Pena V VDH W/ Exhibits A - F - Declaratory Judgement

IN THE CIRCUIT COURT OF THE CITY OF RICHMOND
ANTHONY PENA
PO BOX 8781
VIRGINIA BEACH, VA, 23450
Petitioner,
V. No. _____________________
COLIN GREENE,
in his official capacity as
State Health Commissioner of
Virginia Department of Health;
Madison Building
109 Governor Street
Richmond, Virginia 23219
VIRGINIA DEPARTMENT
OF HEALTH
Madison Building
109 Governor Street
Richmond, Virginia 23219
Respondents.
VERIFIED PETITION AT LAW FOR DECLARATORY JUDGMENT

July 21, 2022
Anthony Pena
fwdquestionshere@gmail.com
PO Box 8781Virginia Beach, VA 23452
(757) 690-1531
1
VERIFIED PETITION AT LAW FOR DECLARATORY JUDGMENT
COMES NOW, before this Honorable Court, Anthony Pena, pro se in
triformis, Executive Director, American Foundation for Informed Consent, a
Virginia limited liability company, and pursuant to the provisions of §8.01-184
state as follows:
JURISDICTION AND VENUE
1. This Court has jurisdiction to hear this matter, and power to issue
declaratory judgments pursuant to Virginia Code § 8.01-184.
2. See also Va. Code § 8.01-186 (authorizing further relief based on a
decree “whenever necessary or proper”).
3. Venue is appropriate under Va. Code § 8.01-261(2) because this is an
action “against one or more officers of the Commonwealth in an official capacity,”
each of whom has official offices in Richmond, Virginia.
PARTIES
4. Petitioner, Anthony Pena, pro se in triformis, Executive Director,
American Foundation for Informed Consent, a Virginia limited liability company
5. Respondent, Virginia Department of Health (VDH)
6. Respondent, Dr. Colin Greene, in his official capacity as State Health
Commissioner
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JUSTICIABLE CONTROVERSY
7. There is a justiciable controversy as to whether VDH must provide
Informed Consent as outlined in Va. Code. § 32.1-162.16 and § 32.1-162.18 for
vaccines provided via Emergency Use Authorization and still in phase 3 medical
trials (i.e. Human Research).
8. That an actual controversy exists is further demonstrated
by VDH Response to Plaintiff via email on 6/15/2022 (Exhibit C): “...no consent
forms are currently being used for COVID-19 vaccination…There are no federal
requirements for informed consent processes for non-research use of any
vaccines…”
9. There is also justiciable controversy as to whether or not the S1
subunit of the spike protein for SARS-CoV-2 is a biologic agent and/or toxin, as it
is a known causative agent of an HHS defined disability “Long Covid'' under the
Americans with Disabilities Act (ADA), as well as inducing other sequelae
appearing under 12VAC5-90-80. List of diseases that shall be reported:
*Coronavirus infection, severe; Hepatitis, other acute viral; *Unusual occurrence
of disease of public health concern.
10. That an actual controversy exists is further demonstrated by VDH
Response to Plaintiff via email on 6/21/2022 (Exhibit E): “We agree with your
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comment that the SARS-CoV-2 spike protein is closely related to the cause of
Long COVID.”
BACKGROUND
11. On August 15, 2021, Governor Northam Announce[d] COVID-19
Vaccine Requirement for State Workers; He said, “The only way to end this
pandemic is to [sic] for everyone to get vaccinated against COVID-19... The time
for waiting is over.”
12. The mandatory nature of participation in human research entailed in
Executive Directive Number Eighteen (2021) (ED-18) Ensuring a Safe Work Place
was rescinded on January 15, 2022, and replaced by ED-2 by Governor Youngkin.
13. On January 20th, 2022, Governor Younkin declared a temporary state
of emergency in EO-11 and concurrently announced his COVID-19 VACCINE
MARSHALL PLAN FOR VIRGINIA.
14. Currently, all publicly-available COVID vaccines have only
“Emergency Use Authorization” (“EUA”) status, and have not received full FDA
approval. Comirnaty, while approved, is NOT being distributed in the US.
15. Vaccines authorized under EUA require complete and voluntary
informed consent, meaning “providing policies allowing knowing and voluntary
agreement, without undue inducement or any element of force, fraud, deceit,
duress, or other form of constraint or coercion, of a person who is capable of
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exercising free power of choice” as defined in Va. Code § 32.1-162.16 and
expounded on § 32.1-162.18.
16. In the case of Human Research, which applies to all publicly-available
COVID vaccines, the “basic elements of information necessary to such consent”
(Basic Elements) shall include:
1. A reasonable and comprehensible explanation to the person
of the proposed procedures or protocols to be followed, their
purposes, including descriptions of any attendant discomforts,
and risks and benefits reasonably to be expected;
2. A disclosure of any appropriate alternative procedures or
therapies that might be advantageous for the person;
3. An instruction that the person may withdraw his consent and
discontinue participation in the human research at any time
without prejudice to him;
4. An explanation of any costs or compensation which may
accrue to the person and, if applicable, the availability of third
party reimbursement for the proposed procedures or protocols;
and
5. An offer to answer and answers to any inquiries by the
person concerning the procedures and protocols.
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17. There does NOT appear to be one example of all 5 “Basic Elements”
of informed consent required as defined in § 32.1-162.16 provided by any agency’s
(DHRM, VDH, DOLI, etc.) ministerial response to the Governor’s discretionary
executive actions, orders, or directives.
18. There appears to only be one department exempt eligible, and even if
deemed exempt the “Activities of the Virginia Department of Health (VDH) [shall
be] conducted pursuant to § 32.1-39” (A) “Where The Board [VDH] shall provide
for the surveillance of and investigation into all preventable diseases and epidemics
in this Commonwealth and into the means for the prevention of such diseases and
epidemics.”
19. Federal Courts have ruled noneconomic activity falls squarely within
the States’ police power. A person’s choice to remain unvaccinated and forego
regular testing is noneconomic activity. Cf. NFIB v Sebilius, 567 U.S. 519, 44 522
(2012) (Roberts, C.J., concurring); see also id. At 652-653 (Scalia, J., dissenting).
And to mandate that a person receive a vaccine or undergo testing falls squarely
within the States’ police power. Zucht v. King, 260 U.S. 174, 176 (1922)
20. The States’ police powers have been activated since the previous
governor’s mandate and now the stated goals of the current COVID-19 Vaccine
Marshall Plan for Virginia.
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FACTS
VDH Denied Informed Consent
21. Following notification of a decision on SCV# 211184, Plaintiff set to
work writing a document titled: S1-Spike Protein Causes PASC, Cytokine Storm, &
Long Covid. (Exhibit A)
22. On or About June 7th, Plaintiff notified VDH of his request for
Informed Consent and additional concerns via phone.
23. On or about June 15th, Plaintiff followed-up on the conversation, sent
initial concerns and Part One of Exhibit A to VDH Call Center Manager, Lee
Moreau via email. (Exhibit B)
24. The email (Exhibit B) notified VDH of a Healthcare-associated
infection related to a Reportable disease and requested designation of the
SARS-CoV-2 spike protein as a Toxic substance as defined 12VAC5-90-10.
Plaintiff requested Epidemiology be notified immediately to confirm the finding,
and Toxicology be notified for their designation under § 32.1-239 for any
substance known to produce this biologic toxin.
25. VDH Responded to Informed Consent request in writing on June 15,
2022 via email (Exhibit C) with “no consent forms are currently being used for
COVID-19 vaccination of the U.S. public. There are no federal requirements for
informed consent processes for non-research use of any vaccines. Details of this
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particular issue are available on the CDC website.”
(https://www.cdc.gov/vaccines/imz-managers/laws/)
26. The CDC Link VDH provided states, “For state and local regulations,
check with your local or state health department.” VDH cannot rely on federal
statute for implementation of State Police Powers. VDH cannot use the absence of
federal jurisdiction in providing Informed Consent as the reason and purpose for
absolving themselves of their duties according to state law.
27. VDH responded “Regarding ‘12VAC5-20-100 Informed consent’, this
also applies to purposes of human research. What is needed is that vaccine
recipients should have access to the fact sheets
(https://www.cdc.gov/vaccines/covid-19/eua/index.html) that discuss the risks and
benefits of the vaccine.” (Exhibit C)
28. The referenced fact sheets are NOT sufficient for Informed Consent as
per Va. Code § 32.1-162.16 and expounded on § 32.1-162.18.
29. “When FDA issues an EUA, it is providing an access mechanism to a
medical countermeasure needed for an emergency response. Under the
EUAs for COVID-19 vaccines, FDA provides maximum flexibility to
emergency response stakeholders (e.g., local, state, and federal public health
and response partners, as defined in the EUAs) by authorizing them to
identify or authorize the types of personnel and responders that would be the
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most appropriate to administer the product to specific populations and
identify the mechanism for authorizing such (e.g., standing order, executive
order, declaration, etc.) …”
(https://www.fda.gov/emergency-preparedness-and-response/mcm-legal-regulatory
-and-policy-framework/vaccine-eua-questions-and-answers-stakeholders)
30. Emergency Response Stakeholders, such as State Governments,
utilizing the access mechanism to distribute medical countermeasures for
COVID-19 must identify the mechanism for authorizing such according to State
Statute within their respective jurisdictions.
VDH Scope of Knowledge on Spike Protein Pathogenicity is Limited
31. VDH stated:
It is certainly true that the COVID-19 spike proteins are potentially harmful
to humans when they are on the outer surfaces of circulating SARS-CoV-2
viruses because those spikes facilitate adhesion of the virus to the surface of
human cells, thus facilitating the subsequent release of a very large number
of new virus particles. These new viral particles then get released into
nearby cells and tissues and into the bloodstream, which can sometimes
cause severe illness.
32. Exhibit A outlines countless observed harmful pathogenic responses
unrelated to adhesion of the cell. The idea that a spike protein may ONLY be
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harmful if facilitating the adhesion of COVID-19 while on the outer surfaces of
circulating SARS-CoV-2 viruses is erroneous. The S1 subunit of the COVID-19
spike protein for Alpha strain B.1.1.7 used as the “therapeutic target” for all
vaccines has been shown to induce Post Acute Severe/Sequelae of Covid (PASC)
on its own, such as Long Covid, absent any other viral particle associated with
SARS-CoV-2.
33. VDH explicitly outlined the limitations in their own knowledge that
Plaintiff’s Exhibit A fulfills when they stated, “...we acknowledge that there could
be some theoretical but as yet undocumented risk(s) associated with the
development and use of mRNA or any other vaccines.”
VDH Admits Spike Protein Associated with Long Covid
34. VDH was also unaware of S1 being the causative agent of Long
Covid on 6/15/2022 (Exhibit C) when they stated:
“Regarding your concern about a possible link between mRNA COVID-19
vaccination and Long COVID, VDH is unaware of any scientific or clinical
studies, either already published or still being reviewed for publication, that
indicate that a vaccine-related spike protein causes Long COVID. We would
be glad to review any studies on that issue that you can refer us to.”
35. For Long Covid, Plaintiff referred VDH to a scientific paper
(https://www.ncbi. nlm.nih.gov/pmc/articles/PMC8784688) and Long Covid
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lecture (https://youtu.be/ h2xyWiMS2Q0) provided by Dr. Bruce Patterson, CEO
of IncellDX, included in Exhibit A, who provided biomarkers for diagnosis, as
well as treatment regimens after improving over 30,000 Long Covid sufferers to
date. Dr. Bruce Patterson specifically cites the S1 subunit, while present in
non-classical monocytes, as the causative agent for Long Covid. (Exhibit D)
36. As a result VDH Responded to Plaintiff via email on 6/21/2022
(Exhibit E): “We agree with your comment that the SARS-CoV-2 spike protein is
closely related to the cause of Long COVID.”
37. On the CDC “Long COVID or Post-COVID Conditions” webpage
(https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects/), Below “What
you need to know”, inside a light blue box, CDC states, “As of July 2021, ‘long
COVID,’ also known as post-COVID conditions, can be considered a disability
under the Americans with Disabilities Act (ADA).”
38. CDC linked Guidance on “Long COVID” to HHS.gov Document
titled: Guidance on “Long COVID” as a Disability Under the ADA, Section 504,
and Section 1557.
(https://www.hhs.gov/civil-rights/for-providers/civil-rights-covid19/guidance-long-
covid-disability/index.html#footnote10_0ac8mdc)
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Causative Agents of Disabling Sequelae are Biologic Toxins
39. 12VAC5-90-280. Defines "Biologic agent" as any microorganism, or
infectious substance, or any naturally occurring, bioengineered, or synthesized
component of any such microorganism or infectious substance, capable of causing
death, disease, or other biological malfunction in a human…
40. 12VAC5-90-280. Defines "Toxin" as the toxic material or product
of… microorganisms (including but not limited to …viruses…); or infectious
substances; or a recombinant or synthesized molecule, whatever the origin and
method of production; and includes any poisonous substance or biological product
that may be engineered as a result of biotechnology or produced by a living
organism.
41. Within the S1 subunit itself there are 4 protein sequences of
pathogenic concern. The First is on the Receptor-Binding Domain (RBD) and
attaches to ACE2 receptors. The second, also on the RBD, is shown to interact
with a7 nAChR receptors of the Nicotine Cholinergic System (NCS), which is
highly indicated on the vagus nerve. The Third sequence is the N-Terminal
Domain, and the fourth sequence, with codons PRRA appearing on the Furin
Cleavage Site (FCS), is a patented human optimized MSH3 gene matching
Hermansky-Pudlak Syndrome, known to cause genetic repair dysregulation when
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binding with MSH2. The S1 subunit of SARS-CoV-2 spike protein is a biologic
toxin. (Exhibit A)
42. The Spike protein for SARS-CoV-2 has been shown to cause syncytia
& lymphocyte elimination; is an inflammagen causing fibrinogenic activity; may
cause amyloidogenesis, micro-clotting, thrombotic thrombocytopenia, ARDS &
cytokine storm; changes the shape of blood cells; may increase phospholipase
production, and lead to autoimmune disorders. The S1 subunit is specifically
known to be the causative agent of Long Covid when expressed in non-classical
monocytes as an antigen or vaccine induced immunogen. Antibody Dependent
Enhancement has been observed leading to pyroptosis, and chronic inflammation
with its own subset of pathogenic consequences as spike induced sequelae. The
Spike protein for SARS-CoV-2 is a biologic toxin. (Exhibit A)
Products Producing Toxins in the Body are Toxic Substances
43. 12VAC5-90-10. Defines "Toxic substance" as any substance,
including any raw materials, intermediate products, catalysts, final products, or
by-products of any manufacturing operation conducted in a commercial
establishment, that has the capacity, through its physical, chemical or biological
properties, to pose a substantial risk of death or impairment either immediately or
over time, to the normal functions of humans…
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44. 12VAC5-90-10. "Healthcare-associated infection" (also known as
nosocomial infection) means a localized or systemic condition resulting from an
adverse reaction to the presence of an infectious agent or agents or its toxin or
toxins that (i) occurs in a patient in a health care setting (e.g., pharmacy, a hospital
or outpatient clinic), (ii) was not found to be present or incubating at the time of
admission unless the infection was related to a previous admission to the same
setting, and (iii) if the setting is a hospital, meets the criteria for a specific infection
site as defined by CDC.
45. Therefore, Plaintiff has a right to receive informed consent of the
possibility of a healthcare associated infection (i.e. Long Covid, others named in
Exhibit A) due to a toxic substance still in Phase 3 Human Research Trials being
used in Virginia as a medical countermeasure for a pathogen of public health
threat.
46. A reasonable and comprehensible explanation to the person of the ...
risks and benefits reasonably to be expected MUST include a description of
adverse effects the spike protein causes, because the spike protein is the element
the vaccines are creating in the body. Risk benefit analysis must apply to any
proposed active agent in the body, as well as ANY currently available vaccine
ingredient, such as Lipid Nano-Particles (LNPs).
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47. Risk-Benefit analysis will also need to be placed in relation to the
current strains in natural circulation, and NOT SARS-CoV-2 Alpha strain B.1.1.7
because the B.1.1.7 is no longer in natural circulation.
WHEREFORE, Plaintiffs respectfully asks this Court for Relief to:
1. Declare Plaintiff’s right to receive informed consent from VDH for
EUA COVID19 vaccines as per state statute.
2. Declare Plaintiff’s right to receive informed consent S1 spike protein
is a biologic toxin.
3. Declare Plaintiff’s right to receive informed consent for any product
producing the SARS-CoV-2 spike protein in the body as a toxic
substance.
4. Declare Plaintiff’s right to receive notice of the possibility of a
healthcare associated infection for any product creating the Spike
protein for SARS-CoV-2
5. Declare Plaintiff’s right to sue VDH via mandamus, or any other legal
filing, to obtain fulfillment of declared statutory rights.
6. Any other relief this Court may find appropriate.
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Date: July 21st, 2022
Respectfully submitted,
_________________________
Anthony Pena
Pro Se In Triformis
Executive Director
American Foundation for Informed Consent
PO Box 8781
Virginia Beach, VA 23452
(757) 690-1531
The taking of evidence is NOT necessary for proper disposition of petition.
Verifications Follow.
Certifications Follow.
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VERIFICATION
Pursuant to VA. CODE § 8.01-4.3, I verify under penalty of perjury that the
foregoing is true and correct to the best of my knowledge.
______________________ ____________________________________
Date Anthony Pena
17
Anthony Pena
Pro Se In Triformis
Executive Director
PO Box 8781
(757) 690-1531
CERTIFICATE
1. On July 21, 2022, Petitioner certifies he requested service from Richmond
Sheriff's office to all Respondents.
2. On July 21, 2022, Petitioner certifies he requested service from Richmond
Sheriff’s Office to the Attorney General’s/Commonwealth Attorney’s Office.
______________________________
Anthony Pena
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EXHIBIT A
S1-Spike Protein Causes PASC,
Cytokine Storm, & Long Covid
An Analysis of Pathologies and Their Origin
By: Anthony Peña
For
https://fwdquestionshere.com/
(757) 690-1531
PO Box 8781
1
Introduction 4
Part 1: Spike Protein Sui Pathogenesis 5
Spike Protein Role in Natural Infection 5
Spike Protein Structure 6
Observed Pathogenicity of Spike Protein 8
Syncytia & Lymphocyte Elimination 11
S1 Inflammagen & Fibrinogenic Activity 12
Amyloidogenesis 14
Micro-Clotting 15
Thrombotic Thrombocytopenia 18
S1 - Alpha7 nAChR Activation 18
ARDS - Cytokine Storm 22
Sui Pathogenesis - Intermission 23
CDC “Harmless” Semantics? 24
PART 2: Blood Cells & Long Covid 26
Long-Term Changes to Blood Cells 26
Severe Covid & Phospholipase 28
Anti-idiotype Antibody & Autoimmunity 32
Long Covid & Non-Classical Monocytes 37
Antibody Dependent Enhancement 41
ADE Pyroptosis 47
NK Cells & ADCC 49
Chronic Inflammation & Cytokines 51
Phagocytosis & Chronic Inflammation 55
2
Immune Regulation & Chronic Inflammation 56
Cytokines & Neurodegeneration 58
Sequence of concern: FCS/PRRA/MSH3 60
PRRARS 65
Genetically Toxic Pathogen 66
Part 3: All About That Vaccine 67
Antibody Targets 68
Vaccine Types 69
mRNA and N1-methylpseudouridine-m1Ψ 69
Adenovirus Vector Vaccines 73
mRNA in Liver converting to DNA 76
Hepatitis (IN CHILDREN) 80
Vaccine Spike induced T-Cell Myocarditis 82
Vaccine Spike Immunogen in Plasma 83
Spike Mediated Pericyte Dysfunction 85
Vaccine Related Neurological Reactions 86
Prion-Like Spike Protein 86
Long Covid & The Vagus Nerve 92
N-Terminal Domain Toxicity 92
Lipid-NanoParticles 93
Pharmacokinetics & Pharmacodistribution 97
Reproductive 99
Innate Immune Suppression 102
3
Child Vaccine Negative All-Cause Efficacy 104
Th1-Th2 Pathways & CD8 Concentration 109
Public Health Gain of Function Research 110
Introduction
This report will cover the biomechanisms involved with the
Spike protein for SARS-CoV-2 as well as various pathogenic
responses it is known to elicit. We will begin with the natural
observation of the spike protein’s role in cellular infection and end
with an examination of the public health theory of using a vaccine
based on spike protein during an active pandemic. Individual
protein and genetic markers within the spike protein as well as
their effects will be provided. In the end, it will be completely
clear to anyone reading that the Spike protein for COVID-19 is
the causative agent for “Long Covid”, which the HHS labels as a
disability under the Americans with Disabilities Act (ADA), and
MUST be designated a biologic toxin, and informed consent for
vaccines expanded to include a warning for the possibility of a
Healthcare-associated infection.
Let us Begin with Natural Infection to grasp S1 sui pathogenesis.
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Part 1: Spike Protein Sui Pathogenesis
Spike Protein Role in Natural Infection

