Towards the emergence of a new form of the neurodegenerative Creutzfeldt-Jakob disease: Twenty six cases of CJD declared a few days after a COVID-19 vaccine

[Emily]

https://la-verite-vous-rendra-libres.org/wp-content/uploads/2022/06/v2cjdperezmoretmontagnierrip2022referencearticle.pdf

Moret-Chalmin, Claire & Montagnier, Luc & Perez, jean-claude. (2022). Towards the emergence of a new form of the neurodegenerative Creutzfeldt-Jakob disease: Twenty six cases of CJD declared a few days after a COVID-19 “vaccine” Jab. 10.13140/RG.2.2.14427.03366. Towards the emergence of a new form of the neurodegenerative Creutzfeldt-Jakob disease:
Twenty six cases of CJD declared a few days after a COVID-19 “vaccine” Jab

Jean Claude Perez, PhD Maths§Computer Science Bordeaux University ; Retired (IBM European Research center on Artificial Intelligence Montpellier France) ; Bordeaux metropole France; https://orcid.org/0000-0001-6446-2042 France jeanclaudeperez2@gmail.com
Claire Moret-Chalmin, MD. Neurologist, 13 rue Roger Martin du Gard 60600 Clermont France clmoret@gmail.com
Luc Montagnier RIP MD. Virologist, Fondation Luc Montagnier Quai Gustave-Ador 62 1207 Genève, Switzerland

KEYWORDS
Creutzfeldt-Jakob desease (CJD), Prion protein, SARS-CoV2 Variants, Spike, COVID-19 mRNA Vaccines, survival, Neuropsychiatric disease, Evolution.

ABSTRACT

We highlight the presence of a Prion region in the different Spike proteins of the original SARS-CoV2 virus as well as of all its successive variants but also of all the “vaccines” built on this same sequence of the Spike SARS-CoV2 from Wuhan.
Paradoxically, with a density of mutations 8 times greater than that of the rest of the spike, the possible harmfulness of this Prion region disappears completely in the Omicron variant. We analyze and explain the causes of this disappearance of the Prion region of the Spike of Omicron.
At the same time, we are analyzing the concomitance of cases, which occurred in various European countries, between the first doses of Pfizer or Moderna mRNA vaccine and the sudden and rapid onset of the first symptoms of Creutzfeldt-Jakob disease, which usually requires several years before observing its first symptoms.
We are studying 26 Creutzfeld Jakob Diseases, in 2021, from an anamnestic point of view, centered on the chronological aspect of the evolution of this new prion disease, without being able to have an explanation of the etiopathogenic aspect of this new entity. We subsequently recall the usual history of this dreadfull subacute disease, and compare it with this new, extremely acute, prion disease, following closely vaccinations. In a few weeks, more 50 cases of almost spontaneous emergence of Creutzfeldt-Jakob disease have appeared in France and Europe very soon after the injection of the first or second dose of Pfizer, Moderna or AstraZeneka vaccines. To summarize, of the 26 cases analyzed, the first symptoms of CJD appeared on average 11.38 days after the injection of the COVID-19 "vaccine". Of these 26 cases, 20 had died at the time of writing this article while 6 were still alive. The 20 deaths occurred only 4.76 months after the injection. Among them, 8 of them lead to a sudden death (2.5 months). All this confirms the radically different nature of this new form of CJD, whereas the classic form requires several decades.

[alert]

If this is a real paper and its reporting is genuine, this is very concerning. However, something about this doesn't pass the smell test to me, and I can't find the text above at the only link in your post.

The virology involved seems a bit over my head, but I've never heard of any virus, including COVID-19, producing prions. If it did, we'd have had a lot bigger issues during this pandemic. And if any vaccine was suspected of containing prions, that would be major worldwide news. We have a few incidents where a researcher accidentally injected themselves with prions during CJD research and they have had nearly a 100% fatality rate.

