células cancerosas y de las neuronas en enfermedades neurodegenerativas como el Alzheimer. manera de producir ATP sin usar oxígeno. Este cambio metabólico hacia la obtención de energía a través de la glucólisis es un rasgo característico de las células cancerosas y de las neuronas en enfermedades neurodegenerativas como el Alzheimer.
En otro experimento, los investigadores demostraron que la proteína espiga puede atravesar la barrera hematoencefálica en ratones y ser captada por las neuronas de todo el cerebro [11]. Es probable que esto también esté mediado por los receptores ACE2 (que también producen las neuronas). Estos mismos investigadores también demostraron que la proteína de punta administrada en la nariz podía llegar al cerebro viajando a lo largo del nervio olfativo. Cuando indujeron la inflamación en el cerebro a través de la exposición al lipopolisacárido (LPS), observaron un aumento en la absorción de la proteína de punta en el cerebro, que según la hipótesis fue causada por una mayor fuga en la barrera. Como verá, estos puntos se vuelven importantes cuando luego consideramos lo que sucede después de una vacuna contra el SARS-CoV-2, que está diseñada para inducir inflamación.
Many people suffering from COVID-19 have experienced symptoms characteristic of the central nervous system such as headache, nausea, dizziness, fatal brain blood clots and encephalitis. In an advanced 3D microfluid model of the human BBB, researchers in the United States showed that the spike protein by itself disrupts the blood brain barrier by inducing an inflammatory state, and they proposed that this could be the source of such symptoms [12].
A published preprint found widespread expression of ACE2 in many parts of the brain. ACE2 was expressed in astrocytes, pericytes (cells that wrap around the endothelial cells lining capillary walls) and in endothelial cells — and all of these are key components of the blood-brain barrier [13]. Perhaps of even greater concern is that ACE2 was highly expressed in the substantia nigra, a brain-stem nucleus where damaged dopaminergic neurons lead to Parkinson’s disease.
Bell’s Palsy, Autism and Parkinson’s Disease
In a paper aptly titled, “Is COVID-19 a Perfect Storm for Parkinson’s Disease?” researchers made a strong case for the possibility that we will see an increase in Parkinson’s disease in the future, due to the COVID-19 pandemic [14]. They refer to three separate cases where acute Parkinsonism developed shortly after a COVID-19 infection. They proposed that systemic inflammation caused by severe COVID-19 could trigger neuroinflammation in the substantia nigra, killing off dopaminergic neurons. These neurons express high levels of the ACE2 receptor, making them highly vulnerable to the spike protein. A viral infection is known to upregulate α-synuclein, which, in high concentrations, forms soluble oligomers that then precipitate out as fibrils and accumulate within “Lewy bodies” that are tightly linked to Parkinson’s disease. Further corroboration of this idea comes from a paper which demonstrated that an infection with SARS-CoV-2 causes brain inflammation in macaques and induces the formation of Lewy bodies [15].
La enfermedad de Parkinson es el segundo trastorno neurodegenerativo más común y el trastorno motor neurodegenerativo más común. Se desconoce la causa raíz de casi el 90% de los casos, pero se ha teorizado que a menudo se trata de infecciones virales. Se puede argumentar que la pérdida del sentido del olfato y/o del gusto en asociación con COVID-19 es un signo de un vínculo parkinsoniano, ya que este síntoma también es un signo temprano de la enfermedad de Parkinson [16].
Las vacunas de ARNm parecen interrumpir la capacidad del cuerpo para evitar que los virus latentes se “despierten” y causen síntomas de enfermedades. Esta observación se basa en el hecho de que el herpes zóster y la parálisis facial (parálisis de Bell) se informan comúnmente en los informes de efectos secundarios en el Sistema de informes de eventos adversos de vacunas de la FDA. Hasta el 21 de mayo de 2021, habían aparecido en VAERS más de 2500 informes de parálisis de Bell después de las vacunas COVID-19. Una de las principales causas de la parálisis de Bell es la activación de infecciones virales latentes, en particular el herpes simple y la varicela zoster, la varicela zoster también es el virus responsable del herpes zóster.