The role of the spike protein in natural infection is
well-known. A brief explanation of its properties help provide
context for understanding reported observations.
Coronavirus disease 2019 is caused by a novel coronavirus,

severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
The spike (S) protein of SARS-CoV-2, which plays a key role in
the receptor recognition and cell membrane fusion process, is
composed of two subunits, S1 and S2. The S1 subunit contains a
receptor-binding domain that recognizes and binds to the host
receptor angiotensin-converting enzyme 2, while the S2 subunit
mediates viral cell membrane fusion by forming a six-helical
bundle via the two-heptad repeat domain.
A large number of glycosylated S proteins cover the surface

of SARS-CoV-2 and bind to the host cell receptor
angiotensin-converting enzyme 2 (ACE2), mediating viral cell
entry. When the S protein binds to the receptor, TM protease
serine 2 (TMPRSS2), a type 2 TM serine protease located on the
host cell membrane, promotes virus entry into the cell by
activating the S protein. Once the virus enters the cell, the viral
5
RNA is released, polyproteins are translated from the RNA
genome, and replication and transcription of the viral RNA
genome occur via protein cleavage and assembly of the
replicase–transcriptase complex. Viral RNA is replicated, and
structural proteins are synthesized, assembled, and packaged in
the host cell, after which viral particles are released.
https://www.nature.com/articles/s41401-020-0485-4
The above link provides further details on the function and

structure of SARS for the purpose of finding a pharmacological
solution. However, the foundation of the solution the article
provides is based on preventing ACE2 binding, or the utilization of
spike as a therapeutic target. TMPRSS2, being a natural enzyme
necessary for cellular intrusion and therefore clinical infection,
listed in the article as “activating the S protein”, is a target
completely ignored.
Spike Protein Structure

The S1 subunit has 2 sections itself: Receptor Binding
Domain (RBD) and the N-Terminal Domain (NTD). RBD must be in
an “up” or “opened” position in order to bind with ACE2.
The fusion peptide (FP) (788–806 residues), heptapeptide

repeat sequence 1 (HR1) (912–984 residues), HR2 (1163–1213
6
residues), TM domain (1213–1237 residues), and cytoplasm
domain (1237–1273 residues) comprise the S2 subunit.
a Schematic representation of the SARS-CoV-2 spike.

b–c The S protein RBD closed and opened status.
d The S protein binds to ACE2 with opened RBD in the S1 subunit.
e The six-helix structure formed by HR1 and HR2 of the S2 subunit.
7
Observed Pathogenicity of Spike Protein
Acute lung injury (ALI) leading to acute respiratory distress
syndrome is the major cause of COVID-19 lethality.
Intratracheally instilled S1 subunit of SARS-CoV-2 spike protein
(S1SP) in K18-hACE2 transgenic mice that overexpress human
ACE2 [showed] signs of COVID-19-associated lung injury 72 h
later.
K18-hACE2 mice that received either saline or whole SP

exhibited little or no evidence of lung injury. Wild Type mice that
received S1SP exhibited a milder form of COVID-19 symptoms,
8
compared with the K18-hACE2 mice. Furthermore, S1SP, but not
full spike protein, decreased cultured human pulmonary
microvascular transendothelial resistance (TER) and barrier
function.
https://journals.physiology.org/doi/full/10.1152/ajplung.00223.2
021
Researchers Show How SARS-COV-2 Spike Protein Causes Ac…
https://youtu.be/BB9Tc6IEA4E
This is the first demonstration of a COVID-19-like response

by an essential virus-encoded protein by SARS-CoV-2 in vivo.
This mouse study serves as clinical evidence of the

pathogenic nature of the S1 spike protein on its own. Evidence of
decreased microvascular transendothelial resistance (TER) is AT
LEAST enough for a warning of this specific pathological result in
vivo. However, it is not the only study with pathogenic findings for
the spike protein.
Data reveals that S protein alone can damage endothelium,

manifested by impaired mitochondrial function and eNOS activity
but increased glycolysis. It appears that S protein in Endothelial
Cells(EC’s) increases redox stress which may lead to AMPK
(AMP-activated protein kinase) deactivation, MDM2 (murine
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double minute 2) upregulation, and ultimately ACE2
destabilization
Mitochondrial fragmentation caused by S1 binding to

ACE2 is an unbelievably important finding, as is the data showing
impairment of Endothelial Nitric Oxide Synthase (eNOS). eNOS
impairment means less Nitric Oxide (NO), which leads to
vasodilation impairment, an increase in VEGF (Vascular
endothelial growth factor) leading to increased localized cellular
proliferation, and reduced antithrombotic activity due to reduced
NO available to inhibit platelet activation. NO is also known to
inhibit Nuclear factor kappa B (NF-κB), which means NO’s
absence or inhibition may cause an increase in NF-kB, leading to
inflammation and increased binding of the immune system on the
cell.
Increased intracellular glycolysis: Glycolosis produces an

increase in reactive oxygen species (ROS). Not normally a cause
of concern on its own, but with reduced Nitric Oxide also comes a
reduction in Superoxide dismutase (SOD). Limited SOD means
less available to counteract ROS, especially when glycolysis is
elevated. ROS may reach such a level as to disrupt or destabilize
ACE2 receptors.
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AMPK is directly responsible for the creation of the ACE2
receptor in the cell. AMPK deactivation means the cell’s ability to
make the ACE2 receptor is inhibited. MDM2 is necessary to
express an ACE2 receptor on the cell surface. An upregulation of
MDM2 means any ACE2 receptor lucky enough to be created in an
already inhibitory environment is still going to have a hard time
making it to the cell membrane to function at all.
The ACE1/ACE2 receptor balance is responsible for the

inflammatory response. ACE1 is inflammatory in nature, and
ACE2 is anti-inflammatory in nature. If ACE2 is destabilized
intracellularly then inflammatory markers of ACE1 will become
dominant as well. Keep in mind all of these effects were observed
occurring due to the SPIKE PROTEIN ALONE.
https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.121.318
902
Spike Protein Cytotoxicity - COVID-19 Primarily A Vascular Di…
https://youtu.be/C6A7REhnOIE
Syncytia & Lymphocyte Elimination

Heterotypic cell-in-cell structures with lymphocytes inside
multinucleated syncytia are prevalent in the lung tissues of
coronavirus disease 2019 (COVID-19) patients. The expression of
the SARS-CoV-2 spike glycoprotein is sufficient to induce a rapid
(~45.1 nm/s) membrane fusion to produce syncytium, which
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could readily internalize multiple lines of lymphocytes to form
typical cell-in-cell structures, remarkably leading to the death of
internalized cells.
A unique bi-arginine motif with the polybasic S1/S2 cleavage

site (FCS) of SARS-CoV-2 spike glycoprotein was identified to be
capable of controlling this process by which syncytia, resulted
from SARS-CoV-2 infection, could target infiltrated lymphocytes
for internalization and CIC mediated death, contributing to
lymphopenia in the patients.
Syncytia are a single cell or cytoplasmic mass containing

several nuclei, formed by fusion of cells or by division of nuclei.
Lymphocytes, aka White blood Cells, play a protective role in your
immune system: B lymphocytes - T lymphocytes - Natural killer
cells. Lymphopenia (also called lymphocytopenia) is a disorder in
which your blood doesn’t have enough Lymphocytes (i.e. immune
cells, antibodies).
S1 Inflammagen & Fibrinogenic Activity

A study on the effect of isolated SARS-CoV-2 spike protein
S1 subunit showed it as a potential inflammagen sui generis.
Using scanning electron and fluorescence microscopy as well as
mass spectrometry, this study investigated the potential of (S1)
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inflammagen to interact with platelets and fibrinogen directly to
cause blood hypercoagulation. Using platelet-poor plasma (PPP),
it has been found that the spike protein interferes with blood flow.
Mass spectrometry also showed that when spike protein S1 is
added to healthy PPP, it results in structural changes to β and γ
fibrin, complement 3, and prothrombin. These proteins were
substantially resistant to trypsinization, in the presence of spike
protein S1.
Trypsinization is the process of cell dissociation using

trypsin, a proteolytic enzyme which breaks down proteins, to
dissociate adherent cells from the vessel in which they are being
cultured. Changes to fibrin structure made them adhere to
endothelial cells in a way natural processes are unable to remove
or dissolve.
Whereas SARS-CoV-2 is widely considered an airborne

respiratory virus, it is IMPOSSIBLE to ignore the effects on the
vascular system. The prevalence of pathologies resulting from S1
are now observed outside the cell with direct interaction and
mutation of fibrin proteins, which creates an additional set of
vascular pathologies.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8380922/
Clots | Blood Vessel Damage - This Is The Most Important Le…
https://youtu.be/ANmkIIxCQCw
13
*Reminder of the role S1 plays in natural infection: How it is
separated from the virus at the furin cleavage site (FCS) by
TMPRSS2, and remains outside of the cell after cellular intrusion
by the virus.
Further reading on Fibrinogen & Fibrin:

https://ashpublications.org/blood/article/126/17/1977/34431/Not
-fibrin-ogen-but-fibrinogen-or-fibrin
Amyloidogenesis
Amyloid fibril assays of peptide library mixtures and
theoretical predictions identified seven amyloidogenic sequences
within the S-protein. Three 20-amino acid long synthetic spike
peptides (sequence 192–211, 601–620, 1166–1185) fulfilled
three amyloid fibril criteria: nucleation dependent polymerization
kinetics by ThT, Congo red positivity, and ultrastructural fibrillar
morphology. Full-length folded S-protein did not form amyloid
fibrils, but amyloid-like fibrils with evident branching were formed
during 24 h of S-protein coincubation with the protease
neutrophil elastase (NE) in vitro.
NE efficiently cleaved (activated) S-protein, rendering

exposure of amyloidogenic segments and accumulation of the
amyloidogenic peptide 194–203, part of the most amyloidogenic
14
synthetic spike peptide. NE is overexpressed at inflamed sites of
viral infection.
Amyloidosis is associated with cerebral amyloid angiopathy,

blood coagulation disruption, fibrinolytic disturbance, FXII
Kallikrein/Kinin activation, and thromboinflammation, suggesting
potential links between S-protein amyloidogenesis and COVID-19
phenotypes.
https://pubs.acs.org/doi/10.1021/jacs.2c03925#
One major causal factor of Alzheimers disease is known to

be extracellular amyloid beta (Abeta) accumulated senile plaques.
Thus amyloidogenesis, as its own pathology caused by the
S1-subunit, may have additional cascading effects within human
physiology. In this context, amyloid cascade hypothesis,
neuroinflammation, oxidative stress, granulovacuolar
degeneration, loss of Wnt signaling, Abeta-related synaptic
alterations, prolonged calcium ions overload and NMDAR-related
synaptotoxicity, and damage signals hypothesis.
https://pubmed.ncbi.nlm.nih.gov/33539020/
Micro-Clotting
SARS-Cov-2-induced infection, the cause of coronavirus
disease 2019 (COVID-19), is characterized by unprecedented
15
clinical pathologies. One of the most important pathologies is
hypercoagulation and microclots in the lungs of patients.
During the progression of the various stages of the

COVID-19, markers of viral replication, as well as von Willebrand
factor (VWF) and fibrinogen depletion with increased D-dimer
levels and dysregulated P-selectin levels, followed by a cytokine
storm, are likely to be indicative of a poor prognosis. This poor
prognosis is further worsened as together with a substantial
deposition of microclots in the lungs. Plasma of COVID-19
patients also carries a massive load of preformed amyloid clots,
and there are also numerous reports of damage to erythrocytes,
platelets, and dysregulation of inflammatory biomarkers.
Receptor binding is certainly responsible for cell-mediated

pathologies, but does not itself explain the coagulopathies. Spike
protein, can however be shed, and it has been detected in various
organs, including the urinary tract. S1 proteins can also cross the
blood–brain barrier. Free S1 particles play a role in the
pathogenesis of the disease.
The fibrin(ogen) production serves like a biological net or

glue. The trapping of VWF itself has a host of known thrombolytic
implications - Von Willebrand factor (VWF) contributes to the
16
pathogenesis of atherosclerosis, the development of arterial and
venous thrombosis, and thromboembolic risks in people with
atrial fibrillation. VWF inhibition may lead to its own CDC defined
disease - https://www.cdc.gov/ncbddd/vwd/facts.html
https://www.sciencedirect.com/topics/medicine-and-dentistry/vo
n-willebrand-factor
Markers used to identify clotting factors become entangled

within the S1 induced fibrin structure, and will NOT show up on
normal lab tests searching for those markers. It is thus preferred
to conduct a TEG Scan (Thromboelastography), to determine the
prevalence of the S1 modified fibrin structures and presence of
microclots.
Research suggests starting antiplatelet and anticoagulants

early on, with professional care, during the initial acute phase if
possible. In dire or chronic cases apheresis may have a positive
outcome. Another suggestion was Heparin induced,
extracorporeal, lipoprotein/fibrinogen precipitation.
Interview with Dr. Resia Pretorius: LongCovid microclots (spi…

https://youtu.be/C8tzTmVwEpM
Details of Microclotting Papers By Prof. Resia Pretorius
https://youtu.be/fflt95jPUYM
17
Thrombotic Thrombocytopenia
Thrombotic thrombocytopenic purpura is a rare disorder that
causes blood clots (thrombi) to form in small blood vessels
throughout the body. These clots can cause serious medical
problems if they block vessels and restrict blood flow to organs
such as the brain, kidneys, and heart.
This is a disease where microclots lead to bleeding. This

diagnosis is the reason the FDA limited Johnson & Johnson
vaccines to over 18 year-olds. With everything preceding this, we
have laid the foundation for the set of S1 induced pathologies
leading to this life-threatening disorder.
https://www.cnbc.com/2022/05/05/fda-limits-use-of-jjs-covid-19
-vaccine-for-adults.html
S1 - Alpha7 nAChR Activation