[sharon sanders]

Here is the text link:

https://www.researchgate.net/publication/358661859_Towards_the_emergence_of_a_new_form_of_the_neurodegenerative_Creutzfeldt-Jakob_disease_Twenty_six_cases_of_CJD_declared_a_few_days_after_a_COVID-19_vaccine_Jab

[Emily]

Alert, your questions and concerns are excellent, but I don't think the paper should be judged as probable misinformation. This is not as alarming as you might think. There are only 26 cases reported here and the window for this aggressive illness looks short, (I did a quick read so could be wrong.) There certainly should be more research done and that is all they ask. I'd like to know if natural infection has a correlation to prion disease and if not, why not? If the vaccine does and the cause is in the spike, then are the vaccinated exposed to different doses or are other components contributing?
But first thing is to see if this has happened to the naturally infected.

I'll post a few links related to the possible links between viruses and prion disease. Never heard of the topic myself, either.

[alert]

Having tracked the apparent false alarm for prion disease in New Brunswick last year, I learned that most developed countries perform surveillance for possible CJD cases. The vast majority of CJD cases worldwide are "sporadic", that is they occur more or less randomly without any known risk factors. Every so often a country detects a "variant" case (i.e. one linked to consumption of mad cow beef), a familial case (one whose genetics cause the illness) or an iatrogenic case (one infected with prions through surgery, often as a result of tissue transplants from a previous case). In a country with 40 million people like Canada, the numbers of those later groups were 1 or 2 cases per year. If ANYTHING, be it a vaccine, a virus, a toxin, or otherwise caused 26 similar cases in a few months, that's an incredibly alarming development.

My understanding is that the classification of what type of CJD a patient has is dependent on the prions themselves, and the incident described in the original paper would surely have tripped national surveillance detections.

(It's worth noting that no prions at all were detected in New Brunswick; nothing here explains the diseases caused there.)

[Emily]

Alert, I posted a few new CJD articles and bumped up two of tetano's. There are a couple of case reports of CJD following infection. Also found a couple more reports of CJD following the vaccine. The emergence of CJD in Nepal is interesting, too. First case was 2019, possibly late 2019, when SARS2 was unknown there but could have been present. Second was in 2021.

[Emily]

Examples of other research examining the relationship between viruses and prion diseases:

https://www.nature.com/articles/s41598-021-89586-6

Hara, H., Chida, J., Uchiyama, K. et al. Neurotropic influenza A virus infection causes prion protein misfolding into infectious prions in neuroblastoma cells. Sci Rep 11, 10109 (2021). https://doi.org/10.1038/s41598-021-89586-6

In this study, we show that infection with a neurotropic IAV strain A/WSN/33 (H1N1) (hereafter referred to as IAV/WSN) induced not only the conversion of PrP^C into PrP^Sc but also the formation of infectious prions in cultured mouse neuroblastoma N2a cells. These results indicate that IAV/WSN infection plays a causal role in misfolding of PrP^C into PrP^Sc and formation of infectious prions, further strengthening the role of virus infections in induction of the protein misfolding or aggregation associated with neurodegenerative diseases.

https://www.nature.com/articles/s41467-018-08180-z

Nan, H., Chen, H., Tuite, M.F. et al. A viral expression factor behaves as a prion. Nat Commun 10, 359 (2019). https://doi.org/10.1038/s41467-018-08180-z
Prions are proteins that can fold into multiple conformations some of which are self-propagating. Such prion-forming proteins have been found in animal, plant, fungal and bacterial species, but have not yet been identified in viruses. Here we report that LEF-10, a baculovirus-encoded protein, behaves as a prion. Full-length LEF-10 or its candidate prion-forming domain (cPrD) can functionally replace the PrD of Sup35, a widely studied prion-forming protein from yeast, displaying a [PSI⁺]-like phenotype. Furthermore, we observe that high multiplicity of infection can induce the conversion of LEF-10 into an aggregated state in virus-infected cells, resulting in the inhibition of viral late gene expression. Our findings extend the knowledge of current prion proteins from cellular organisms to non-cellular life forms and provide evidence to support the hypothesis that prion-forming proteins are a widespread phenomenon in nature.

