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https://21a86421-c3e0-461b-83c2-cfe4628dfadc.filesusr.com/ugd/659775_4e00147b79904ba3a2594a7a47bac1fa.pdfCOVID-19 RNA Based Vaccines and the Risk of Prion Disease
Classen Immunotherapies, Inc.,
3637 Rockdale Road, Manchester, MD21102,E-mail:
[email protected].
J. Bart Classen, MD*
Citation: Classen JB. COVID-19 RNA Based Vaccines and theRisk of Prion Disease. Microbiol Infect Dis. 2021; 5(1): 1-3.
* Correspondence: J. Bart Classen, MD, ClassenImmunotherapies, Inc.,
3637 Rockdale Road, Manchester, MD21102,Tel: 410-377-8526. Received: 27 December 2020; Accepted: 18 January 2021
ABSTRACT
Development of new vaccine technology has been plagued with problems in the past. The current RNA based SARSCoV-2 vaccines were approved in the US using an emergency order without extensive long term safety testing. In
this paper the Pfizer COVID-19 vaccine was evaluated for the potential to induce prion-based disease in vaccine
recipients. The RNA sequence of the vaccine as well as the spike protein target interaction were analyzed for the
potential to convert intracellular RNA binding proteins TAR DNA binding protein (TDP-43) and Fused in Sarcoma
(FUS) into their pathologic prion conformations. The results indicate that the vaccine RNA has specific sequences
that may induce TDP-43 and FUS to fold into their pathologic prion confirmations. In the current analysis a total
of sixteen UG tandem repeats (ΨGΨG) were identified and additional UG (ΨG) rich sequences were identified. Two
GGΨA sequences were found. Potential G Quadruplex sequences are possibly present but a more sophisticated
computer program is needed to verify these. Furthermore, the spike protein, created by the translation of the vaccine
RNA, binds angiotensin converting enzyme 2 (ACE2), a zinc containing enzyme. This interaction has the potential
to increase intracellular zinc. Zinc ions have been shown to cause the transformation of TDP-43 to its pathologic
prion configuration. The folding of TDP-43 and FUS into their pathologic prion confirmations is known to cause
ALS, front temporal lobar degeneration, Alzheimer’s disease and other neurological degenerative diseases. The
enclosed finding as well as additional potential risks leads the author to believe that regulatory approval of the
RNA based vaccines for SARS-CoV-2 was premature and that the vaccine may cause much more harm than benefit.
*
Correspondence:
J. Bart Classen, MD, Classen Immunotherapies, Inc., 3637
Rockdale Road, Manchester, MD 21102, Tel: 410-377-8526.
Received: 27 December 2020; Accepted: 18 January 2021
Microbiology & Infectious Diseases
ISSN 2639-9458
Keywords
COVID-19, Vaccines, Diabetes, Immunity.
Introduction
Vaccines have been found to cause a host of chronic, late developing
adverse events. Some adverse events like type 1 diabetes may not
occur until 3-4 years after a vaccine is administered [1]. In the
example of type 1 diabetes the frequency of cases of adverse events
may surpass the frequency of cases of severe infectious disease
the vaccine was designed to prevent. Given that type 1 diabetes is
only one of many immune mediated diseases potentially caused by
vaccines, chronic late occurring adverse events are a serious public
health issue.
The advent of new vaccine technology creates new potential
mechanisms of vaccine adverse events. For example, the first
killed polio vaccine actually caused polio in recipients because
the up scaled manufacturing process did not effectively kill
the polio virus before it was injected into patients. RNA based
vaccines offers special risks of inducing specific adverse events.
One such potential adverse event is prion based diseases caused
by activation of intrinsic proteins to form prions. A wealth of
knowledge has been published on a class of RNA binding proteins
shown to participating in causing a number of neurological
diseases including Alzheimer’s disease and ALS. TDP-43 and
FUS are among the best studied of these proteins [2].
The Pfizer RNA based COVID-19 vaccine was approved by the
US FDA under an emergency use authorization without long term
safety data. Because of concerns about the safety of this vaccine a
study was performed to determine if the vaccine could potentially
induce prion based disease.
Methods
Pfizer’s RNA based vaccine against COVID-19 was evaluated for
the potential to convert TDP-43 and or FUS to their prion based
Microbiol Infect Dis, 2021 Volume 5 | Issue 1 | 2 of 3
disease causing states. The vaccine RNA was analyzed for the
presence of sequences that can activate TDP-43 and FUS. The
interaction of the transcribed spike protein with its target was
analyzed to determine if this action could also activate TDP-43
and FUS.
Results
Analysis of the Pfizer vaccine against COVID-19 identified two
potential risk factors for inducing prion disease is humans. The RNA
sequence in the vaccine [3] contains sequences believed to induce
TDP-43 and FUS to aggregate in their prion based conformation
leading to the development of common neurodegerative diseases.
In particular it has been shown that RNA sequences GGUA [4],
UG rich sequences [5], UG tandem repeats [6], and G Quadruplex
sequences [7], have increased affinity to bind TDP-43 and or
FUS and may cause TDP-43 or FUS to take their pathologic
configurations in the cytoplasm. In the current analysis a total of
sixteen UG tandem repeats (ΨGΨG) were identified and additional
UG (ΨG) rich sequences were identified. Two GGΨA sequences
were found. G Quadruplex sequences are possibly present but
sophisticated computer programs are needed to verify these.