Si bien la parálisis de Bell generalmente se resuelve con el tiempo, puede haber algunas consecuencias graves a largo plazo. Las mujeres embarazadas a las que se les diagnostican infecciones herpéticas activas durante el embarazo tienen un riesgo 2 veces mayor de tener un hijo varón autista a partir de ese embarazo [17]. Esto debería hacer que una mujer embarazada dude en vacunarse contra el SARS-CoV-2. La parálisis de Bell también puede ser un factor de riesgo para la enfermedad de Parkinson mucho más tarde en la vida. Un estudio de casi 200 pacientes con enfermedad de Parkinson en comparación con controles emparejados por edad y sexo encontró que seis de los pacientes con Parkinson habían tenido un diagnóstico anterior de parálisis de Bell, mientras que ninguno de los pacientes de control lo había hecho [18]. También existe un vínculo entre el autismo y la enfermedad de Parkinson. Un estudio en adultos autistas mayores de 39 años encontró que un tercio de ellos tenía síntomas que cumplían con los criterios para el diagnóstico de Parkinson [19].
Prion Diseases
Prion diseases are a group of severe neurodegenerative diseases that are caused by misfolded prion proteins. The most common prion disease in humans is the always-fatal sporadic Creutzfeldt-Jakob disease (CJD), which accounts for more than 85% of the cases [20]. Prion diseases are more specifically called transmissible spongiform encephalopathies (TSEs), and infection can spread through exposure to misfolded proteins as “infective” agents, without requiring a live pathogen [20]. PrP is the name given to the specific prion protein associated with these TSEs. Misfolded PrP proteins act as a seed or catalyst that then recruits other molecules of PrP to misfold in the same way and glom together into pathogenic fibrils.
MADCOW, the disease that affected a large number of cows in Europe beginning in the 1990s, is probably the best-known TSE. While eating beef from an infected animal is a very rare risk factor, most cases of Creutzfeldt-Jakob disease occur for unknown reasons, and no other risk factors have been identified. A study based in Switzerland confirmed that many patients who died of Creutzfeldt-Jakob disease had detectable levels of a prion protein in their spleen and muscles, in addition to the olfactory lobe and the central nervous system [21]. More generally, diseases involving misfolded PrPs have consistently been found to involve an initial early phase of prion replication in the spleen which happens long before overt symptoms appear [22, 23]. This point becomes important when we consider whether the COVID-19 vaccines might cause prion diseases.
PrP has a unique feature that it contains multiple copies of a characteristic motif in its amino acid sequence that is called a “GxxxG” motif, also known as a “glycine zipper” [24]. These proteins normally fold into a characteristic shape called an alpha helix, which allows the protein to penetrate the plasma membrane. The glycines in the zipper motif play an essential role in cross-linking and stabilizing alpha helices [25]. This glycine zipper motif is also a common characteristic of many transmembrane proteins (proteins that cross the membrane of the cell).
Indeed, the coronavirus spike protein has a GxxxG motif in its transmembrane domain (specifically, GFIAG — glycine, phenylalanine, isoproline, alanine, glycine) [26]. There is a platform called “Uniprot” where you can look up the sequence of specific proteins. The Uniprot entry for the SARS-CoV-2 spike protein has five glycine zipper sequences altogether [27]. According to J. Bart Classen, the SARS-CoV-2 spike protein has the ability “to form amyloid and toxic aggregates that can act as seeds to aggregate many of the misfolded brain proteins and can ultimately lead to neurodegeneration.” [28]
Many neurodegenerative diseases have been linked to specific proteins that have prion-like properties, and these diseases are characterized as protein-misfolding diseases or proteopathies [29]. Like PrP, prion-like proteins become pathogenic when their alpha helices misfold as beta sheets, and the protein is then impaired in its ability to enter the membrane. These diseases include Alzheimer’s, amyotrophic lateral sclerosis (ALS), Huntington’s disease and Parkinson’s disease, and each of these is associated with a particular protein that misfolds and accumulates in inclusion bodies in association with the disease. We already saw that Parkinson’s disease is characterized by Lewy bodies in the substantia nigra that accumulate misfolded α-synuclein.