https://www.nature.com/articles/npre.2009.3887.1

Bandea, C. Endogenous Viral Etiology of Prion Diseases. Nat Prec (2009). https://doi.org/10.1038/npre.2009.3887.1
Transmissible spongiform encephalopathies (TSEs), or prion diseases, are a group of incurable neurodegenerative disorders, including Kuru and Creutzfeldt-Jakob disease in humans, “mad cow” disease in cattle, and scrapie in sheep. This paper presents structural, genetic, and evolutionary evidence supporting an endogenous TSE virus model that integrates the three major traditional views on the nature of TSE pathogens, the conventional virus view, the prion hypothesis, and the virino concept, into a novel conceptual and evolutionary framework. According to this model, the TSE pathogens are symbiotic endogenous viruses that inadvertently produce transmissible viral particles that lack the viral genome and are composed primarily of the viral prion protein (PrP). Production of defective viral particles that contain a partial genome or lack the viral genome entirely is a relatively common event in the life cycle of many viruses. Similar to the normal viral particles, which contain a genome, these defective viral particles can be transmitted to new host cells. Obviously, in the absence of viral genome, these protein-only viral particles cannot establish a productive infection. However, if these viral particles enter a host cell that carries the parental or a related virus and induce the production of similar protein-only particles, then they would appear as self-replicating, protein-only infectious pathogens if mistakenly taken out from the context of the viral life cycle. This misconception, which is rooted into the current dogma of viruses as viral particles, led to the development of the prion theory. The endogenous TSE virus model is consistent with the TSE data and offers solutions to many enigmatic features associated with TSE, including the function of PrP that, despite more than two decades of TSE research conducted primarily within the framework of the prion hypothesis, is still not known. According to the TSE endogenous virus model, PrP is the protein of an endogenous virus that has co-evolved with their vertebrate hosts by providing a protective function against pathogenic viruses. The evidence for the endogenous TSE virus model and for the antiviral protective function of PrP is strong, and they are fully open to additional experimental testing. The endogenous virus model opens the TSE research field to new interpretations and directions, both in basic research and in associated biomedical and public health fields, and could lead to development of new diagnostic and therapeutic approaches.

https://www.sciencedirect.com/science/article/pii/S0042682208008039

Prion expression is activated by Adenovirus 5 infection and affects the adenoviral cycle in human cells
Paola Caruso,Romina Burla,Stefania Piersanti,Gioia Cherubini,Cristina Remoli,Yuri Martina,Isabella Saggio
Virology
Elsevier
15 March 2009

The prion protein is a cell surface glycoprotein whose physiological role remains elusive, while its implication in transmissible spongiform encephalopathies (TSEs) has been demonstrated. Multiple interactions between the prion protein and viruses have been described: viruses can act as co-factors in TSEs and life cycles of different viruses have been found to be controlled by prion modulation.
We present data showing that human Adenovirus 5 induces prion expression. Inactivated Adenovirus did not alter prion transcription, while variants encoding for early products did, suggesting that the prion is stimulated by an early adenoviral function. Down-regulation of the prion through RNA interference showed that the prion controls adenovirus replication and expression.
These data suggest that the prion protein could play a role in the defense strategy mounted by the host during viral infection, in a cell autonomous manner. These results have implications for the study of the prion protein and of associated TSEs.

[tetano]

Studies 1,3 and 4 do not indicate a direct production of priones by viruses, but only a stimulus to produce them on the host tissues (1 and 4) or an alteration of the viral replication that can generate ( it's only a hypothesis) defective viruses without genome (3).
Studio 2 is the only one that indicates a possible direct production of a prion protein, but from a virus that infects only insects.

[Emily]

Thank you, tetano.

[sharon sanders]

I think it is important to put everything into perspective.

It is estimated that there have been 12 BILLION doses of COVID-19 given in the world. link

There are always risks with every medicine. Some people, unfortunately, suffer bad consequences.

If you have any medical questions, including vaccines, please consult your medical practitioner.

Do not take medical advice from the internet.