Alpha7 nicotinic acetylcholine receptor (α7 nAChR) is an
important part of the cholinergic nerve system in the brain.
Moreover, it is associated with a cholinergic anti-inflammatory
pathway in the termination of the parasympathetic nervous
system.
18
AChR activation will influence enzyme acetylcholinesterase
(AChE) availability in the neurosynaptic cleft normally present to
quickly terminate the Acetylcholine (ACh) neurochemical signal.
Antagonists of α7 nAChR are a wide group represented by

conotoxin and bungarotoxin. Alzheimer’s disease drug memantine
acting as an antagonist in its side pathway belongs in this group.
Agonists of α7 nAChR are suitable for treatment of multiple
cognitive dysfunctions such as Alzheimer’s disease or
schizophrenia.
19
S1 epitope coincides with the well-described cryptic epitope
for the human antibody CR3022 and with the epitope for the
recently described COVA1-16 antibody.
The NCS is an important pathway which regulates the

response to inflammation. Its effects on macrophages and other
immune cells are mainly regulated by the vagus nerve and by
alpha7 nicotinic acetylcholine receptors (nAChRs). This so-called
“cholinergic anti-inflammatory pathway” has been found
beneficial in preventing inflammatory conditions such as sepsis
and Acute Respiratory Distress Syndrome (ARDS) in animal
models. Dysregulation of the NCS could therefore be a possible
cause for the uncontrolled inflammatory response in COVID-19.
20
SARS-CoV-2 S1 glycoproteins (A7J8L4, P0DTC2) with
Neurotoxin homolog NL1 (Q9DEQ3). SARS-CoV-2 Receptor
Binding Domain (RBD) (aa 306-527) Spike glycoproteins (the
domain through which the spike protein recognizes the ACE2 on
the host’s cell surface) neighboring to the ACE2 Receptor Binding
Motif (aa 437-508). This sequence is exposed while spike protein
is in a closed/down position and after S1 is cleaved.
https://www.biorxiv.org/content/10.1101/2020.08.20.259747v1.f
ull
21
ARDS - Cytokine Storm
Cytokines are any of a number of substances, such as
interferon, interleukin, and growth factors, which are secreted by
certain cells of the immune system and have an effect on other
cells.
Cytokine storm and cytokine release syndrome are

life-threatening systemic inflammatory syndromes involving
elevated levels of circulating cytokines and immune-cell
hyperactivation. Cytokine Storm is the clinical cause of mortality;
Its removal and reduction is the goal of any clinician.
https://www.cell.com/cell/fulltext/S0092-8674(20)31542-7
Synergism of TNF-α and IFN-γ Triggers Inflammatory Cell Death,
Tissue Damage, and Mortality in SARS-CoV-2 Infection and
Cytokine Shock Syndromes
https://youtu.be/qOLksb6PMoA
Acute respiratory distress syndrome (ARDS) is a serious lung

condition that causes low blood oxygen. People who develop
ARDS are usually ill due to another disease or a major injury.
In ARDS, fluid builds up inside the tiny air sacs of the lungs, and
surfactant breaks down.
https://www.nhlbi.nih.gov/health/ards
22
Pulmonary surfactant is a surface-active complex of
phospholipids and proteins formed by type II alveolar cells.[1] The
proteins and lipids that make up the surfactant have both
hydrophilic and hydrophobic regions. By adsorbing to the
air-water interface of alveoli, with hydrophilic head groups in the
water and the hydrophobic tails facing towards the air, the main
lipid component of surfactant, dipalmitoylphosphatidylcholine
(DPPC), reduces surface tension.
This may also be characterized as decreased cultured human

pulmonary microvascular transendothelial resistance (TER) and
barrier function as discussed earlier in “Observed Pathogenicity of
Spike Protein”. ARDS appears to be a lung diagnosis when S1
induced cytokines sui generis cascade into numerous
inflammatory pathologies.
Sui Pathogenesis - Intermission

“The Science” necessitates observable reality. Long Covid is
an extension of pathologies (Sequelae) occurring during the acute
phase via S1 sui pathogenesis. Inflammation has many
characteristics and consequences. Knowing the S1 sui
pathogenesis cascade provides a context to understand its
chronic phase, conditions, and sequelae.
23
Understanding acute S1-induced physiologies provides a
foundation to approach PASC (Post-Acute Severe Covid, aka
Post-Acute Sequelae Covid19), Long Covid, Multi-System
Inflammatory Syndrome (MIS-C), Myocarditis, Hepatitis, etc.
Diagnosing “inflammation” is akin to prescribing Motrin in

the military. Whereas specialists are trained to label inflammation
in an organ with a specific word, greater understanding needs to
be given to the characteristics and specific pathophysiologies
resulting in abnormal growth and function.
When the “experts” finally get around to telling you the

originating cascade for a host of chronic conditions now being
seen in the actuarial tables of life insurance agencies as a 40%
increase in all-cause mortality, rest assured you have already
read what you would expect them now to tell you…
https://thehill.com/changing-america/well-being/longevity/58873
8-huge-huge-numbers-death-rates-up-40-percent-over-pre/
CDC “Harmless” Semantics?

ALL VACCINES TARGET the S1 subunit for production.
24
For some reason the CDC refers to the spike protein as
“harmless”.
Knowing what we know now, how is it possible to call the spike

protein harmless?
Now we will go into the immune response, and finish with Long
Covid, which *spoiler alert* is caused by spike protein.
Please take a moment to digest this: How is it possible for S1 sui

pathogenesis to be known to “Average Person” using
peer-reviewed publicly available research and information, yet
25
NOT provided for Informed Consent by “public health experts”,
WHO officials, or other mandating entity?
S1 is a toxin
PART 2: Blood Cells & Long Covid

With a foundation in the S1 sui pathogenesis we will now
look at the blood, immune cells, and Long Covid. Chronic
conditions may be the result of secondary pathologies. Science
must always begin with natural observations to gain an
understanding of physiological mechanisms related to their
existence. With understanding comes methodologies of clinical
and/or diagnostic confirmation.
Long-Term Changes to Blood Cells

Scientists have observed significant changes in lymphocyte
stiffness, monocyte size, neutrophil size and deformability, and
heterogeneity of erythrocyte deformation and size. Although
some of these changes recovered to normal values after
hospitalization, others persisted for months after hospital
discharge, evidencing the long-term imprint of COVID-19 on the
body.
Change in physical form may happen at the phospho-lipid

bilayer cell membrane like TER, “inflammation”, a mutation in
26
genetics, or a change in microtubule (tubulin) genetic expression
and natural function. The authors hypothesize a “cytoskeleton,
responsible for determining cell function, has changed”; likely
referencing microtubule (tubulin) structures.
COVID-19 Causes Long-Term Blood Cell Changes

https://www.youtube.com/watch?v=721WMC5pZ5A
https://www.sciencedirect.com/science/article/pii/S00063495210
04549?via%3Dihub
27
‘We suspect that the immune cells’ cytoskeleton, which is
responsible for determining cell function, has changed,’ explains
Markéta Kubánková, lead author of the research article. In her
opinion, real-time deformability cytometry could potentially be
used routinely for diagnosing Covid-19, and even act as an early
warning system in the future for detecting as yet unknown
viruses with the potential of triggering a new pandemic.
https://www.fau.eu/2021/06/21/news/research/long-term-chang
es-to-blood-cells-triggered-by-covid-19-infection/
Severe Covid & Phospholipase

Analyzed blood samples from two COVID-19 patient cohorts
found that circulation of the enzyme – secreted phospholipase A2
group IIA, or sPLA2-IIA, – may be the most important factor in
predicting which patients with severe COVID-19 eventually
succumb to the virus.
Early lipidomic studies revealed that severe COVID-19

modifies the circulating lipidome, with decreases in plasma levels
of phospholipids and elevated quantities of lysophospholipids
(lyso-PLs), unesterified unsaturated fatty acids (UFAs), and
acylcarnitines. This lipidomic pattern suggests that severe
COVID-19 may be accompanied by cellular or circulating
28
phospholipase(s) that cleave intact phospholipids from cellular
and mitochondrial membranes to form lyso-PLs and UFAs.
Phospholipases are a ubiquitous group of enzymes that

share the property of hydrolyzing a common substrate,
phospholipid. Nearly all share another property; they are more
active in aggregated substrate above the phospholipids critical
micellar concentration (cmc). Phospholipases have low Activity
on monomeric substrate but become activated when the
substrate concentration exceeds the cmc. Their functions go
beyond their role in membrane homeostasis; they also function in
such diverse roles from the digestion of nutrients to the formation
of bioactive molecules. There are indications that a few
phospholipases may carry out a biological function independent of
their catalytic activity by binding to a regulatory membrane
receptor. Phospholipase-like proteins with toxic properties, which
lacked a functional catalytic site, are found in venoms. It is of
interest that most, but not all, phospholipases studied in detail
thus far are soluble proteins. The soluble nature of many
phospholipases suggests that their interaction with cellular
membranes is one of the regulatory mechanisms that exist to
prevent membrane degradation.
29
Page 211 -
https://books.google.com/books?id=EGMuwXqDbkcC&lpg=PP1&o
ts=pTMYwT1knM&dq=biochemistry%20of%20lipids%20lipoprotei
ns%20and%20membranes%20%22Moseley%20waite%22&lr&pg
=PA212#v=onepage&q=waite&f=false
Esterase-Phospholipase balance is important to cmc and

balance each other - if esterase dysregulation occurs, perhaps
due to excess a7 nAChR activation releasing AChRE into the
synaptic cleft, phospholipase will increase to counteract, and may
begin degrading the phospho-lipid bilayers making up every cell
membrane of every cell type in the body. Like a tailored biological
acid the body itself produces.
30
The role of the sPLA2-IIA enzyme has been the subject of
study for half of a century and it is "possibly the most examined
member of the phospholipase family," Chilton explained.
Charles McCall, lead researcher from the Wake Forest School

of Medicine on the study, refers to the enzyme as a "shredder" for
its known prevalence in severe inflammation events, such as
bacterial sepsis, as well as hemorrhagic and cardiac shock.
Previous research has shown how the enzyme destroys

microbial cell membranes in bacterial infections, as well as its
similar genetic ancestry with a key enzyme found in snake
venom.
The protein "shares a high sequence homology to the active

enzyme in rattlesnake venom and, like venom coursing through
the body, it has the capacity to bind to receptors at
neuromuscular junctions and potentially disable the function of
these muscles," Chilton said.
https://news.arizona.edu/story/venom-coursing-through-body-re
searchers-identify-mechanism-driving-covid-19-mortality
Is There Snake Venom in SARS-COV-2?
https://youtu.be/NjJeT1daDIE
31
Anti-idiotype Antibody & Autoimmunity
One way of thinking about the complexity of the immune
response is through the lens of anti-idiotype immune responses.
The Network Hypothesis, formulated in 1974 by Niels Jerne,
described a mechanism by which the antibody responses to an
antigen themselves induced downstream antibody responses
against the antigen-specific antibody.
Every antibody that is induced and specific for an antigen

(termed “Ab1” antibody) has immunogenic regions, particularly in
their variable-region antigen-binding domains, that are unique as
a result of genetic recombination of immunoglobulin variable,
diversity, and joining (VDJ) genes; VDJ recombination results in
new and therefore immunogenic amino acid sequences called
idiotopes, which are then capable of inducing specific antibodies
against Ab1 antibodies as a form of down-regulation.
However, these regulatory immune responses are also

capable of doing much more. The paratopes, or antigen-binding
domains, of some of the resulting anti-idiotype (or “Ab2”)
antibodies that are specific for Ab1 can structurally resemble that
of the original antigens themselves (like the spike protein). Thus,
the Ab2 antigen-binding region can potentially represent an exact
mirror image of the initial targeted antigen in the Ab1 response,
32
and Ab2 antibodies have even been examined for potential use as
a surrogate for the antigen in vaccine studies.
However, as a result of this mimicry, Ab2 (Anti-idiotype)

antibodies also have the potential to bind the same receptor that
the original antigen was targeting. Ab2 antibodies binding to the
original receptor on normal cells therefore have the potential to
mediate profound effects on the cell that could result in
pathologic changes, particularly in the long term — long after the
original antigen itself has disappeared.
https://www.nejm.org/doi/full/10.1056/NEJMcibr2113694
33
Whereas ACE2 will be the first anti-idiotype to come to
mind, it is also important to remember CR3022 and COVA1-16
antibody with the epitope for the recently described a7 nAChR.
There is also another sequence of concern, aside from ACE2 and
a7nAChR binding amino acid sequences, that we will get into
later…
34
Autoimmune Disease after Infection or Vaccine in Some (Arti…
https://youtu.be/kE9UUX7NV5Q
https://www.nobelprize.org/prizes/medicine/1984/jerne/lecture/
https://www.nobelprize.org/uploads/2018/06/jerne-lecture.pdf
https://health.ucdavis.edu/news/headlines/antibodies-mimicking-
the-virus-may-explain-long-haul-covid-19-rare-vaccine-side-effec
ts/2021/11
This anti-idiotype mechanism may help explain the Syncytial

Lymphocyte Elimination observed in Part 1: “… SARS-CoV-2 spike
glycoprotein was identified to be capable of controlling this
process by which syncytia, resulted from SARS-CoV-2 infection,
could target infiltrated lymphocytes for internalization and CIC
(cell-in-cell) mediated death, contributing to lymphopenia in the
patients.”
These studies show for the first time that ACE2 antibodies
are present after SARS-CoV-2 infection. This finding is consistent
with a hypothesis that ACE2 antibodies may be involved in a
process that leads to immune activation. While we do not have
data about the association of ACE2 antibodies and PASC in this
cohort, we hypothesize that antibodies could initiate a cascade of
effects that lead to the symptoms of PASC. (A cascade like was
shown in Part 1…)
35
It is important to note that when two antibodies combine,

the resulting “immune complex” may circulate until finally settling
on a tissue, which will then activate macrophages and cause
damage to the tissue or organ they are on.
There are a number of ways to manage this autoimmune

response from causing damage. Whereas treatment is NOT a
focus of this report, the below video reviews biological
mechanisms and potential management approaches.
Autoimmune disease caused by spike protein and potential m…
https://youtu.be/uuaz8CpnV7I
36
Long Covid & Non-Classical Monocytes
The recent COVID-19 pandemic is a treatment challenge in
the acute infection stage but the recognition of chronic COVID-19
symptoms termed post-acute sequelae SARS CoV-2 infection
(PASC) may affect up to 30% of all infected individuals. PASC is
synonymous with Long Covid.
The levels of both intermediate (CD14+, CD16+) and

non-classical monocytes (CD14Lo, CD16+) were significantly
elevated in PASC patients up to 15 months post acute infection
compared to healthy controls (P=0.002 and P=0.01,
respectively). A statistically significant number of non-classical
monocytes contained SARS-CoV-2 S1 protein in both severe
(P=0.004) and PASC patients (P=0.02) out to 15 months post
infection. Non-classical monocytes are capable of causing
inflammation throughout the body in response to
fractalkine/CX3CL1 and RANTES/CCR5.
37
HC, Healthy Control - Severe, Acute Covid - LH, PASC (Long Haul)
Classical monocytes have a circulating lifespan of

approximately one day before they either migrate into tissues,
die, or turn into intermediate and subsequently non-classical
monocytes. Non-classical monocytes expressing high levels of
CX3CR1 are involved in complement and Fc gamma-mediated
phagocytosis and antiviral responses.
During early stages of the disease, PASC group have

reduced classical monocyte and increased intermediate monocyte
percentages compared with healthy controls. There is an increase
in non-classical monocytes in PASC group 6-15 months post
infection, and higher percentages of intermediate and
non-classical monocytes at day 0 in severe cases, suggesting
38
augmented classical-intermediate-non-classical monocyte
transition in both groups but with different kinetics.
The clinical relevance of monocyte activation in COVID-19

patients and the significance of these cells as viral protein
reservoirs in PASC is supported by data reporting the presence of
S1 protein within non-classical monocytes. Viral particles
and/or viral proteins can enter monocyte subpopulations in
distinct ways, and this appears to be regulated differently in
individuals that will develop severe disease or PASC. Classical
monocytes are primarily phagocytes and express high levels of
the ACE-2 receptor.
The hallmark of PASC is the heterogeneity of symptoms

arising in a variety of tissues and organs. The CD14lo, CD16+, S1
protein+ monocytes could be preferentially recruited into
anatomic sites expressing fractalkine and contribute to vascular
and tissue injury during pathological conditions in which this
monocyte subset is expanded in non-classical monocytes
without S1 protein. Previously, CD16+ monocytes were
demonstrated to migrate into the brain of AIDS patients
expressing high levels of CX3CL1 (fractalkine) and SDF-1, and
mediate blood-brain barrier damage and neuronal injury in
HIV-associated dementia via their release of proinflammatory
cytokines and neurotoxic factors. Interestingly, a number of
39
papers have been written discussing the increased mobilization of
CD14lo, CD16+ monocytes with exercise. These data could help
to explain reports of worsening PASC symptoms in individuals
resuming pre-COVID exercise regimens.
It is important to note that the S1 protein detected in these

patients appears to be retained from prior infection or
phagocytosis of infected cells undergoing apoptosis and is NOT
the result of persistent viral replication. The S1 subunit itself,
while present in non-classical monocytes, is recognized as a
CAUSATIVE AGENT responsible for PASC, one of the most
chronically severe forms of Long Covid. That is why the US Dept.
of HHS has labeled Long Covid a disability under the Americans
with Disability Act (ADA).
Spike Proteins In Immune Cells - Dr. Bruce Patterson Discuss…
https://youtu.be/JwjJs5ZHKJI
Dr. Bruce Patterson outlines the pathophysiology of natural and

vaccine induced S1 protein caused PASC/Long Covid, biomarker
assays to diagnose, and treatment protocols used successfully on
27,000 patients to date.
Dr Bruce Patterson Presentation at Georgetown University on…
https://youtu.be/h2xyWiMS2Q0
40
Antibody Dependent Enhancement
In the defense against invading pathogens, Immunoglobulins
are formed by B cells. These bind the pathogen via their Fab
domains and subsequently activate both complement but also
immune cells by immunoglobulin (Fraction constant)
Fc-receptors. The largest portion are Immunoglobulin γ (IgG)
antibodies that mediate their effector functions through Fc
gamma receptors (FcγR)(CD16+) on myeloid (Granulocytes,
monocytes, macrophages, and dendritic cells (DCs) represent a
subgroup of leukocytes/lymphocytes) and Natural Killer (NK)
cells. Antibody dependent cellular cytotoxicity (ADCC) is one of
the major Fc-dependent effector functions of IgG, that is
particularly important in the clearance of viral infections and is
mostly mediated by NK cells. NK cells mediate ADCC through
binding of antibody opsonized target cells by membrane
expressed FcγRIIIa and induce cytotoxicity by releasing
granzymes and perforins stored in intracellular granules.
https://www.frontiersin.org/articles/10.3389/fimmu.2020.00740/
full
To block viral attachment to target cells, antibodies that

target the viral surface proteins specifically are secreted, which
bind and neutralize the viruses. However, in some viruses, the
binding of specific antibodies to viral surface proteins can
promote viral invasion into certain types of cell instead, and
41
enhance viral infection. This effect is called antibody-dependent
enhancement (ADE)
ADE happens in two main cases:

1. When viral-specific antibody promotes viral entry into
host monocytes/macrophages and granulocytes, and
2. When it enhances viral infection in cells via interplay
with the Fc receptor (FcR) and/or complement receptor.
Studies so far have presumed that there are five

mechanisms that underlie ADE and that various viruses work
under different mechanisms and are not necessarily facilitated by
a single mechanism.
1. The first mechanism of ADE is dependent on FcR. The viral

surface protein combines with the antibody to form a
virus–antibody complex. The complex strengthens viral
adhesion through interaction of the Fc portion on the
antibody and its receptor on the surface of particular cells.
2. Complement C3 is activated in the classical pathway through

the binding of antibody to viral surface protein, following
which the interaction between complement C3 and
corresponding receptor enhances viral adhesion in the form
of virus–antibody–complement complex
42
3. Virus–antibody complexes are combined by C1q, promoting
fusion between the viral capsule and cell membrane through
the deposition of the combination of C1q and its receptor.
4. The fourth mechanism of ADE is the suppression of the

expression of antiviral genes via the stimulation and
enhancement of certain target cell effects, such as
endocytosis, or the suppression of the antiviral genes, such
as those for tumor necrosis factor (TNF) and induced nitric
oxide synthase (NOS), hence helping the virus with
immunological escape.
5. The fifth mechanism of ADE is the enhancement of the

fusion of viruses and cells via a change in the conformation
of viral protein through its binding with antibody (Figure 1E).
This was found in HIV infection by Sullivan and co-workers.
Monoclonal antibodies recognize the glycoprotein gp120 on
the outer membrane of HIV and combine with one of its
subunits under a sub-neutralizing concentration. This then
induces a conformational change in the residual subunits
and promotes membrane fusion of viruses and target cells
via the activation of viral glycoprotein. The specific antibody
towards gp120 will also regulate the interaction between
gp120 and virus ligand CCR5.
43
44
Up until 2019, the mechanism of ADE in SARS-CoV remained
unclear. Then Chen et al. developed the first SARS vaccine in
2005, which encodes the complete SARS-CoV viral spike in the
modified attenuated poxvirus vector. It was found to induce the
production of large amounts of neutralizing antibodies (S-IgG)
soon after injection. Although these antibodies can effectively
reduce the viral load in the upper respiratory tract, they also
enhance lung injury. A positive correlation has been found
between the amount of neutralizing antibody in serum and the
degree of pathological injury in the lung. Further studies found
that the virus enters macrophages with the help of FcR during
ADE.
Antibody against SARS-CoV spike alters the function of M2

macrophages (non-classical monocytes) through binding with
FcR. Endocytosis of glycoprotein and immunodepression in
macrophages are then weakened while the enrichment of
cytokines increases. M1 macrophages, which should repair
pathological injury in the lung, then convert into cells that
promote inflammation. This conversion partially relies on the role
of FcγR. *SARS1
07311#fig0005
45
CD169+ macrophages have ACE2 and are susceptible to
SARS-CoV-2 infection. Both M1- and M2-type macrophages are
susceptible to SARS-CoV-2 infection. These observations are
likely linked by antibody-dependent enhancement of coronavirus
infection of macrophages. The pathophysiology of moderate and
severe SARS and COVID-19 diseases fits a proposed model of
antibody-dependent infection of macrophages as the key gate
step in disease progression from mild to moderate and severe
symptoms contributing to dysregulated immune responses
including apoptosis for some T cells/T cell lymphopenia,
proinflammatory cascade with macrophage accumulation, and
cytokine and chemokine accumulations in lungs with a cytokine
storm in some patients. Infected phagocytic immune cells may
enable the virus to spread to additional organs prior to viral
sepsis.
https://www.frontiersin.org/articles/10.3389/fimmu.2021.640093
/full
If macrophages become infected, Ivermectin is critical in

denying viral load transference into the nucleus for viral
replication. No other drug, currently in pharmacology, has
exhibited influence on this pathway. It must be approved for
those showing elevated humoral response, or antibody dependent
enhancement, in order to prevent cytokine storm, Severe COVID,
PASC, and Long Covid.
46
Cytokine Storm with ADE - Antibody-dependent Enhancemen…
https://youtu.be/qOLksb6PMoA
Non-neutralizing antibodies are what cause ADE.

Neutralizing antibodies prevent ADE. What are the implications of
continuously inducing vaccine-generated neutralizing antibodies
from a two year old strain no longer in natural circulation that
wane over time, in an environment of homologous endemic virae,
such as coronaviruses?
ADE Pyroptosis
Monocytes and macrophages are sentinel cells that sense
invasive infection to form inflammasomes that activate caspase-1
and gasdermin D, leading to inflammatory death (pyroptosis) and
the release of potent inflammatory mediators. About 6% of blood
monocytes of patients with COVID-19 are infected with
SARS-CoV-2. Monocyte infection depends on the uptake of
antibody-opsonized virus by Fcγ receptors (ADE Mechanism #1).
SARS-CoV-2 begins to replicate in monocytes, but infection

is aborted, and infectious virus is not detected in the
supernatants of cultures of infected monocytes. Instead, infected
cells undergo pyroptosis mediated by activation of NLRP3 and
AIM2 inflammasomes, caspase-1 and gasdermin D.
47
Moreover, tissue-resident macrophages, but not infected
epithelial and endothelial cells, from lung autopsies from patients
with COVID-19 have activated inflammasomes. Taken together,
these findings suggest that antibody-mediated SARS-CoV-2
uptake by monocytes and macrophages triggers inflammatory cell
death that aborts the production of infectious virus but causes
systemic inflammation that contributes to COVID-19
pathogenesis.
Increased chronic inflammation is associated with ageing

(inflammaging) and the comorbidities linked to severe disease,
and severe disease is linked to signs of inflammation. When
myeloid cells sense invasive infection, they activate
inflammasomes to sound an innate immune alarm.
Inflammasome activation is required to process and release
interleukin-1 (IL-1)-family cytokines, arguably the most potent
inflammatory mediators. However, activation of NF-κB, the TNF
receptor superfamily and T helper 17 (TH17) cell cytokines can
also cause severe inflammation. When inflammasomes sense
infection, they recruit the ASC adaptor and assemble into large
complexes that recruit and activate caspase-1, which in turn
processes IL-1 pro-cytokines and the pore-forming gasdermin D
(GSDMD) to disrupt the cell membrane, leading to cell death and
cytokine release. Pyroptotic cell membrane rupture releases
cytokines, chemokines and other alarmins that recruit immune
48
cells to infection sites. LDH release is pathognomonic for
pyroptosis and other forms of necrotic cell death and elevated
LDH is one of the best correlates of severe COVID-19.
Summary - ADE in Severe COVID Causing Massive Inflamma…
https://youtu.be/cH0FrweXwrs
NK Cells & ADCC

While immune responses of the adaptive immune system
have been in the focus of research, the role of NK (Natural Killer,
CD16+) cells in COVID-19 are extremely important. Antibody
opsonization is the process of antibody binding as a marker, and
awaiting an Fc-receptor to conduct elimination of the cell.
Antibody-dependent cellular cytotoxicity (ADCC) is the process
after recognition, by which phagocytes envelope, or NK cells
attack with perforins and granzymes. Perforins perforate the cell
membrane, granzymes, stored in granules, are then inserted to
“digest” the cell.
49
Serum samples from SARS-CoV-2 resolvers induced
significant CD107a-expression by NK cells in response to S1 and
NC, while serum samples from SARS-CoV-2-negative individuals
did not. Serum samples from individuals that received the
BNT162b2 vaccine induced strong CD107a expression by NK cells
that increased with the second vaccination and was significantly
higher than observed in infected individuals.
S1-specific CD107a responses by NK cells were significantly

correlated to NK cell-mediated killing of S1-expressing cells.
Interestingly, screening of serum samples collected prior to the
50
COVID-19 pandemic identified two individuals with cross-reactive
antibodies against SARS-CoV-2 S1, which also induced
degranulation of NK cells.
Taken together, these data demonstrate that antibodies

induced by SARS-CoV-2 infection and anti-SARS-CoV-2 vaccines
can trigger significant NK cell-mediated ADCC activity, and
identify some cross-reactive ADCC-activity against SARS-CoV-2
by endemic coronavirus-specific antibodies.
Natural Killer Cells and Antibody Dependent Cellular Cytotoxi…
https://youtu.be/GGl1pLaV2o0
Chronic Inflammation & Cytokines

Inflammation is the principal process used by the innate arm
to combat & clear out microbes or damaged cells due to;
infection, injury, cancer, environmental irritants, toxic
substances, sui pathogenesis, etc.
When there is a continual process of inflammation then

slowly the area damaged may get scarred with calcium or
amyloid deposits, leading to permanent damage. All tissues have
sentinel (sensor) cells, such as Dendritic cells, macrophages, and
mast cells. Sensor cells within the tissue have multiple functions:
51
1. Diagnose origin of tissue damage
2. Engage with foreign substance
3. Signal additional responses
Liver = Kupfffer’s cells, Spleen = Splenic macrophages,

Nervous = MicroGlia, Lungs = Alveolar Macrophages (Dust cells),
Peritoneum = Peritoneal Macrophages, Epithelial (Skin) Cells =
Langerhans cells; are system specific sentinel cells of the innate
arm of immunity.
Toll-like Receptors on sentinel cells, have two forms:

1. Damage Associated Molecular Pattern (DAMP)
2. Pathogen Associated Molecular Pattern (PAMPs)
Cellular material will initiate a response from DAMP. Foreign

substances, such as microbes, bacteria, and pathogens, trigger
PAMPs. The activation of toll-like receptors (DAMP, PAMPs) in
sentinel cells will cause the production of cytokines. If doctors
understand the pathologies associated with cytokines present in
the system, they will be better able to diagnose the nature of
disease, and formulate treatment solutions.
TNF, (Interleukin) IL-1, IL-6, IL-10, IL-12, IL-15, IL-18,

IL-23, IL-27, IFNα,β are all types of Cytokines. There are more.
52
Chemokines are specialized Cytokines principally resulting in
cellular recruitment to a site:
1. CCL2, 3, 4, 5, 11, 17, 19, 21, 22, 25, 27
2. CXCL 1, 8, 9, 10, 12, 13
3. XCL1 (Lymphotactin)
4. CX3CL1 (Fractalkines)
TNFα, IL-1, & IL-6 being the most critical. Most Cytokines
operate in a localized paracrine action. However, it is possible for
them to be released into the bloodstream and operate as an
endocrine, possibly causing a pathogenic cascade, anywhere
connected to the system.
For example: Interleukin has been shown to produce acute

phase reactant proteins in the Liver. Cytokines in the Brain can
affect temperature regulation in the hypothalamus. A humoral
response may be triggered in the bone marrow. These are all
distinct examples of what may happen when a disease enters a
chronic phase, and release of cytokines cascades into other
pathologies downstream of tissue undergoing infection, apoptosis,
pyroptosis, etc.
Cytokines have Three primary functions:
1. Regulate Local Innate/Inflammatory response
2. Inhibit Viral Replication
3. Activate Adaptive Arm of Immune System
53
The sequence of events of inflammation:
1. TLR/PRR/DAMP/PAMP sensory receptors detect damage

or pathogens, and begin releasing cytokines.
2. Permeability of nearby capillaries is increased and
dilated to open channels to areas of infection/damage.
3. Blood flow increases in the area and Antibodies,
Collectins, Complement proteins, pentraxins, etc begin
flowing into the site.
4. TNF & IL-1 act on epithelial cells to begin producing
ligands. Ligands (Integrins, E-Selectins, ICAM-1,
VCAM-1, etc) are specialized signal receptors for White
Blood Cell recruitment from blood vessels to affected
tissue.
5. White Blood Cells release cell adhesion molecules to
bind with ligands formed on the blood vessel.
6. Transmigration occurs when the ligand fuses with the
cell adhesion molecule and the White Blood Cell creates
a path from the blood vessel to enter the affected
tissue.
7. White Blood Cells then become inflammatory-infiltrate
and begin working in the affected area.
Chronic Inflammation (Lecture 1)
https://youtu.be/oy06PqhoaAg
54
Phagocytosis & Chronic Inflammation
Phagocytosis is the process of a cell internalizing (eating,
surrounding, etc.) a pathogenic substance for elimination. While
in a normal resting state phagocytes (macrophages and
neutrophils) are NOT producing cytokines or actively engaged in
elimination. Once activated after DAMP/PAMP receptor binding,
cytokines will be released and the phagocyte will envelop the
microbe.
In order for phagocytosis to occur, the pathogen/microbe will

need to be opsonized with antibodies. Fc Receptors on the
phagocyte bind with Fractional constant proteins of the antibody.
Complement factors, such as C3b, produced by the liver as an
acute phase reactant protein, may also bind to the microbe in
order to opsonize it just like an antibody.
When a pathogen is internalized by a phagocytosis, it will be

held in a vesicle called a Phagolysosome. Lysosomes, enzyme
packed vesicles within the phagocyte, will then fuse with the
Pathogenic phagolysosome and release its enzymatic contents.
Reactive Oxygen Species (ROS), critical in chronic inflammation,
are made to a greater extent in neutrophils, Nitric Oxide is made
to a greater extent in macrophages. Inducing Nitric Oxide
Synthase (iNOS) converts arginine to citrulline in order to
produce NO. Oxidase producing ROS are also activated by IFN-γ
55
and TLRs(DAMP/PAMP). If ROS and NO are unable to degrade the
pathogen inside the phagolysosome, the macrophage will become
“frustrated” and may self-select to Pyroptosis, leading to the
release of inflammatory cytokines into the body.
Chronic Inflammation - Pathogen Killing - Phagocytosis (Lect…
https://youtu.be/VaU0wf21cEU
Immune Regulation & Chronic

Inflammation
Immune system regulation between the innate and adaptive
(acquired) arms of immunity are meant to Amplify each other
until a pathogen or disease is eliminated, as well as to return
back to homeostasis when the threat has been dealt with.
Regulation helps prevent excessive activation and protect from
the immune system attacking on the body. The duration, location,
and intensity of the immune response need to be carefully
coordinated. If immune cells begin unnecessarily attacking our
own body then it may lead to an autoimmune induced state of
chronic inflammation.
Antigen tolerance development, immune exhaustion, genetic

factors, memory cells, and molecular mimicry all play a role in the
speed and nature of response, as well as duration of activity.
56
The adaptive arm of immunity begins when the innate arm
(macrophages & dendritic cells) present a protein from the
pathogen (antigen) to “Naive” CD4+ T-helper cells. If IL-4 is
present and IL-12 is absent, then the “Naive” CD4+ T-helper cell
will convert down the Th2 pathway, or humoral response, and
later convert into a B-Cell. If IL-12 is present, then the T-helper
cell will go down the Th1 pathway, and later convert to a
cytotoxic CD8+ Killer T-Cell.
Th17 and T-Reg cells are T-helper cells mainly geared toward
regulating the response of both the innate and adaptive arms of
immunity. IL-10 is an immuno-modulator of inhibition or
deactivation of the innate arm.
Suppressors of Cytokine Signaling (SoCS) receptors are

formed after innate arm activation of TLR (DAMP/PAMP), on the
cell itself. SoCS receptors are presented as a feedback
mechanism for the cell to deactivate the cell with an inhibitory
cytokine, such as IL-10. SoCS receptors, if activated, will inhibit
the Jak-stat signal pathway in the cell from functioning if the cell’s
cytokine receptors are activated, thus suppressing the production
and influence of cytokines within the cell. Every single cell has its
own regulatory mechanism.
57
IFN-γ, when released by Th1 cells, will upregulate the innate
arm and increase inflammation by raising the activity of major
histocompatibility complexes (MHC). MHC-2 is required for the
innate arm to present an antigen to the adaptive immune cells.
The more antigens to present, the higher the inflammation.
If a B-cell becomes active in generating antibodies after an

antigen binds to one of its antigen receptors, it may become
down-regulated if an Fc on an antibody-antigen complex binds to
an FcγRIIβ on the B-cell at the same time as the antigen it is
attached to. In this case, ITim would be activated in the B-cell,
thus inhibiting any further antigen binding. If there are any
mutations on either the Fc or the FcR preventing binding, then
there will be no inhibitory signal to stop production of antibodies
within the B-Cell.
Chronic Inflammation - Immune System Regulation (Lecture …
https://youtu.be/7reYtV-Ab0I
https://www.cell.com/cell/fulltext/S0092-8674(20)31542-7
Cytokines & Neurodegeneration