Glycines within the glycine zipper transmembrane motifs in the amyloid beta precursor protein (APP) play a central role in the misfolding of amyloid beta linked to Alzheimer’s disease (Decock et al., 2016). APP contains a total of four GxxxG motifs (one fewer than the spike protein).
A case study presented the case of a man who developed CKD simultaneously with symptomatic COVID-19. The authors proposed that infection with SARS-CoV-2 precipitates or accelerates neurodegenerative diseases [30]. A theoretical paper published by researchers in India showed that the spike protein binds to a number of aggregation-prone prion-like proteins, including amyloid beta, α-synuclein, tau, PrP and TDP-43. They argued that this could initiate aggregation of these proteins in the brain, leading to neurodegeneration [31].
Tracing the Vaccine Trail to the Spleen
It is important to understand what happens to the contents of a vaccine after it is injected into the arm. Where does it travel in the body, and what does it do in the places where it settles in?
Vaccine developers are keen to know whether the vaccine induces a strong immune response, reflected in high antibody production against the spike protein, in the case of COVID-19 vaccines. And to do this, they need to trace its movement in the body.
CD8+ T-cells are cytotoxic immune cells that can kill cells that are infected with a virus. They detect an immune complex with viral proteins that are exposed on the surface of an infected cell. A study on an adenovirus-vector based vaccination of mice used clever methods to produce a marker that could track the activity of CD8+ T-cells in the lymph system and the spleen, in the days following vaccination [32]. It can be inferred that immune cells (antigen-presenting cells, where the “antigen” is the spike protein) were initially present at the arm muscle injection site and synthesized the virus spike protein from the vaccine DNA code, exposing it on their surface. Once activated by the foreign protein, they translocated into the draining lymph nodes and finally made their way to the spleen via the lymph system. The CD8+ T-cells are idly waiting within the lymphatics until they spot an infected immune cell. Researchers could detect activation of CD8+ immune cells over time and inferred that this was caused by the arrival of the contents of the vaccine to the site where these immune cells reside. Activated CD8+ T-cells first appeared in the draining lymph nodes, but after five days began to show up in the spleen. Their numbers there peaked sharply by 12 days and then remained high with a slow decay up to 47 days, when the researchers stopped looking. What this means is that the vaccine is picked up by antigen-presenting cells at the injection site and carried to the spleen via the lymph system. The carrier cells then hang out in the spleen for a long time. And this is where the danger lies in terms of the potential to cause prion disease.
In the paper that Greg Nigh and I published recently on the mRNA vaccines, we argued that the mRNA vaccines are rather perfectly set up to produce a very dangerous situation in the spleen that is poised to launch a prion disease. Given the fact that the DNA vector vaccines also end up concentrated in the spleen, I think that the same thing holds true for them as well. The spleen is where the action is for seeding misfolded prion proteins. The vaccine-infected cells have been programmed to produce large amounts of spike proteins. Prion proteins misfold into damaging beta-sheet oligomers when there are too many of them in the cytoplasm. Might the spike protein do the same?