The spike protein encoded by the vaccine binds angiotensin
converting enzyme 2 (ACE2), an enzyme which contains zinc
molecules [8]. The binding of spike protein to ACE2 has the
potential to release the zinc molecule, an ion that causes TDP-43
to assume its pathologic prion transformation [9].
Discussion
There is an old saying in medicine that “the cure may be worse
than the disease.” The phrase can be applied to vaccines. In the
current paper the concern is raised that the RNA based COVID
vaccines have the potential to cause more disease than the
epidemic of COVID-19. This paper focuses on a novel potential
adverse event mechanism causing prion disease which could be
even more common and debilitating than the viral infection the
vaccine is designed to prevent. While this paper focuses on one
potential adverse event there are multiple other potential fatal
adverse events as discussed below.
Over the last two decades there has been a concern among certain
scientists that prions could be used as bioweapons. More recently
there has been a concern that ubiquitous intracellular molecules
could be activated to cause prion disease including Alzheimer’s
disease, ALS and other neurodegenerative diseases. This concern
originates due to potential for misuse of research data on the
mechanisms by which certain RNA binding proteins like TDP-43,
FUS and others can be activated to form disease causing prions.
The fact that this research, which could be used for bioweapons
development, is funded by private organizations including the Bill
and Melinda Gates Foundation, and Ellison Medical Foundation
[2] without national/international oversight is also a concern.
In the past, for example, there were prohibitions for publishing
information pertaining to construction of nuclear bombs.
Published data has shown that there are several different factors that
can contribute to the conversion of certain RNA binding proteins
including TDP-43, FUS and related molecules to their pathologic
states. These RNA binding proteins have many functions and are
found in both the nucleus and the cytoplasm. These binding proteins
have amino acid regions, binding motifs that bind specific RNA
sequences. Binding to certain RNA sequences when the proteins
are in the cytoplasm is believed to causes the molecules to fold in
certain ways leading to pathologic aggregation and prion formation
in the cytoplasm [2]. The current analysis indicates Pfizer's RNA
based COVID-19 vaccine contains many of these RNA sequences
that have been shown to have high affinity for TDP-43 or FUS
and have the potential to induce chronic degenerative neurological
diseases.
Zinc binding to the RNA recognition motif of TDP-43 is another
mechanism leading to formation of amyloid like aggregations [9].
The viral spike protein, coded by the vaccine RNA sequence, binds
ACE2 an enzyme containing zinc molecules [8]. This interaction
has the potential to increase intracellular zinc levels leading to
prion disease. The initial binding could be between spike proteins
on the surface of the cell transfected by the vaccine and ACE2
on the surface of an adjacent cell. The resulting complex may
become internalized. Alternatively, the interaction could initially
take place in the cytoplasm of a cell that makes ACE2 and has been
transfected with the vaccine RNA coding for the spike protein.
The interaction is quite concerning given the belief that the virus
causing COVID-19, SARS-CoV-2, is a bioweapon [10,11] and it
is possible that the viral spike protein may have been designed to
cause prion disease.
Another related concern is that the Pfizer vaccine uses a unique
RNA nucleoside 1-methyl-3'-pseudouridylyl (Ψ). According to
FDA briefing documents, this nucleoside was chosen to reduce
activation of the innate immune system [12]. RNA molecules
containing this nucleoside will undoubtedly have altered binding
[13]. Unfortunately, the effect on TDP-43, FUS and other RNA
binding proteins is not published. The use of this nucleoside in
a vaccine can potentially enhance the binding affinity of RNA
sequences capable of causing TDP-43 and FUS to assume toxic
configurations.
There are many other potential adverse events that can be induced
by the novel RNA based vaccines against COVID-19. The vaccine
places a novel molecule, spike protein, in/on the surface of host
cells. This spike protein is a potential receptor for another possibly
novel infectious agent. If those who argue that the COVID-19 is
actually a bioweapon are correct, then a second potentially more
dangerous virus may be released that binds spike protein found on
the host cells of vaccine recipients. Data is not publicly available
to provide information on how long the vaccine RNA is translated
in the vaccine recipient and how long after translation the spike
protein will be present in the recipient’s cells. Such studies
pertaining to in vivo expression will be complex and challenging.
Genetic diversity protects species from mass casualties caused by
infectious agents. One individual may be killed by a virus while
Microbiol Infect Dis, 2021 Volume 5 | Issue 1 | 3 of 3
another may have no ill effects from the same virus. By placing
the identical receptor, the spike protein, on cells of everyone in a
population, the genetic diversity for at least one potential receptor
disappears. Everyone in the population now becomes potentially
susceptible to binding with the same infectious agent.
Autoimmunity and the opposing condition, metabolic syndrome,
are well know adverse events caused by vaccines [14]. COVID-19
infections are associated with the induction of autoantibodies
and autoimmune disease [15,16] making it more than plausible
a vaccine could do the same. One author has found amino acid
sequences coded by the spike protein to be identical to sequences
in human proteins including proteins found in the CNS [17].