The dysregulation of cytokines and chemokines is a central
feature in the development of neuroinflammation,
neurodegeneration, and demyelination both in the central and
peripheral nervous systems and in conditions of neuropathic pain.
58
Pathological states within the nervous system can lead to
activation of microglia.
The latter may mediate neuronal and glial cell injury and
death through production of proinflammatory factors such as
cytokines and chemokines. These then help to mobilize the
adaptive immune response.
Although inflammation may induce beneficial effects such as

pathogen clearance and phagocytosis of apoptotic cells,
uncontrolled inflammation can result in detrimental outcomes via
the production of neurotoxic factors that exacerbate
neurodegenerative pathology. In states of prolonged
inflammation, continual activation and recruitment of effector
cells can establish a feedback loop that perpetuates inflammation
and ultimately results in neuronal injury.
A critical balance between repair and proinflammatory

factors determines the outcome of a neurodegenerative process.
In the field of neuroimmunology, the classical view that regarded
the central nervous system (CNS) as an immune-privileged site
by virtue of its shield, the blood brain barrier (BBB), has evolved
to a view of significant CNS-immune system interactions.
59
Cytokines and chemokines are involved in the regulation of
CNS-immune system interactions besides being important for the
coordination of immune responses throughout the body. They are
produced primarily not only by white blood cells or leukocytes but
also by a variety of other cells as a response to various stimuli
under both pathological and physiological conditions. In the
nervous system, cytokines and chemokines function as
neuromodulators and regulate neurodevelopment,
neuroinflammation, and synaptic transmission.
This review will focus on how cytokines and chemokines

affect neuroinflammation and disease pathogenesis in bacterial
meningitis and brain abscesses, Lyme neuroborreliosis, human
immunodeficiency virus encephalitis, and neuropathic pain.
Sequence of concern: FCS/PRRA/MSH3

Among numerous point mutation differences between the
SARS-CoV-2 and the bat RaTG13 coronavirus, only the
12-nucleotide furin cleavage site (FCS) exceeds 3 nucleotides. A
BLAST search revealed that a 19 nucleotide portion of the
SARS.Cov2 genome encompassing the furin cleavage site is a
100% complementary match to a codon-optimized proprietary
(patented) sequence that is the reverse complement of the
human mutS homolog (MSH3).
60
While numerous point mutation differences exist between
SARS-CoV-2 and RaTG13, only one insertion and dissimilarity
exceeding 3 nucleotides (nt): a 12-nucleotide insertion coding for
four amino acids (aa 681-684, PRRA) in the SARS-CoV-2 S
protein has been discovered. This polybasic FCS differentiates
SARS-CoV-2 from other b-lineage betacoronaviruses or any other
sarbecovirus. An FCS addition enhanced the infectivity of SARS
Co-V-2 in 2019. The absence of this FCS results in attenuated
SARS-CoV-2 variants useful for animal vaccination, accentuating
its relevance to human infection. This FCS is vital for human and
ferret transmission, expands viral tropism to human cells, and is
requisite for severe disease in two animal models of SARS-CoV-2.
61
A BLAST search for the 12-nucleotide insertion led to a
100% reverse match in a proprietary sequence (SEQ ID11652, nt
2751-2733) found in the US patent 9,587,003 filed on Feb. 4,
2016. It is important to note that gene do NOT have to be an
exact match in order to produce an identical protein. Codons are
sequences of 3 genes producing a protein. I have used the term
“homologous” in the past, and that is to indicate relation to two
proteins, even though the codons (genes) producing them may
be different.
The proprietary sequence SEQ ID11652, read in the forward

direction, encodes a 100% amino acid match to the human mut S
homolog 3 (MSH3). MSH3 is a DNA mismatch repair protein (part
of the MutS beta complex). SEQ ID11652 is transcribed to a
MSH3 mRNA that appears to be codon optimized for humans. We
62
did not find the 19-nucleotide sequence
CTCCTCGGCGGGCACGTAG in any eukaryotic or viral genomes
except SARS-CoV-2 with 100% coverage and identity in the
BLAST database.
Overexpression of MSH3 is known to interfere with mismatch

repair (MSH2 sequestration from the MutS alpha complex
comprising MSH2 and MSH6 results in MSH6 degradation and
MutS alpha depletion), which holds virologic importance.
Induction of DNA mismatch repair deficiency results in
permissiveness of influenza A virus (IAV) infection of human
respiratory cells and increased pathogenicity. Mismatch repair
deficiency may extend shedding of SARS-CoV-2.
https://www.frontiersin.org/articles/10.3389/fviro.2022.834808/f
ull#B15
MSH3, MSH2, and MSH6 are responsible for DNA repair. If

there is an imbalance of any of these genes then there may be
disruption, repair inhibition, or mutation of the host genome. At a
point of genetic damage, genetic repair will occur or the cell will
lose function. The primary genetic respondents to genetic
damage are MSH2 & MSH6. MSH3 is known to bind to MSH2. If
MSH2 is not available to bind with MSH6 for genetic repair, then
genetic dysregulation may occur.
63
An investigation must be conducted. MSH3 leads to more
severe disease, longer recovery times, and is carcinogenic. It is a
genetic pathogen.
Spike Genes Have Patented DNA Sequences. This is Dangero…
https://youtu.be/zPoZTtruaB0
The protein encoded by this MSH3 forms a heterodimer with

MSH2 to form MutS beta, part of the post-replicative DNA
mismatch repair system. MutS beta initiates mismatch repair by
binding to a mismatch and then forming a complex with MutL
alpha heterodimer. This gene contains a polymorphic 9 bp tandem
repeat sequence in the first exon. The repeat is present 6 times in
the reference genome sequence and 3-7 repeats have been
reported. Defects in this gene are a cause of susceptibility to
endometrial cancer.
https://www.ncbi.nlm.nih.gov/gene/4437
At this moment the idea of inducing MSH2 production may

seem advisable to counteract an abundance of MSH3. However,
the presence of MSH2 implies damage and usually induces the
creation of cytokines. MSH3, in this case, is a patented human
optimized genetic codon sequence, meant for oncology (cancer)
related proteins and peptides, that occured naturally in a wet
market…
64
PRRARS
Scientists scanned the human databases (Taxon 9606) and
found that the exact sequence PRRARS was present only in two
human proteins:
1. AAB17869.1, Hermansky-Pudlak syndrome protein

(HPS1) - Hermansky-Pudlak syndrome (HPS) is a rare,
hereditary disorder that consists of two characteristics:
decreased pigmentation (albinism) with visual
impairment, and blood platelet dysfunction with
prolonged bleeding. Some patients have lung fibrosis,
colitis, or an abnormal storage of a fatty-like substance
(ceroid lipofuscin) in various tissues of the body.
https://rarediseases.org/rare-diseases/hermansky-pudl
ak-syndrome/ , and
2. AAF79955.1, RhoGEF (RhoGEF domain is a structural

domain of guanine nucleotide exchange factors for
Rho/Rac/Cdc42-like GTPases. It is also called
"Dbl-homologous" (DH) domain.)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7833556/#appse
c1
65
Genetically Toxic Pathogen
I did not think I would find a patented protein when this
began. Much less a carcinogenic human codon optimized MSH3
gene that could cause genetic repair dysregulation. I believe
PRRA on the SARS-CoV-2 Spike protein furin cleavage site fits the
definition of a genetic toxin.
I can only imagine the wisdom in artificially creating the

spike protein intracellularly with human optimized mRNA known
to dysregulate genetic repair, with a technology capable of
infiltrating monocytes for reproduction. ADE was already found to
be an issue with this spike protein, but might as well give them a
head start…
Those saying the spike protein has been modified with

primers and prolines to prevent any of this from happening are
lying. 2 prolines have been added to keep the S2 subunit in a
prefusion/closed state ONLY. There have been NO
MODIFICATIONS when it comes to the S1 subunit, which is

the therapeutic target. If S1 is the therapeutic target then it
MUST be cleaved from S2 thus exposing the most pathogenic part
of SARS-CoV-2 within the cell.
66
Part 3 will be all about vaccines. Vaccines attempt to
stimulate your immune system, and you now have full context of
the immune mechanisms involved with generating the antibodies
necessary to “combat COVID19”. You also have full knowledge of
the toxic structure and effects. What we don’t know are every
possible mutagenic consequence of its application.
In this sense “Long COVID”, outside of ADE S1 infected

monocytes and chronic inflammation, may even be hereditary.
S1 is a toxin
Part 3: All About That Vaccine

mRNA, adenoviral vector as well as inactivated whole-virus
vaccines are now in widespread use, and a subunit vaccine is in a
final stage of authorization. They all rely on the native viral spike
protein (S) of SARS-CoV-2 for inducing potently neutralizing
antibodies, but the presentation of this key antigen to the
immune system differs substantially between the different
categories of vaccines.
In this part we will explore the way the vaccine presents the spike
protein, lipid nano-particles, as well as a review on how the public
67
policy of using a spike protein based vaccine during an active
SARS pandemic evolved.
Antibody Targets
The potency of antibodies depends on high-affinity
interactions with specific parts of the complex three-dimensional
structure of the spike in a native conformation.
B-cell humoral immunity is the target for “long-term”

immunity for any pathogen. Efficient formation of such antibodies
by B cells requires helper functions of CD4 T cells that are
specifically stimulated by peptides derived from the same antigen
in complex with MHCII molecules (innate immune system).
Other components of cellular immunity, such as CD8 T cells,

also contribute to immune responses after SARS-CoV-2 infection
or vaccination, although their role in COVID-19 infections and
protection from disease is still incompletely resolved.
It is a significant note to cite the role of CD8+ T-cells as

being “incompletely resolved”. Government agencies have been
using “Waning immunity” as the epidemiological purpose of
requiring booster shots. This recommendation is being forwarded
from the foundation of the loss of CD8+ T-cell concentration in
68
the blood. From part 2, we learned consistent exposure to an
antigen may prime the immune system for ADE. With that
knowledge, as well as the scientific admission that B-cell
immunity is preferred, what reason can a pharmaceutical
regulator allow for policy to be based on CD8+ T-cell
concentration?
Vaccine Types
Irrespective of vaccine type, all have to cope with the
intrinsic problem of conformational instability of the spike protein,
whether it is synthesized in the vaccinee after genetic vaccination
or in cell culture systems for production of conventional vaccines.
The first category type is mRNA and the second are

adenoviral vector vaccines, both of which do not contain the
spike protein but provide genetic information for its biosynthesis
in body cells of the vaccinee.
mRNA and N1-methylpseudouridine-m1Ψ

RNA vaccines contain fully functional mRNAs that can be
translated directly into the S protein. Additional biosynthetic steps
are required with adenovirus vector vaccines, including
intranuclear transcription of the vector DNA into RNA and
processing to generate functional mRNAs. It is believed that
69
muscle cells, fibroblasts, endothelial cells, and/or immune cells
such as dendritic cells contribute to the expression of S after
intramuscular vaccination
ER—endoplasmic reticulum; ERGIC—endoplasmic reticulum Golgi

intermediate compartment; TGN—Trans Golgi Network;
RNP—Ribonucleoprotein; Viral proteins: S—spike, M—membrane;
E—envelope; N—nucleoprotein.
BioNTech-Pfizer and Moderna contain codon-optimized

sequences for efficient expression of the full-length S protein and
use the authentic signal sequence for its biosynthesis. Both
constructs include the two stabilizing mutations in S2 (K986P and
V987P).
https://www.nature.com/articles/s41541-021-00369-6#Fig3
Both mRNA vaccines have modulated 5′ and 3′ untranslated

sequences to optimize mRNA stability and translation efficiency,
and all uridines are replaced by N1-methylpseudouridine (m1Ψ)
70
to further increase RNA stability and to reduce innate immune
responses.
Non-natural RNA nucleobase N1-methylpseudouridine

(m1Ψ); enhances immune evasion and protein production.
71
● A 5′-cap (m7(3′OMeG)(5′)ppp(5′)(2′OMeA)pG, commonly
referred to as trinucleotide “cap 1”) that helps recruit the
ribosome and protect the RNA from degradation.
● A 5′-untranslated region (UTR) derived from the human
α-globin mRNA with an optimized Kozak sequence that helps
drive high levels of translation from the correct start codon.
● A codon-optimized coding sequence that specifies production
of the transmembrane-anchored immunogenic SARS-CoV-2
spike glycoprotein.
● A 3′-UTR consisting of two sequences derived from the
amino-terminal enhancer of split mRNA and the
mitochondrial encoded 12S rRNA, which aids high levels of
protein expression by stabilizing the RNA.
● An unusual 3′-terminus consisting of two segmented
poly(adenosine) tracts. The poly(adenosine) stretches
increase mRNA stability, while the segmented structure
helps reduce unwanted recombination during plasmid
production.
It is important to note that in many studies, the specific

contributions of each of these mechanisms to mRNA
immunogenicity have not been explicitly defined. In such cases,
an mRNA modification may be exerting its activity by altering
antisense transcript synthesis, mRNA structure, immune
recognition, or some combination thereof.
72
Incorporation of m1Ψ increases the size and abundance of
polysomes, leading them to propose that the more rapid
translation initiation and slower elongation of m1Ψ mRNAs may
coordinately increase their half-life as well as induce productive
interactions with the ribosome.
Further studies provided support for a model in which

secondary structure in the coding sequence, which can be
enforced by m1Ψ, may increase mRNA functional half-life
independent of codon optimality.
While the modular nature of mRNA vaccines has led to

considerable enthusiasm, the combinatorial space of elements
that contribute to their activity (including caps, coding sequence,
codons, UTRs, and modifications) is massive in scale, and
relatively few RNA modifications have been comparatively
evaluated in a systematic manner.
https://pubs.acs.org/doi/10.1021/acscentsci.1c00197
Adenovirus Vector Vaccines

Compared to mRNA vaccines, adenovirus-vector vaccines
comprise several additional layers of complexity (including
production in mammalian cell cultures) that can lead to
heterogeneities of immune reactions and adverse effects.
73
Variations include (but are not limited to) the type of adenovirus
used as a vector (Janssen-Johnson&Johnson—human adenovirus
#26), genetic modifications of the vector, the cell lines used for
vaccine production, procedures for purification, and the specific
design of the gene for expressing S.
The current adenovirus-vaccine vectors are the replacement

of one of the early adenoviral genes (E1) for the full-length
SARS-Cov-2 S gene in the adenoviral DNA and the additional
deletion of E3. Production cell lines are derived from human
embryonic retinal cells (PER.C6) for the Janssen vaccine.
Although in vitro model studies with one of the current

adenovirus vector vaccines (ChAdOx1 nCoV-19) have shown that
S-coding transcripts dominate the transcription patterns, rare
aberrant splicing or polyadenylation site usage were observed.
Alternative splice events might lead to the formation of
C-terminally truncated and therefore soluble S protein. Such
secreted forms may bind to ACE2-expressing endothelial cells and
could contribute to thrombotic events via ADE mechanism.
Janssen vaccine contains the two prolines in S2 but and mutated
the S1/S2 furin cleavage site from 682-RRAS-685 to SRAG to
avoid conversion of S into the post-fusion structure.
https://www.nature.com/articles/s41541-021-00369-6#Tab1
74
75
mRNA in Liver converting to DNA
Preclinical studies of COVID-19 mRNA vaccine BNT162b2,
developed by Pfizer and BioNTech, showed reversible hepatic
effects in animals that received the BNT162b2 injection.
Furthermore, a recent study showed that SARS-CoV-2 RNA can
be reverse-transcribed and integrated into the genome of human
cells.
The safety profile of BNT162b2 is currently only available

from short-term clinical studies. Less common adverse effects of
BNT162b2 have been reported, including pericarditis, arrhythmia,
deep-vein thrombosis, pulmonary embolism, myocardial
infarction, intracranial hemorrhage, and thrombocytopenia.
In pharmacokinetics data provided by Pfizer to European

Medicines Agency (EMA), BNT162b2 biodistribution was studied in
mice and rats by intra-muscular injection with radiolabeled LNP
and luciferase modRNA. Radioactivity was detected in most
tissues from the first time point (0.25 h), and results showed that
the injection site and the liver were the major sites of
distribution, with maximum concentrations observed at 8–48 h
post-dose
Intracellular accumulation of LNP in hepatocytes (liver cells)

has been demonstrated in vivo. A preclinical study on BNT162b2
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showed that BNT162b2 enters the human cell line HEK293T
(kidney) cells and leads to robust expression of BNT162b2
antigen.
A previous study on mRNA vaccines against H10N8 and

H7N9 influenza viruses using a similar LNP delivery system
showed that the mRNA vaccine can distribute rather
nonspecifically to several organs such as liver, spleen, heart,
kidney, lung, and brain, and the concentration in the liver is
roughly 100 times lower than that of the intra-muscular injection
site. In the assessment report on BNT162b2 provided to EMA by
Pfizer, the pharmacokinetic distribution studies in rats
demonstrated that a relatively large proportion (up to 18%) of
the total dose distributes to the liver.
Liver cells also present the vaccine-derived SARS-CoV-2

spike protein, which could potentially make the liver cells targets
for previously primed spike protein reactive cytotoxic T cells.
There have been case reports on individuals who developed
autoimmune hepatitis after BNT162b2 vaccination.
BNT162b2 can be reverse transcribed to DNA in liver cell line