Three out of the four COVID-19 vaccines currently on the market in the U.S. and Europe (Pfizer, Moderna, and J&J) use a genetic code for the spike protein that has been slightly tweaked, in order to produce a more potent antibody response [33]. Normally, after binding to the ACE2 receptor, the spike protein spontaneously changes its shape in a dramatic way in order to fuse with the membrane of the cell. In a Web publication, Ryan Cross described this action very graphically based on a spring-like model, as follows: “When the spike protein binds to a human cell, that spring is released, and the two helices and the loop straighten into one long helix that harpoons the human cell and pulls the virus and human membranes close together until they fuse.” [33]. As Cross explains, through trial and error, but taking structural information into account, researchers came up with the idea of swapping out two adjacent amino acids for prolines in the membrane fusion domain in order to stabilize the shape of the spike protein in its pre-fusion form. In this form, it exposes critical antigenic areas, and this assures more rapid formation of matching antibodies, the only goal of the vaccine design. This also prevents the protein from fusing with the plasma membrane of a host cell. I’d imagine that the spike protein attaches to the ACE2 receptor and then gets stuck there, like a sitting duck. But a worrisome thought is whether this open state, not fused with the membrane, might more closely resemble the shape of a misfolded prion-like protein like amyloid beta than does the collapsed shape it needs to go into the membrane?
Tetz and Tetz have argued in a published online preprint that prion-like domains in the spike protein enable higher affinity for the ACE2 receptor, making the virus more virulent than its earlier cousins [34]. These same authors published an earlier peer-reviewed journal paper where they observed that many other viruses have proteins in their coat that have distinct features of prion proteins [35].
Germinal Centers and Parkinson’s Disease
Germinal centers in the spleen are a primary factory where antibodies against specific antigens (such as the spike protein) are manufactured and perfected. Makers of the mRNA vaccines were pleased to see that antigen-presenting cells (mainly dendritic cells), originally attracted to the site of the injection, take up the mRNA particles and then migrate via the lymph system to the spleen in high numbers and induce high levels of antibody production in these germinal centers [36].
Unfortunately, these same germinal centers are a primary site for the initiation of a process of producing and distributing misfolded prion proteins, often seeded by viral proteins, and triggered by an acute inflammatory response [37].
B cells, also known as B lymphocytes, are a type of immune cell that is the key player in the process that leads to the production of specific antibodies to a foreign antigen [38]. They originate from precursor cells in the bone marrow, and then migrate to the spleen and other lymphoid organs, where they bind to antigens presented to them by antigen-presenting cells, such as the dendritic cells. A maturation process beginning with a multipotent progenitor B cell ends with a mature “memory” B cell that has gone through a complex process to perfect its antibody production process to specifically match the antigen it has been assigned to (e.g., the spike protein). B cells also go through another process called class switching, which changes the type of antibody they produce from one class to another, without changing its specificity to the antigen.
Antibodies are also known as immunoglobulins (Igs), and the possible classes include IgM, IgG, IgA and IgE. IgM is the first immunoglobulin class that is produced (primarily in the spleen), and it is converted into IgG through class switching. IgG is the dominant class in the blood, making up 75% of the serum antibodies, and it is essential for clearing infections in the tissues. Long-lived mature memory B cells cruise the blood stream looking for any appearances of the antigen they have been assigned to, but they are useless for anything else. When the virus they’ve been trained to match mutates to the point where their antibodies no longer match well, they become useless even for the disease they’re trained to fight.
When mice are injected with PrP in the abdomen (intraperitoneal injection), the PrP shows up very quickly in the spleen. From there, the PrP travels along the spinal cord and the vagus nerve to reach the brain, causing prion disease [39]. As we will soon see, α-synuclein, the prion-like protein linked to Parkinson’s disease, also makes its way to the brain from the spleen along the vagus nerve. The mRNA vaccines set up perfect conditions in the spleen for the formation and distribution of conglomerates made up of misfolded α-synuclein, PrP and spike protein.
While α-synuclein causes neurodegenerative disease when it misfolds, in its normal shape it is an active participant in the immune response. α-Synuclein facilitates the processes that lead to antibody production in response to foreign antigens. Dendritic cells express α-synuclein, and it is upregulated (over-expressed) in response to stressors, such as the mRNA, the cationic lipids, and the PEG in the mRNA vaccines. Much can be learned by studying mice that have been genetically engineered to have a defective version of α-synuclein [40]. These mice have a decreased capacity to clear pathogens through phagocytosis, and an impairment in the ability to generate B cells from precursor stem cells. They also had a four-fold reduction in progenitor B cells in the bone marrow. The amount of immunoglobulin G was reduced compared to wildtype, suggesting impaired class switching. Altogether, they are unable to mount an effective immune response to antigens, whether they come from a natural threat or a vaccine.