[Emily]

https://www.ijvtpr.com/index.php/IJVTPR/article/view/66

Perez, J.-C., Moret-Chalmin, C., & 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), 727–770. Retrieved from https://www.ijvtpr.com/index.php/IJVTPR/article/view/66

Abstract

Creutzfeldt-Jakob Disease, the formerly rare but universally fatal prion disease in humans, normally progresses over several decades before it leads to death. In the Appendix to this paper, we highlight the presence of a prion region in the spike protein of the original SARS-CoV-2, and in all the “vaccine” variants built from the Wuhan virus. The prion region in the spike of SARS-CoV-2 has a density of mutations eight times greater than that of the rest of the spike, and, yet, strangely that entire prion region disappears completely in the Omicron variant. In the main body of our text, we present 26 cases of Creuzfeldt-Jacob Disease, all diagnosed in 2021 with the first symptoms appearing within an average of 11.38 days after a Pfizer, Moderna, or AstraZeneca COVID-19 injection. Because the causal progression, the etiopathogenesis, of these atypical and new cases of human prion disease — cases of what is apparently a totally new form of rapidly developing Creuzfeldt-Jacob Disease — we focus on the chronology of the symptomatic development. We consider it from an anamnestic point of view — one in which we compare the typical development of pre-COVID cases of Creuzfeldt-Jacob Disease to the extremely accelerated development of similar symptoms in the 26 cases under examination. By such an approach, we hope to work out the etiopathogenesis critical to understanding this new and much more rapidly developing human prion disease. By recalling the sequential pathway of that the formerly subacute and slowly developing disease followed in the past, and by comparing it with this new, extremely acute, rapidly developing prion disease — one following closely after one or more of the COVID-19 injections — we believe it is correct to infer that the injections caused the disease in these 26 cases. If so, they have probably also caused a many other cases that have gone undiagnosed because of their rapid progression to death. By late 2021, 20 had died within 4.76 months of the offending injection. Of those, 8 died suddenly within 2.5 months confirming the rapid progression of this accelerated form of Creuzfeldt-Jacob Disease. By June 2022, 5 more patients had died, and at the time of this current writing, only 1 remains still alive.

Author Biography

Luc Montagnier, Virology; discoverer of the human immunodeficiency virus and Nobel Laureate 2008


Luc Montagnier, MD, and Nobel Laureate, esteemed colleague and friend, passed from this world on February 8, 2022 not long after the completion of the preliminary draft of this work which his co-authors have carried forward to this updated report with some additional cases and new information. Perhaps this may be the most important work of Luc’s lifetime expressing his incredible genius and spirit. While hospitalized, he continued to attach the greatest importance to the publication of this article. He is honored by the Luc Montagnier Foundation Quai Gustave-Ador 62 1207, Geneva, Switzerland.

INTRODUCTION
Prions are self-templating protein aggregates that stably perpetuate distinct biological states. On the
occasion of the Nobel Prize in Physiology or Medicine1997, the committee gave a good definition of the
prion research breakthrough spearheaded by Stanley B. Prusiner:
Creutzfeldt-Jakob disease and related illnesses affecting people and animals involve the degeneration of brain cells. In
1982 Stanley Prusiner was able to isolate a suspected infectious agent, a protein that he called a prion. He identified the
gene behind the prion protein, but determined that it is also present in healthy people and animals. Stanley Prusiner
showed that the prion molecules are folded in a different way than the normal proteins and that the folding of the
prion can be transferred to normal proteins. This is the basis for the illness.
Prions are proteins that can switch from non-aggregated states to self-templating highly ordered
aggregates. This property allows them to confer stable changes in biological states, and in doing so, to
cause fatal disease in animals and humans.

A PRION REGION IN COVID-19 SARS-COV-2 AND IN THE“VACCINES”

It has been suggested (Seneff & Nigh,2021;
Classen, 2021b; Tetz & Tetz,2022), that
there is a prion region in all spike proteins
produced by the SARS-CoV-2 virus.T he
presence of the prion region in the SARS-
CoV-2 spike embedded in the COVID-19
injectables was formally demonstrated by
Tetz and Tetz (2022) as summed up in
Figure1. And, in Perez, Lounnas, and
Montagnier(2021), we showed that all
SARS-CoV-2 Wuhan strain variants, and all
of the COVID-19 vaccines have this prion
region, although it disappears totally in the
Omicron variant (for the details of that
disappearance, see the Appendix to this
paper)...