Huh7, and this may give rise to the concern if BNT162b2-derived
DNA may be integrated into the host genome and affect the
integrity of genomic DNA, which may potentially mediate
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genotoxic side effects. At this stage, we do not know if DNA
reverse transcribed from BNT162b2 is integrated into the cell
genome. Further studies are needed to demonstrate the effect of
BNT162b2 on genomic integrity, including whole genome
sequencing of cells exposed to BNT162b2, as well as tissues from
human subjects who received BNT162b2 vaccination.
Human autonomous retrotransposon LINE-1 (long

interspersed nuclear element-1) is a cellular endogenous reverse
transcriptase and the only remaining active transposon in
humans, able to retrotranspose itself and other nonautonomous
elements, and ~17% of the human genome are comprised of
LINE-1 sequences. A recent study showed that endogenous
LINE-1 mediates reverse transcription and integration of
SARS-CoV-2 sequences in the genomes of infected human cells.
Furthermore, expression of endogenous LINE-1 is often increased
upon viral infection, including SARS-CoV-2 infection.
Previous studies showed that LINE-1 retrotransposition

activity is regulated by RNA metabolism, DNA damage response,
and autophagy. Efficient retrotransposition of LINE-1 is often
associated with cell cycle and nuclear envelope breakdown during
mitosis, as well as exogenous retroviruses, which promotes
entrance of LINE-1 into the nucleus.
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It is worth noting that gene transcription is regulated by
chromatin modifications, transcription factor regulation, and the
rate of RNA degradation, while translational regulation of protein
involves ribosome recruitment on the initiation codon, modulation
of peptide elongation, termination of protein synthesis, or
ribosome biogenesis. These two processes are controlled by
different mechanisms, and therefore they may not always show
the same change patterns in response to external challenges.
The Pfizer EMA assessment report also showed that

BNT162b2 distributes in the spleen (<1.1%), adrenal glands
(<0.1%), as well as low and measurable radioactivity in the
ovaries and testes (<0.1%). No data on placental transfer of
BNT162b2 is available from Pfizer EMA assessment report.
Results showed that BNT162b2 mRNA readily enters Huh7

cells at a concentration (0.5 µg/mL) corresponding to 0.5% of the
local injection site concentration, induce changes in LINE-1 gene
and protein expression, and within 6 h, reverse transcription of
BNT162b2 can be detected.
https://www.mdpi.com/1467-3045/44/3/73/htm
Pfizer Vaccine Becomes DNA in Liver Cells. (In-vitro Swedish …
https://youtu.be/MjxlvduyJyc
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Hepatitis (IN CHILDREN)
Recently, there have been reports of children with a severe
acute form of hepatitis in the UK, Europe, the USA, Israel, and
Japan. No common environmental exposures have been found,
and an infectious agent remains the most plausible cause.
Hepatitis viruses A, B, C, D, and E have not been found in these
patients, but 72% of children with severe acute hepatitis in the
UK who were tested for an adenovirus had an adenovirus
detected, and out of 18 subtyped cases in the UK, all were
identified as adenovirus 41F. However, adenovirus 41F has not
previously been reported to cause severe acute hepatitis.
SARS-CoV-2 viral persistence in the gastrointestinal tract

can lead to repeated release of viral proteins across the intestinal
epithelium, giving rise to immune activation. Such repeated
immune activation might be mediated by a superantigen motif
within the SARS-CoV-2 spike protein that bears resemblance to
Staphylococcal enterotoxin B, triggering broad and non-specific
T-cell activation. This superantigen-mediated immune-cell
activation has been proposed as a causal mechanism of
multisystem inflammatory syndrome (MIS-C) in children.
Acute hepatitis has been reported in children with

multisystem inflammatory syndrome, but co-infection of other
viruses was not investigated. We hypothesize the recently
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reported cases of severe acute hepatitis in children could be a
consequence of adenovirus infection with intestinal trophism in
children previously infected by SARS-CoV-2 and carrying viral
reservoirs.
In mice, adenovirus infection sensitizes to subsequent

Staphylococcal-enterotoxin-B-mediated toxic shock, leading to
liver failure and death. This outcome was explained by
adenovirus-induced type-1 immune skewing, which, upon
subsequent Staphylococcal enterotoxin B administration, led to
excessive IFN-γ production and IFN-γ-mediated apoptosis of
hepatocytes (liver cells).
Suggestion is that children with acute hepatitis be

investigated for SARS-CoV-2 persistence in stool, T-cell receptor
skewing, and IFN-γ upregulation, because this could provide
evidence of a SARS-CoV-2 superantigen mechanism in an
adenovirus-41F-sensitized host. If evidence of
superantigen-mediated immune activation (i.e. ADE) is found,
immunomodulatory therapies should be considered in children
with severe acute hepatitis.
01662
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COVID19 vaccination can elicit a distinct T cell-dominant
immune-mediated hepatitis with a unique pathomechanism
associated with vaccination induced antigen-specific
tissue-resident immunity requiring systemic immunosuppression.
02343
Spike Protein and Mysterious Hepatitis in Children (Research …
https://youtu.be/mpls43FaMaw
Vaccine Spike induced T-Cell Myocarditis

In a cohort study of 23.1 million residents across 4 Nordic
countries, risk of myocarditis after the first and second doses of
SARS-CoV-2 mRNA vaccines was highest in young males aged 16
to 24 years after the second dose. For young males receiving 2
doses of the same vaccine, data were compatible with between 4
and 7 excess events in [only the first] 28 days per 100 000
vaccinees after second-dose BNT162b2, and between 9 and 28
per 100 000 vaccinees after second-dose mRNA-1273.
https://jamanetwork.com/journals/jamacardiology/fullarticle/279
1253
Clinical markers of T-Cell cardiac infiltration and damage

have been shown to numerically increase and raise PULS scores
from 11% to 25% for 5-year risk of Acute Coronary Syndrome
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(ACS) in a clinical setting of post-vaccinated patients. 11% to
25% is more than 100% increased risk after vaccination.
https://www.ahajournals.org/doi/abs/10.1161/circ.144.suppl_1.1
0712
The S protein may elicit vascular cell dysfunction through

CD147, independently from the infection. A recombinant S
protein alone elicits cellular signaling through the CD147 receptor
in cardiac pericytes, thereby inducing cell dysfunction and
microvascular disruption.
Soluble S protein can potentially propagate damage to

organs distant from sites of infection, promoting microvascular
injury. Blocking the CD147 receptor in patients may help protect
the vasculature not only from infection, but also from the
collateral damage caused by the S protein.
https://portlandpress.com/clinsci/article/135/24/2667/230273/Th
e-SARS-CoV-2-Spike-protein-disrupts-human
SARS-COV-2 Spike Damages Heart Tissue and Vessels (IN-VI…
https://youtu.be/QZyBUmuIQP4
Vaccine Spike Immunogen in Plasma

SARS-CoV-2 proteins were measured in longitudinal plasma
samples collected from participants who received two doses of
mRNA-1273 vaccine. 84% of Participants showed detectable
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levels of S1 spike protein as early as day 1 after first vaccine
injection. Clearance of detectable SARS-CoV-2 protein correlated
with production of immunoglobulin G (IgG) and immunoglobulin A
(IgA).
https://academic.oup.com/cid/article/74/4/715/6279075?login=f
alse
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Spike Mediated Pericyte Dysfunction
ACE2 expression in human brain vascular pericytes was
increased upon S protein exposure. Pericytes exposed to S
protein underwent profound phenotypic changes associated with
an elongated and contracted morphology accompanied with an
enhanced expression of contractile and myofibrogenic proteins,
such as α-smooth muscle actin (α-SMA), fibronectin, collagen I,
and neurogenic locus notch homolog protein-3 (NOTCH3); Is this
Ceroid Lipofuscin?
On the functional level, S protein exposure promoted the

acquisition of calcium (Ca2+) signature of contractile
ensheathing pericytes characterized by highly regular oscillatory
Ca2+ fluctuations. Furthermore, S protein induced lipid
peroxidation, oxidative and nitrosative stress in pericytes as well
as triggered an immune reaction translated by activation of
nuclear factor-kappa-B (NF-κB) signaling pathway, which was
potentiated by hypoxia, a condition associated with vascular
comorbidities that exacerbate COVID-19 pathogenesis. S protein
exposure combined to hypoxia enhanced the production of
pro-inflammatory cytokines involved in immune cell activation
and trafficking, namely macrophage migration inhibitory factor
(MIF).
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Collectively, these findings suggest that SARS-CoV-2 S
protein impairs the vascular and immune regulatory functions of
brain pericytes, which may account for vascular-mediated brain
damage.
Vaccine Related Neurological Reactions

Various peripheral neuropathies, particularly those with
sensory and autonomic dysfunction may occur during or shortly
after acute COVID-19 illnesses. These appear most likely to
reflect immune dysregulation. Observational studies suggest that
a variety of neuropathic symptoms may manifest after
SARS-CoV-2 vaccinations and in some patients might be an
immune-mediated (ADE) process.
https://www.medrxiv.org/content/10.1101/2022.05.16.22274439
v1
First Ever NIH/NIND Study on Vaccine Caused Neurological I…
https://youtu.be/9XGpe6MTaFg
Prion-Like Spike Protein

Prion diseases are a collection of neurodegenerative diseases
that are induced through the misfolding of important bodily
proteins, which form toxic oligomers that eventually precipitate
out as fibrils causing widespread damage to neurons. The CDC
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website on prion diseases states that “prion diseases are usually
rapidly progressive and always fatal.” It is now believed that
many neurodegenerative diseases, including Alzheimer’s,
Parkinson’s disease, and amyotrophic lateral sclerosis (ALS) may
be prion diseases, and researchers have identified specific
proteinaceous infectious particles linked to these diseases
(Weickenmeier et al., 2019).
Prion proteins become toxic when the α-helices misfold as

β-sheets, and the protein is then impaired in its ability to enter
the membrane (Prusiner, 1982). Glycines within the glycine zipper
transmembrane motifs in the amyloid-β precursor protein (APP)
play a central role in the misfolding of amyloid- β linked to
Alzheimer’s disease (Decock et al., 2016). APP contains a total of
four GxxxG motifs.
When considering that the SARS-CoV-2 spike protein is a

transmembrane protein, and that it contains five GxxxG motifs in
its sequence, it becomes extremely plausible that it could behave
as a prion. A paper published by J. Bart Classen (2021) proposed
that the spike protein in the mRNA vaccines could cause
prion-like diseases, in part through its ability to bind to many
known proteins and induce their misfolding into potential prions.
Idrees and Kumar (2021) have proposed that the spike protein’s
S1 component is prone to act as a functional amyloid and form
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toxic aggregates. These authors wrote that S1 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.” According to Tetz and Tetz
(2020), the form of the spike protein in SARS-CoV-2 has prion
regions that are not present in the spike proteins for other
coronaviruses.
Parkinson’s disease is a neurodegenerative disease

associated with Lewy body deposits in the brain, and the main
protein found in these Lewy bodies is α-synuclein. There are
many parallels between α-synuclein and the spike protein,
suggesting the possibility of prion-like disease following
vaccination. We have already shown that the mRNA in the vaccine
ends up in high concentrations in the liver and spleen, two organs
that are well connected to the vagus nerve. The cationic lipids in
the vaccine create an acidic pH conducive to misfolding, and they
also induce a strong inflammatory response, another predisposing
condition.
Germinal centers are structures within the spleen and other

secondary lymphoid organs where follicular dendritic cells (innate
immune system) present antigens to B cells, which in turn perfect
their antibody response. Researchers have shown that mRNA
vaccines, in contrast with recombinant protein vaccines, elicit a
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robust development of neutralizing antibodies at these germinal
centers in the spleen (Lederer et al., 2020). However, this also
means that mRNA vaccines induce an ideal situation for prion
formation from the spike protein, and its transport via exosomes
along the vagus nerve to the brain.
Studies have shown that prion spread from one animal to

another first appears in the lymphoid tissues, particularly the
spleen. Differentiated follicular dendritic cells are central to the
process, as they accumulate misfolded prion proteins (Al-Dybiat
et al., 2019). An inflammatory response upregulates synthesis of
α-synuclein in these dendritic cells, increasing the risk of prion
formation. Prions that accumulate in the cytoplasm are packaged
up into lipid bodies that are released as exosomes (Liu et al.,
2017). These exosomes eventually travel to the brain, causing
disease.
https://dpbh.nv.gov/uploadedFiles/dpbhnvgov/content/Boards/BO
H/Meetings/2021/SENEFF~1.PDF
https://rumble.com/vsm3vh-covid-shots-could-cause-crippling-ne
urodegenerative-disease-in-young-people.html
https://www.mdpi.com/2076-2607/10/2/280/htm
https://www.americaoutloud.com/alarming-new-data-confirms-co
vid-vaccine-link-to-fatal-brain-disorder/
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A prion is a type of protein that can trigger normal proteins
in the brain to fold abnormally. Prion diseases can affect both
humans and animals and are sometimes spread to humans by
infected meat products. The most common form of prion disease
that affects humans is Creutzfeldt-Jakob disease (CJD).
https://www.hopkinsmedicine.org/health/conditions-and-diseases
/prion-diseases
The number of Creutzfeldt-Jacob Disease (CJD)/prion

disease reports in VAERS since the deployment of the COVID-19
injections has far surpassed the background rate for the U.S. for
the year. Prion proteins or cellular prion proteins (PrPc), are
native to humans, are in our brains, and expressed all the time.
When these particular proteins mis-fold, then, Houston, we have
a problem. These mis-folded proteins are called prions
(mis-folded prion protein (PrPSc - Sc is for Scrapie2 3)) and are
associated with neuro-degenerative diseases like Alzheimer’s
disease. It seems that they can transform or ‘teach’ other prion
proteins to mis-fold (transmissible), as well. It’s not really
teaching as much as proximal disallowance of proper folding. This
‘enables’ an autocatalytic reaction whereby the PrPSc catalyzes
the mis-folding of PrPc to produce more PrPSc due to the fact that
prions are resistant to proteolysis - the process of ‘removal’ of
mis-folded proteins.
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https://jessicar.substack.com/p/rsfiedllfnkv-are-we-looking-at-we
aponized?s=r
S1 Spike Protein meets the definition of a prion:

1. S1 when binding to ACE2 causes inflammation, down
regulates ACE2 formation, and ACE2 expression on the cell
surface, thus upregulating ACE1.
2. a7 nAChR may also be activated. If AChEsterase
concentration exceeds cmc then Phospholipase concentration
may “misfold” the phospho-lipid bilayer cell membrane.
3. If MSH3 PRRA interacts with MSH2 at the site of neural
genetic repair, or begins generating amyloid ceroid lipofuscin
a la hermansky-pudlak syndrome sui generis in the brain
misfolding platelets in an observed fibrinogenic characterized
response, then S1 is a prion.
4. If cytokine concentration from pyroptosis occurs in the
microglia of the nervous system and degrades the myelin
sheath, thus leading to a “misfolding” of neurons, then S1 is
a prion.
5. Research has also shown a displacement of zinc ions from
the protein structure when S1 binds to ACE2, which causes
them to misfold. The Displaced Zinc may further displace
zinc embedded in other protein structures leading to further
misfolding of proteins.
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Long Covid & The Vagus Nerve
Findings point at vagus nerve dysfunction as a central
pathophysiological feature of long COVID. Some of the most
common symptoms of long COVID include fatigue, headaches,
shortness of breath, loss of smell and taste, and muscle
weakness. In a pilot evaluation, most long COVID subjects with
vagus nerve dysfunction symptoms had a range of significant,
clinically-relevant, structural and/or functional alterations in their
vagus nerve, including nerve thickening, trouble swallowing, and
symptoms of impaired breathing," Findings so far thus point at
vagus nerve dysfunction as a central pathophysiological feature of
long COVID.
https://www.zerohedge.com/covid-19/breakthrough-research-fin
ds-link-between-long-covid-and-vagus-nerve-damage
https://www.jpost.com/health-and-wellness/article-696452
N-Terminal Domain Toxicity