Dendritic cells under stress accumulate prion proteins and release them into small lipid particles called exosomes, which are then distributed throughout the body, either along nerve fibers or in the general circulation [41]. There is reason to believe that these vaccines will accelerate the release of exosomes containing misfolded prion-like spike proteins that are being produced in large amounts under instruction from the vaccines. These spike proteins will act as seeds to cause α-synuclein and PrP to also misfold and form toxic oligomers together with the spike protein, which are released into the extracellular space as exosomes. These exosomes, released under the severe stress conditions induced by the vaccine, then carry prion proteins into the brain along the vagus nerve, to initiate prion diseases [42].
Impaired Immune Response due to Over-vaccination
A characteristic of the elderly is an impaired ability to mount antibodies against new pathogenic threats, and this is reflected in a failure to generate protective antibodies in response to vaccination. It has been demonstrated in experiments with mice that aged mice have an overabundance of long-lived memory (antigen-experienced) B cells, and this is paired with an inability to generate new B cells from progenitor cells in the bone marrow, as well as impairment in the process of refinement of the antibody response in germinal centers in the spleen and the associated class switching that produces effective IgG antibodies [43, 44]. A significant reduction in the number of naive follicular B cells, combined with an impaired ability to convert them into mature memory B cells leaves these aged mice highly vulnerable to new infections. It is likely that the same principle applies to humans. A plausible conclusion is that aggressive vaccination campaigns accelerate the pace at which an individual’s immune system reaches an ”aged” status due to exuberant generation of memory B cells in response to the artificial stimuli induced by repeated vaccination.
It has now been confirmed that the S1 component of the spike protein shows up in the blood one day after the first mRNA vaccine and remains detectable for up to a month after vaccination, becoming cleared as IgA and IgG antibodies become available [45]. For immune compromised people, it likely stays in the blood much longer, exposing all the tissues — the spleen, the heart, the brain, the gonads, etc. – to the toxic prion-like spike protein.
Today’s children are by far the most vaccinated generation in the history of humankind. If we decide in the near future to deliver a booster COVID-19 shot to them every year, as seems possible given the current climate of enthusiasm for these vaccines, are we inviting disaster for them in years to come? Will their immune system “age” much faster than that of previous generations, due to the exhaustion of the pool of progenitor B cells by all these vaccines? Will they succumb to Parkinson’s disease or other debilitating prion-based neurodegenerative diseases much sooner and in much greater numbers than previous generations? This is an experiment that I hope we finally decide not to carry out.
Summary
There are many reasons to be wary of the COVID-19 vaccines, which have been rushed to market with grossly inadequate evaluation and aggressively promoted to an uninformed public, with the potential for huge, irreversible, negative consequences. One potential consequence is to exhaust the finite supply of progenitor B cells in the bone marrow early in life, causing an inability to mount new antibodies to infectious agents. An even more worrisome possibility is that these vaccines, both the mRNA vaccines and the DNA vector vaccines, may be a pathway to crippling disease sometime in the future. Through the prion-like action of the spike protein, we will likely see an alarming increase in several major neurodegenerative diseases, including Parkinson’s disease, CKD, ALS and Alzheimer’s, and these diseases will show up with increasing prevalence among younger and younger populations, in years to come. Unfortunately, we won’t know whether the vaccines caused this increase, because there will usually be a long time separation between the vaccination event and the disease diagnosis. Very convenient for the vaccine manufacturers, who stand to make huge profits off of our misfortunes — both from the sale of the vaccines themselves and from the large medical cost of treating all these debilitating diseases.
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STEPHANIE SENEFF
August 19, 2020
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