Autoimmunity can also be induced by epitope spreading when a
foreign antigen, like the spike protein, is presented by an antigen
presenting cell that also has self molecules attached to its MHC
molecules.
Finally, others working in the field have published additional support
that COVID-19 vaccines could potentially induce prion disease.
Authors [18] found prion related sequences in the COVID-19 spike
protein which were not found in related coronaviruses. Others [19]
have reported a case of prion disease, Creutzfeldt-Jakob disease,
initially occurring in a man with COVID-19.
Many have raised the warning that the current epidemic of
COVID-19 is actually the result of an bioweapons attack released
in part by individuals in the United States government [10,11].
Such a theory is not far fetched given that the 2001 anthrax attack
in the US originated at Fort Detrick, a US army bioweapon facility.
Because the FBI’s anthrax investigation was closed against the
advice of the lead FBI agent in the case, there are likely conspirators
still working in the US government. In such a scenario the primary
focus of stopping a bioweapons attack must be to apprehend the
conspirators or the attacks will never cease. Approving a vaccine,
utilizing novel RNA technology without extensive testing is
extremely dangerous. The vaccine could be a bioweapon and even
more dangerous than the original infection.
References
1. Classen JB, Classen DC. Clustering of cases of insulin
dependent diabetes (IDDM) occurring three years after
Hemophilus influenza B (HiB) immunization support causal
relationship between immunization and IDDM. Autoimmunity.
2002; 35: 247-253.
2. King OD, Gitler AD, Shorter J. The tip of the iceberg: RNAbinding proteins with prion-like domains in neurodegenerative
disease. Brain Res. 2012; 1462: 61-80.
3. WHO, International Non Proprietary Names Program: 11889.
9/2020.
4. Kapeli K, Pratt GA, Vu AQ, et al. Distinct and shared functions
of ALS-associated proteins TDP-43, FUS and TAF15 revealed
by multisystem analyses. Nature Communications. 2016; 7:
12143.
5. Kuo P, Chiang C, Wang Y, et al. The crystal structure of TDP43 RRM1-DNA complex reveals the specific recognition for
UG- and TG-rich nucleic acids. Nucleic Acids Research. 2014;
42: 4712-4722.
6. Tollervey JR, Curk T, Rogelj B, et al. Characterizing the RNA
targets and position-dependent splicing regulation by TDP-43;
implications for neurodegenerative diseases. Nat Neurosci.
2011; 14: 452-458.
7. Imperatore JA, McAninch DS, Valdez-Sinon AN, et al. FUS
recognizes G quadruplex structures within neuronal mRNAs.
Frontiers in Molecular Biosciences. 2020; 7: 6.
8. Shang J, Ye G, Shi K, et al. Structural basis of receptor
recognition by SARS-CoV-2. Nature. 2020; 581: 221-225.
9. Garnier C, Devred F, Byrne D, et al. Zinc binding to RNA
recognition motif of TDP-43 induces the formation of amyloidlike aggregates. Sci Rep. 2017; 7: 6812.
10. Classen JB. COVID-19, MMR vaccine, and bioweapons.
Diabetes & its Complications.2020; 4: 1-8.
11. Classen JB. Evidence supporting the hypothesis that the 2019
epidemic of E-vaping acute lung injury (EVALI) was caused in
part by COVID-19. Diabetes & Complications. 2020; 4: 1-2.
12. Pfizer-Biotech: COVID-19 Vaccine (BNT162, PF-07302048),
Vaccines and Related Biological Products Advisory Committee
Briefing Document. Meeting Date: 10 December 2020.
13. Roundtree IA, Evans ME, Pan, et al. Dynamic RNA
modifications in gene expression regulation. Cell. 2017; 169:
1187-1200.
14. Classen JB. Review of Vaccine Induced Immune Overload and
the Resulting Epidemics of Type 1 Diabetes and Metabolic
Syndrome, Emphasis on Explaining the Recent accelerations in
the Risk of Prediabetes and other Immune Mediated Diseases. J
Mol Genet Med. 2014; S1: 025.
15. Amiral J. Can COVID-19 Induce an autoimmune disease
associated with long- lasting symptoms and delayed
complications? Ann Clin Immunol Microbiol. 2020; 2: 1014.
16. Wang EY, Mao T, Klein J, et al. Diverse functional autoantibodies
in patients with COVID-19. medRxiv preprint. 2020.
17. Lyons-Weiler J. Pathogenic priming likely contributes to serious
and critical illness and mortality in COVID-19 via autoimmunity.
Journal of Translational Autoimmunity. 2020; 3: 100051.
18. Tetz G, Tetz V. SARS-CoV-2 prion-like domains in spike
proteins enable higher affinity to ACE2. Preprint. 2020.
19. Young MJ, O’Hare M, Matiello M, et al. Creutzfeldt-Jakob
disease in a man with COVID-19: SARS-CoV-2-accelerated
neuro degeneration? Brain, Behavior, and Immunity. 2020; 89:
601-603.
© 2021 Classen JB. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License