Zebrafish injected with fragment 16 to 165 (rSpike), which
corresponds to the N-terminal portion of the protein, presented
mortalities and adverse effects on liver, kidney, ovary and brain
tissues. The conserved genetic homology between zebrafish and
humans might be one of the reasons for the intense toxic effects
followed inflammatory reaction from the immune system of
zebrafish to rSpike which provoked damage to organs in a similar
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pattern as happen in severe cases of COVID-19 in humans, and,
resulted in 78.6% of survival rate in female adults during the first
seven days. The application of spike protein in zebrafish was
highly toxic that is suitable for future studies to gather valuable
information about ecotoxicological impacts, as well as vaccine
responses and therapeutic approaches in human medicine.
Lipid-NanoParticles
Lipid nanoparticles are next generation liposomes that use
nanotechnology and are well suited to stable and efficient delivery
of various therapeutics. Liposomes are closed lipid bilayer vesicles
that spontaneously form in water (see fig. 1A) – essentially a
fatty capsule. They were discovered in the 1960s and their
potential as effective drug delivery systems was almost
immediately recognized.
Liposomes have proven to be an extremely versatile

nanocarrier platform because they can transport either
hydrophilic drugs within the enclosed aqueous interior, or
hydrophobic drugs within the hydrocarbon chain region of the
lipid bilayer
93
To enhance tissue targeting, the liposomes’ surface may be
modified with ligands or antibodies which allow the liposome to
recognise and bind to specific receptors on the cells. These are
referred to as immunoliposomes.
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To improve longevity in the blood stream, the surface may
be coated in biocompatible inert polymers such as PEG, which
goes undetected, like in the current Covid mRNA vaccines.
Presently, the most widely used non-viral vector system

includes a synthetic positively charged (cationic) lipid. These form
stable complexes known as lipoplexes with negatively charged
(anionic) nucleic acids. Decorated by positively charged lipids,
nucleic acids are more stable and resistant to nuclease
degradation.
Despite their clear advantages for drug delivery, lipid

nanoparticles have an unwanted side-effect; they have the
potential to induce an allergic reaction, particularly for those who
suffer with severe allergies. Researchers estimate a rate of 1.1
cases of anaphylaxis for every million first doses of the
Pfizer/BioNTech COVID-19 vaccine.
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https://www.cas.org/resource/blog/understanding-nanotechnolog
y-covid-19-vaccines
LNPs used in many preclinical studies are highly

inflammatory in mice. Intradermal injection of these LNPs led to
rapid and robust inflammatory responses, characterized by
massive neutrophil infiltration, activation of diverse inflammatory
pathways, and production of various inflammatory cytokines and
chemokines. The same dose of LNP delivered intranasally led to
similar inflammatory responses in the lung and resulted in a high
mortality rate.
The intradermal inoculation of LNPs in mice led to the

secretion of large amounts of major and minor pyrogens,
IL-1β/IL-6 and macrophage inflammatory protein-α (CCL3) and
macrophage inflammatory protein-β (CCL4), respectively (Figures
2B and 2C). Furthermore, the observed activation of other
inflammatory pathways and cell death could further accentuate
the experienced side effects. However, further studies will be
needed to determine the exact nature of the inflammatory
responses triggered by mRNA-LNP vaccines in humans and how
much overlap there might be with the inflammatory signatures
documented here for mice.
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Pharmacokinetics &
Pharmacodistribution
Initially, 21 male rats were dosed at 100 ug mRNA/animal.
Some adverse clinical signs were observed after approximately 24
hours post-dose and a subsequent review of the data showed
concentrations were well detected in tissues. After discussions
with the Sponsor, the target dose level was lowered to 50 ug
mRNA/animal by amendment for the remainder of the study.
18.05% of the 50 ug dose accumulates in the liver after just

8 hours and remains at this concentration up to the 48-hour
mark. It is unknown if this plateau trend continued or if the
increase in percentage injected amount continued. The target
dose level is 50 ug mRNA per animal with 1.29 mg total lipid per
animal. So this means that the liver cells that contained the lipids
had accumulations of 9 ug of mRNA and 0.23 mg of total lipid
after just 8 hours.
Although greatest mean tissue concentration remained at

the injection site, biodistribution was clearly demonstrated and
lipids were found in high concentrations in the liver, spleen,
adrenals and ovaries following a short time period of 48 hours.
Whether or not the accumulation continued following this time
period is unknown.
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https://jessicar.substack.com/p/the-pfizer-document-dump-pertai
ning?s=r
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Reproductive
The European Medicines Agency's safety committee
reviewed reports of heavy menstrual bleeding and absence of
menstruation from women who had received COVID vaccines
from Pfizer/BioNTech and Moderna.
After reviewing the available evidence, the EMA's

Pharmacovigilance Risk Assessment Committee (PRAC) said it
decided to request an evaluation of all available data, including
reports from patients and healthcare professionals, clinical trials
and the published literature.
https://www.reuters.com/business/healthcare-pharmaceuticals/e
u-investigates-reports-menstrual-disorders-after-mrna-covid-shot
s-2022-02-11/
Over more than 100 years, fewer than 40 cases of decidual

cast shedding — during which the uterus’ thick mucous lining is
shed, intact — have been reported. But over a 7.5 month period
in 2021, 292 women experienced it, raising questions about
whether Covid-19 vaccines could be to blame.
https://expose-news.com/2022/05/13/unprecedented-number-of
-women-gynaecological-event/
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IVF clinics started having problems starting in March. And
they’ve talked to other IVF clinics who are having similar
problems:
1. In March thru May, there was a huge spike in miscarriage

rates. It is normally 25% to 30%. In these months it shot up
over 50%. They’ve never seen anything like that before.
2. One woman had very reliably donated 30 or more eggs each

time she came in which yielded 5 to 8 embryos. In May, she
got her second shot of the vaccine and then came in to
donate a couple of weeks later. The clinic was shocked: all of
the embryos had all arrested when they checked them on
day 5. None of them reached the stage where the
trophectoderm forms. I’m told this sort of thing is exactly
what you’d expect from the vaccine (see “What happened in
Singapore” below).
3. They are seeing an unknown contaminant in the wells with

the embryos. They started noticing this in August, but it
could have started sooner than that. They only notice it
under high power magnification and it is only the wells with
the embryos. They still don’t know what it is or how it got
there. Multiple clinics report the exact same thing. This
means it is either coming from the sperm or the egg.
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In one month, 2 of 10 women in their clinic are having
serious problems. They both had 38 eggs but produced only 1 or
2 embryos, way below normal.
https://stevekirsch.substack.com/p/ivf-clinics-started-having-seri
ous?r=oybif&s=r
Various testicular cells including Leydig, Sertoli,

spermatogonia and spermatozoa express ACE2 and related
proteases resulting with viral fusion. Cytokine storm-induced
dysfunction, autophagy regulation and damaged blood-testis
barrier were also suggested as possible pathogenic mechanism
for testicular damage. Clinical reports of orchitis, supported by
histological findings, further emphasized testicular involvement.
Detrimental impact on both spermatogenesis and testosterone
production seem an obvious outcome; they evaluated donors
from 3 sperm banks over a longitudinal period commencing
before pfizer vaccine and following up after.
Post day 150, sperm concentration was -15.9% vs baseline,

lower even than in the 75-120 day period. Average time post
vaxx for T3 collection was 174 +/- 26.8 days so we’re talking
about 6 months post vaxx with NO recovery in sperm
concentration. Total motile count was slightly recovered from T2,
but was still down 19.4% vs baseline, seeming to make up
somewhat in volume what is lost in concentration. Both results
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were statistically significant at a 95% confidence interval and
nearly so even at T3.
https://boriquagato.substack.com/p/pfizer-vaccine-effects-on-tot
al-motile
Innate Immune Suppression

The BNT162b2 vaccine modulated the production of
inflammatory cytokines by innate immune cells upon stimulation
with both specific (SARS-CoV-2) and non-specific (viral, fungal
and bacterial) stimuli. The response of innate immune cells to
TLR4 and TLR7/8 ligands was lower after BNT162b2 vaccination,
while fungi-induced cytokine responses were stronger. In
conclusion, the mRNA BNT162b2 vaccine induces complex
functional reprogramming of innate immune responses, which
should be considered in the development and use of this new
class of vaccines.
v1
Innate Immune System Reprogramming By Pfizer-BioNTech V…
https://www.youtube.com/watch?v=jcl0B9FdSf8
Vaccination induces a profound impairment in type I

interferon signaling, which has diverse adverse consequences to
human health. Immune cells that have taken up the vaccine
nanoparticles release into circulation large numbers of exosomes
102
containing spike protein along with critical microRNAs that induce
a signaling response in recipient cells at distant sites.
Seneff, et al also identified potential profound disturbances

in regulatory control of protein synthesis and cancer surveillance.
These disturbances potentially have a causal link to
neurodegenerative disease, myocarditis, immune
thrombocytopenia, Bell's palsy, liver disease, impaired adaptive
immunity, impaired DNA damage response and tumorigenesis.
This innate immune suppression is combined with immune

system priming and may lead to antibody dependent
103
enhancement of future pathogens infiltrating CD16+ or other
primed macrophages upon natural infection or reexposure.
Anti-Idiotype antibodies have been observed as a result of
vaccination as well.
https://youtu.be/NY9Wrpw3igs
Child Vaccine Negative All-Cause Efficacy

Top epidemiologist Professor John Ioannidis has published a
new study which concludes that the survival rate of people under
the age of 20 who catch COVID is 99.9987%.
“From analysis of 25 seroprevalence surveys across 14

countries, Prof. Ioannidis and his colleague found the IFR varied
from 0.0013% in the under-20s (around one in 100,000) to
0.65% in those in their 60s,” writes Will Jones.
https://www.zerohedge.com/covid-19/covid-survival-rate-under-
20s-999987-stanford-epidemiolgy-prof-study
The mRNA COVID vaccines begin a process of spike protein

production throughout the body. Spike protein effects on ACE 2
104
receptors in the vascular endothelium serve to vasoconstrict. The
result may obstruct the body’s supply of increased blood flow and
oxygen, just when the demands are greatest, during exertion.
Spike protein associated immune and inflammatory factors can
also affect perivascular and periarterial cells, as well as CD8 and
NK T-cell infiltration. All of these can reduce coronary
vasodilation.
Further compounding the problem of blood delivery to

peripheral and coronary tissues are the spike protein positions
and effects. Jutting from the endothelial surface, spike proteins
are docked onto ACE-2 receptors. These are thought to adversely
affect blood flow through turbulent rather than laminar flow. As
stagnant blood pools, the clotting cascade begins ubiquitously
throughout the body. Such micro-clotting thickens and slows the
blood, which would further impair the delivery of blood and
oxygen to the capillary beds in the heart and in the periphery.
Thus, coronary blood flow can be adversely affected by high
viscosity, which is also caused by spike protein induced RBC
aggregation from adhesion through CD 147. As a result, the
heart is burdened to push a more viscous liquid than normal
blood through the body’s arterioles and capillaries. Does this
explain recent youth and athlete Sudden Death?
https://colleenhuber.substack.com/p/vaccinated-athletes-perform
-worse?s=r
105
The Office for National Statistics has revealed without
meaning to that children are 82 to 303x more likely to die
following Covid-19 vaccination than children who have not had
the Covid-19 vaccine.
https://expose-news.com/2022/05/20/kids-death-risk-increases-
8100percent-covid-vaccination/
There have also been reports of vaccine efficacy for children

being 12% for 28 days. Combined with clinically observed ONS
data, and the 99.9987% innate immunity, what is the medical
justification to inject healthy children with this experimental gene
106
therapy to produce the known biologic toxin as well as the
inflammatory lipid-nanoparticles???
https://youtu.be/lzMCstQ5VJw
Results indicate that while T cells play a role in the recovery

of rhesus macaques from acute SARS-CoV-2 infections, their
depletion does not induce severe disease, and T cells do not
account for the natural resistance of rhesus macaques to severe
COVID-19. Neither primed CD4+ nor CD8+ T cells appeared
critical for immunoglobulin class switching, the development of
immunological memory, or protection from a second infection.
https://journals.asm.org/doi/10.1128/mBio.01503-21
What reason is there to artificially induce the creation of

CD8+ Tcells in children with “boosters” when Alpha strain B.1.1.7
is no longer in natural circulation?
Boosters May Weaken The Immune System Says European M…
https://youtu.be/7nhyhLVD-Hs
A Lancet study comparing vaccinated and unvaccinated

people in Sweden was conducted among 1.6 million individuals
over nine months. It showed that protection against symptomatic
COVID-19 declined with time, such that by six months, some of
the more vulnerable vaccinated groups were at greater risk than
their unvaccinated peers.
107
Doctors are calling this phenomena in the repeatedly
vaccinated “immune erosion” or “acquired immune deficiency”,
accounting for elevated incidence of myocarditis and other
post-vaccine illnesses that either affect them more rapidly,
resulting in death, or more slowly, resulting in chronic illness.
https://americasfrontlinenews.com/post/vaccine-acquired-immun
e-deficiency-syndrome-vaids-we-should-anticipate-seeing-this-im
mune-erosion-more-widely
Using national epidemiological and whole genome

sequencing surveillance data from March to August 2021 in the
Netherlands, our analysis provides evidence for an increased risk
of infection by the Beta, Gamma, or Delta variants compared to
the Alpha variant after full vaccination, regardless of the vaccine
used. This indicates lower vaccine effectiveness against infection
with the Beta, Gamma and Delta variant compared to the Alpha
variant. No clear differences between vaccine type were observed
as confidence intervals largely overlap.
v1
Children under 18 are also 51 times more likely to die from

the jab than they are to die from COVID if not vaccinated.
https://www.theepochtimes.com/the-alarming-trends-in-covid-ja
b-side-effects_4319841.html
108
https://www.naturalnews.com/2021-11-19-covid-vaccines-suppre
ssed-immunity-hiv-hpv-herpes.html#
Th1-Th2 Pathways & CD8 Concentration

CD4+ cells are the earliest state of existence any adaptive
antibody can be. All antibodies originate as CD4+ T-helper (Th)
cells.
CD4+ cells of the adaptive arm of the immune system may turn
into Th1 or Th2 cells:
1. Th1 cells turn into CD8+ Killer T-Cells.
2. Th2 cells turn into B-memory cells.
Fauci, WHO, CDC, and the medical establishment have sold

the world on the idea that CD8+ cytotoxic killer T-cell antibodies
must be present at a specific concentration, in order for
“immunity” to exist within the body.
To solely rely on a quantitative measure of the adaptive

immune system, thinking an increase on the Th1 pathway to
CD8+ cells is the ONLY way to treat a viral SARS/Airborne
pandemic, completely discounts the efficacy of the innate immune
system; An innate immune system upon which accounts for a
99.99% “natural immunity” in children, and is responsible for
processing biological matter into the protein antigens needed to
program CD4+ cells in the first place…
109
Public Health Gain of Function Research
Th2 immune pathology is based on a subset of CD4+
pathways the adaptive immune system may take regarding a
vaccine or any other pathogen. “Th1 cells drive the type-1
pathway ("cellular immunity") to fight viruses and other
intracellular pathogens, eliminate cancerous cells, and stimulate
delayed-type hypersensitivity (DTH) skin reactions. Th2 cells
drive the type-2 pathway ("humoral immunity") and up-regulate
antibody production to fight extracellular organisms; type 2
dominance is credited with tolerance of xenografts and of the
fetus during pregnancy.”
The Th2 humoral response is held in concert with Th1. Th2

immune pathology is science speak for when Th2 becomes
dominant over Th1. Th1 is considered preferential in viral
immunology, because the cellular immune response leads to the
creation of CD8+, cytotoxic specialized killer T-cells. CD8+ cells
are “antibodies” pharma companies use as the “gold standard” for
proof of efficacy and continuing Emergency Use Authorizations…
In 2014 Evaluation of available SARS-based

immune-therapeutic and prophylactic modalities revealed poor
110
efficacy; both monoclonal antibody and vaccine approaches failed
to neutralize and protect from infection with CoVs using the novel
spike protein.
Doubly inactivated vaccines induced a Th2 immune

pathology associated with massive influxes in the numbers of
eosinophils and neutrophils, effectively causing a gain in virus
pathogenic potential in an unpredictable manner (Bolles et al.,
2012). The resulting increased immune pathology can sometimes
progress to fatal disease and similar findings have been reported
in primates.
https://www.nature.com/articles/nm.3985
Dr. Baric, of WIV, Wuhan, China fame, cited research that

inducing T-Helper 2 (CD4+) cells associated with an increase in
white blood cells effectively causes a “gain of virus pathogenic
potential”. Baric, et al synthetically re-derived an infectious
full-length SHC014 recombinant virus and demonstrated robust
viral replication both in vitro and in vivo. The work suggested a
potential risk of SARS-CoV re-emergence from viruses currently
circulating in bat populations. When biological mechanisms
involving the immune system make a virus WORSE it gave reason
for a moratorium on pathogenic research in 2014.
111
Public Policy was forced to shift and create the Potential
Pandemic Pathogens (PPPs) and was buffered by Cambridge
Working Group Consensus Statement on the Creation of Potential
Pandemic Pathogens (PPPs):
“For any experiment, the expected net benefits should
outweigh the risks. Experiments involving the creation of
potential pandemic pathogens should be curtailed until there
has been a quantitative, objective and credible assessment
of the risks, potential benefits, and opportunities for risk
mitigation, as well as comparison against safer experimental
approaches.”
http://www.cambridgeworkinggroup.org/documents/statement.p
df
This approach must be considered in the context of the US

government–mandated pause on gain-of-function (GOF) studies.
On the basis of previous models of emergence, the creation of
chimeric viruses such as SHC014-MA15 was not expected to
increase pathogenicity. Although SHC014-MA15 is attenuated
relative to its parental mouse-adapted SARS-CoV, similar studies
examining the pathogenicity of CoVs with the wild-type Urbani
spike within the MA15 backbone showed no weight loss in mice
and reduced viral replication. Thus, relative to the Urbani
spike–MA15 CoV, SHC014-MA15 shows a gain in pathogenesis.
112
Gain in pathogenesis = Gain of Function. The moratorium on
gain of function was tailored to reduce the amount of antibodies
ultimately produced by the Th2 humoral response in order to limit
the overproduction of non-neutralizing eosinophils and
neutrophils which caused further damage. Today’s medical lexicon
may call this action Antibody Dependent Enhancement.
Whatever term “gain of function” may have for public policy

experts, the observable effects of an MSH3 gene, known to be
associated with ceroid lipofuscin formation and bleeding disorders
MUST be looked at closer. As well as, N-Terminal, ACE2 effects, a7
nAChR effects, lipid-nanoparticle effects, and spike protein sui
pathogenesis in general.
Emerging viruses exist in swarms of heterologous but

related viruses, thus, Future outbreaks could be derived from
other precursor strains which are antigenically and genetically
distinct. Antigenic variation could obviate the potency and efficacy
of SARS vaccines and immunotherapeutics or erode the
therapeutic potency of antiviral drugs.
Vaccines using the SARS S glycoprotein do not protect

against lethal heterologous Spike challenge, Especially in aged
animals; Thus, current SARS vaccines will fail to protect against
these precursor strains should they seed future outbreaks. In
113
fact, the doubly inactivated vaccines don't protect but do
stimulate the Th2 immune pathology noted above
“Gain-of-function” research produces the unwanted result of

an increased pathogenic, non-neutralizing response within the
immune system. Gain of function implies harm to the organism
itself via an increased biological functioning, leading to greater or
increased pathogenicity within the body or host. No scientist will
admit conducting research leading to harm being done to people.
If they did, they would in essence, be providing a function for a
system antithetical to medical ethics. The creation of the PPP
distinction insulated the scientific community by providing a
whipping boy the erudite establishment could collectively scoff at
and label “Gain-of-function” in disdain.
https://dockek.substack.com/p/they-knew-the-danger
Recall the antibody targets at the beginning of Part 3 for the

current vaccines being B-Cells, i.e. Th2 response. The emerging
variants of concern are precursor strains exposed to
non-neutralizing antibodies. Many believe the “new” variants have
evolved from SARS-CoV-2 Alpha B.1.1.7 strain, and that is NOT
the case, as variants are categorized by changes in spike protein
ONLY, and may NOT be related to SARS phylogenetically.
114
The schism of “gain of function” by the creation of the PPP
label is what Dr. Fauci and other public policy experts hide behind,
because no one else delineates pathogenic research, in all of its
forms, from “gain of function”. However, there is little doubt
continuing to inject a spike protein from a virus two years ago, no
longer in natural circulation, will only go to forwarding the
probability of a gain in pathogenesis in those continuing to be
injected, to include children.
CD8+ concentration CANNOT be used as a measure for

“immunity” because scientific research has shown elevated
concentrations to be associated with a gain of function, or gain in
pathogenesis of the antigen within the host’s body. The effects on
the host’s body are unknown for chronic exposure. Informed
Consent must be provided on each item contained herein to
ensure proper medical disclosures are provided, and patients
made fully aware of the cascade of effects, to include mutagenic
influence on their own genome.
Many Blessings
115
EXHIBIT B
7/18/22, 2:03 PM Gmail - Informed Consent
Anthony Pena <fwdquestionshere@gmail.com>
Informed Consent
Anthony Pena <fwdquestionshere@gmail.com> Wed, Jun 15, 2022 at 10:20 AM
To: lee.moreau@vdh.virginia.gov
Good Morning,
I am notifying you this morning of a Healthcare-associated infection related to a Reportable disease and am requesting
designation of a Toxic substance as defined 12VAC5-90-10.
As per 12VAC5-90-100; The local health director or his designee shall review reports of diseases received from his
jurisdiction and follow up such reports.
The attached Pathophysiological report shows SARS-CoV-2 Spike Protein is a biologic toxin that causes Post-Acute
Sequelae, Cytokine Storm, & the HHS defined ADA disability Long Covid.
Epidemiology must be notified immediately to confirm the finding.
Toxicology will also need to be notified for their designation under § 32.1-239 for any substance known to produce this
biologic toxin.
Under 12VAC5-90-90. Those required to report. -
Physicians. Directors of laboratories. Persons in charge of a medical care facility. Persons in charge of a residential or
day program, service, or facility licensed or operated by any agency of the Commonwealth, or a school, child care center,
or summer camp. Persons in charge of hospitals, nursing facilities or nursing homes, assisted living facilities, and
correctional facilities.
E. Local health directors. The local health director shall forward any report of a disease or report of evidence of a disease
which has been made on a resident of his jurisdiction to the Office of Epidemiology within three days of receipt. This
report shall be submitted immediately by the most rapid means available if the disease is one requiring rapid
communication, as required in 12VAC5-90-80 C. All such rapid reporting shall be confirmed in writing and submitted to
the Office of Epidemiology, by either a paper report or entry into a shared secure electronic disease surveillance system,
within three days. Furthermore, the local health director shall immediately forward to the appropriate local health director
any disease reports on individuals residing in the latter's jurisdiction or to the Office of Epidemiology on individuals
residing outside Virginia. The Office of Epidemiology shall be responsible for notifying other state health departments of
reported illnesses in their residents and for notifying CDC as necessary and appropriate.
Many Blessings,
Anthony Pena 757-814-9885
S1 Spike Pathologies causes PASC & Cytokine Storm Sui Pathogenesis.pdf
1958K
https://mail.google.com/mail/u/2/?ik=86eea6d442&view=pt&search=all&permmsgid=msg-a%3Ar294162758926045232&simpl=msg-a%3Ar294162758… 1/1
EXHIBIT C
7/13/22, 12:24 PM Gmail - Vaccine Research
Vaccine Research
covid19-questions-VDH, rr <covid19-questions@vdh.virginia.gov> Wed, Jun 15, 2022 at 11:51 AM

To: fwdquestionshere@gmail.com
Dear Mr. Anthony Pena,
Thank you for your inquiry to the Virginia Department of Health.
Regarding vaccine research, because there are federal requirements for informed consent in medical research, Pfizer-
BioNTech, Moderna, and Johnson and Johnson (Janssen) obtained informed consent from the participants in their
research studies in 2020 that were used to develop their vaccines. You may be able to obtain copies of those informed
consent documents from the individual companies.
Regarding public use of each COVID-19 vaccine once that vaccine has received an Emergency Use Authorization (EUA)
from the Food and Drug Administration, no consent forms are currently being used for COVID-19 vaccination of the U.S.
public. There are no federal requirements for informed consent processes for non-research use of any vaccines. Details
of this particular issue are available on the CDC website.
Regarding “12VAC5-20-100 Informed consent”, this also applies to purposes of human research. What is needed is that
vaccine recipients should have access to the fact sheets that discuss the risks and benefits of the vaccine.
Regarding your concern about a possible link between mRNA COVID-19 vaccination and Long COVID, VDH is unaware
of any scientific or clinical studies, either already published or still being reviewed for publication, that indicate that a
vaccine-related spike protein causes Long COVID. We would be glad to review any studies on that issue that you can
refer us to.
We can share some information on what is known about Long COVID:

1. People who get infected with SARS-CoV-2, the virus that causes COVID-19, develop Long COVID relatively
often.
2. By effectively preventing the development of SARS-CoV-2 infection and COVID-19 illness, COVID-19 vaccine
helps protect against the development of Long COVID. The exact amount of protection is still uncertain but no
study has shown a higher rate of Long COVID among vaccinated people.
3. People who get breakthrough infections after COVID-19 vaccination develop Long COVID less often than
unvaccinated COVID-19 patients.
It is certainly true that the COVID-19 spike proteins are potentially harmful to humans when they are on the outer surfaces
of circulating SARS-CoV-2 viruses because those spikes facilitate adhesion of the virus to the surface of human cells,
thus facilitating the subsequent release of a very large number of new virus particles. These new viral particles then get
released into nearby cells and tissues and into the bloodstream, which can sometimes cause severe illness.
Spike proteins are common components of the outer surfaces of many highly infectious viruses. For example, the
influenza virus carries a spike protein called “hemagglutinin” that is responsible in part for the virus’ effective adherence to
cells during the infection process. For a more detailed description of the virus-related spike protein issue, see the
introduction to: https://journals.asm.org/doi/10.1128/mSphere.01339-20?.
In addition, the Infectious Disease Society of America (IDSA) estimates that the spike proteins generated by COVID-19
vaccines last up to a few weeks at most, like nearly all other proteins made by the body. Antibodies from the immune
system quickly identify, attack, and destroy these spike proteins. Dr. Shin Jie Yong has written a detailed discussion of
various aspects of the spike protein mRNA vaccine that is available here. As mentioned by Dr. Yong, “The mRNA
vaccines are designed in such a way that the vaccine-derived spike proteins are anchored onto the cell surface... Hence,
spike proteins made by muscle cells at the injection site will stay at the injection site.”
More specifically, the distribution and circulation of vaccine-generated spike proteins is different from that of the spike
proteins on the actual viruses. A detailed discussion of the difference between spike proteins from infection and spike
proteins from vaccination can be found here. In sum, VDH does not consider the spike proteins generated by COVID-19
vaccine to be toxic substances.
https://mail.google.com/mail/u/2/?ik=86eea6d442&view=pt&search=all&permmsgid=msg-f%3A1735716557612799343&simpl=msg-f%3A1735716557… 1/2

In initial studies of COVID-19 vaccine in laboratory mice, a small amount of vaccine-related chemicals was identified in
the liver of mice that were injected. No significant impact on liver function was found in those mouse studies. More
recently, public media widely misinterpreted the results of a Swedish study that found that human liver cancer cells
isolated in a laboratory could accumulate COVID-19 vaccine. The authors’ clarification of the study results and its DNA-
related implications can be found here and in a fact-check review of the study.
There is a small but increased risk of myocarditis after mRNA COVID-19 vaccines. However, it is important to know that
cardiovascular effects such as myocarditis are anywhere from 6-8 times more common after COVID-19 disease than after
COVID-19 vaccination.

We also note (1) that more than one million Americans, including more than 20,000 Virginians, have now died from
COVID-19 disease; (2) that the hospitalization and death rates from COVID-19 are far higher in people who are
unvaccinated against COVID-19 than in people up to date with COVID-19 vaccination; (3) that the multiple federal and
other surveillance systems in use to identify and study adverse effects in people given COVID-19 vaccine make this
vaccine by far the most heavily monitored vaccine development effort in U.S. history; and (4) that, as of early June 2022,
more than 580 million doses of COVID-19 vaccine have been given out in the United States with only rare documentation
of significant adverse effects.
Finally, we acknowledge that there could be some theoretical but as yet undocumented risk(s) associated with the
development and use of mRNA or any other vaccines. However, at the moment, scientific data indicate that those
theoretical risks are far outweighed by the clear benefits provided by being up to date with COVID-19 vaccination.

We hope that these comments are helpful.
EXHIBIT D
Vaccine Research
Anthony Pena <fwdquestionshere@gmail.com> Tue, Jun 21, 2022 at 12:32 PM

To: "covid19-questions-VDH, rr" <covid19-questions@vdh.virginia.gov>
Cc: grace.akol@vdh.virginia.gov, dwight.flammia@vdh.virginia.gov, VBEpi@vdh.virginia.gov, delgdavis@house.virginia.gov
I am not interested in the original trials or anything federally related. I am approaching a state agency regarding its
statutory duty to provide Informed Consent regarding Emergency Use Authorized injections being deployed in Virginia on
a phase 3 trial experimental basis.
The admission that no Informed Consent forms are being used is astounding, and I appreciate the candor. Nevertheless,
it does NOT absolve VDH from the statutory and administrative duty to provide it according to state law and policy.
CDC Answered this Question and even they say this falls to the States…
Q: In the COVID-19 Vaccine EUAs, is FDA’s reference to pharmacists who may be acting pursuant to state law under a
standing order intended to suggest that standing orders are required for pharmacists to administer COVID-19 vaccine?
A: No. When FDA issues an EUA, it is providing an access mechanism to a medical countermeasure needed for an
emergency response. Under the EUAs for COVID-19 vaccines, FDA provides maximum flexibility to emergency response
stakeholders (e.g., local, state, and federal public health and response partners, as defined in the EUAs) by authorizing
them to identify or authorize the types of personnel and responders that would be the most appropriate to administer the
product to specific populations and identify the mechanism for authorizing such (e.g., standing order, executive order,
declaration, etc.) in accordance with applicable official response plans and HHS authorizations.
EUA is only an access mechanism. It does NOT absolve “emergency response stakeholders”, such as the VDH, from
their own statutory duties as defined in State Law, such as providing Informed Consent.
There are no federal requirements for the informed consent process because State Police Powers govern non-economic
activity such as providing Informed Consent for phase 3 trials of experimental vaccines available to the general public as
an EUA MCM and fall within the bailiwick of the Virginia Department of Health. Federal Courts have ruled noneconomic
activity falls squarely within the States’ police power. A person’s choice to remain unvaccinated and forego regular testing
is noneconomic activity. Cf. NFIB v Sebilius, 567 U.S. 519, 44 522 (2012) (Roberts, C.J., concurring); see also id. At 652-
653 (Scalia, J., dissenting). And to mandate that a person receive a vaccine or undergo testing falls squarely within the
States’ police power. Zucht v. King, 260 U.S. 174, 176 (1922) 109. The States’ police powers have been activated since
the previous governor’s mandate and now ED-2. The Governor, and every agency, company, and organization in Virginia
mandating or “supporting” vaccines under ANY CONDITION is obliged to follow statute as it pertains to Human Research
and MUST provide Informed Consent.
*My Issues are relegated to state law, NOT federal. All EUA vaccines are currently undergoing phase 3 trials, meaning
human research is being conducted, and VDH is statutorily required to ensure informed consent is provided as per state
law. Federal mandates were declared unconstitutional because State Police Powers regulate non-economic activity.
The referenced fact sheets are NOT sufficient. What is needed is full compliance with statutory authority for
administrative code § 32.1-12 & § 32.1-12.1. Federal Courts have placed responsibility for Informed Consent within State
Police Power’s, which statutorily are situated under § 32.1-162.16 - § 32.1-162.20.
Regarding Long Covid:
Long Covid results from the S1 subunit in non-classical monocytes, as per Bruce Patterson. https://www.ncbi.
nlm.nih.gov/pmc/articles/PMC8784688/
He recently went over biomarkers, diagnosis, and treatment at a conference in Georgetown. https://youtu.be/
h2xyWiMS2Q0
His research specifically notates the S1 subunit as a causative agent.
Within the S1 subunit itself there are 3 protein sequences of pathogenic concern. The First is on the Receptor-Binding
Domain (RBD) and attaches to ACE2 receptors. The second, also on the RBD, is shown to interact with a7 nAChR
receptors of the Nicotine Cholinergic System (NCS), which is highly indicated on the vagus nerve. And the third
sequence, with codons PRRA appearing on the Furin Cleavage Site (FCS), is a human optimized MSH3 gene known to
cause genetic repair dysregulation when binding with MSH2.
Please see below links for cited literature among multiple documented pathogenicities of the spike protein.
https://fwdquestionshere.com/2022/06/14/s1-spike-protein-causes-pasc-cytokine-storm-long-covid/
https://fwdquestionshere.com/2022/06/20/part-2-blood-cells-long-covid-s1-spike-protein-causes-pasc-
cytokine-storm-long-covid/amp/
I am familiar with the structure of the spike protein and conformational changes made to keep the S2 subunit in a
closed/pre-fusion state, in order to keep S2 from attaining the “hairpin” structure it takes after being cleaved from S1 by
TMPRSS2. However, the S1 protein is the “therapeutic target” of the vaccine requiring S1 to be separated. Furthermore,
research has shown that whereas it is assumed PRRAR.S will be cleaved by TMPRSS2 at "S", there are other enzymes
capable of cleaving the FCS at PRRA. RS. Meaning MSH3 would be completely exposed. https://www.ncbi.nlm.
nih.gov/pmc/articles/PMC7833556/#appsec1
The human neutralizing antibody response in SARS-CoV-2 infection appears to be dominated by RBD-specific
antibodies, which—on average—were shown to contribute 90% of the total neutralizing activity of human post-infection
sera. It is therefore a major goal of all COVID-19 vaccines to present the spike and its RBD (S1) in a most native
conformation for inducing a high proportion of potently neutralizing antibodies after vaccination. https://www.
nature.com/articles/s41541-021-00369-6
mRNA spike proteins have been found in the blood, so the idea they “are anchored onto the cell surface” is false.
https://academic.oup.com/cid/article/74/4/715/6279075?login=false
Previous LNP studies have shown LNPs to travel lymphatically to the brain, heart, liver, spleen, and ovaries of patients,
not just the Japan study Dr. Yong referenced.
mRNA has been found to be converted and incorporated into the host’s DNA in the Liver, how is this possible if 1. spikes
stay anchored to the cell surface, and/or 2. LNPs do not migrate from injection site… https://pubmed.ncbi.nlm.nih.
gov/33958444/
Clinical markers of T-Cell cardiac infiltration and damage have been shown to numerically increase and raise PULS
scores from 11% to 25% for 5-year risk of Acute Coronary Syndrome (ACS) in a clinical setting of post-vaccinated
patients. 11% to 25% is more than a 100% increase… https://www.ahajournals.org/doi/abs/10.
1161/circ.144.suppl_1.10712
The notes on the benefits of this spike based vaccine against COVID-19 do not explain a 40% increase in all-cause
mortality among the working-age population, where a 10% increase is a 1 in 200 year event, that Life Insurance executive
from the companies cutting checks say is NOT COVID-19. https://thehill.com/changing-america/well-being/
longevity/588738-huge-huge-numbers-death-rates-up-40-percent-over-pre/
You mentioned there could be some theoretical but as yet undocumented risk(s) associated with the development and
use of mRNA or any other vaccines.
US patent 9,587,003 - is a direct match for PRRA, which is at the Furin cleavage site (FCS) where S1/S2 subunits are
separated. TMPRSS2 is known to "cleave" the two subunits. However, there are other enzymes capable of cleaving
PRRA. The FCS Codons are written PRRAR.S, where "S" is the point of TMPRSS2 binding. PRRA is an MSH3 (HPS-1)
gene. Enzymes Capable of cleaving PRRA .RS mean MSH3 would be exposed; especially if codons were optimized for
humans, and even IF the code were part of a longer set of proteins, such as what is made by a vaccine... Are doctors,
professionals, "scientists", health ministers, epidemiologists, educators, etc NOT ethically bound to notify others of the
presence of a genetic toxin that has already led to a worldwide pandemic of public health threat and is shown to be a
major driver of the S1 protein studies that have shown S1 to be the causative agent of Long Covid, which is defined as an
ADA disability by HHS??
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7833556/#appsec1
S1 spike is a biologic toxin.
MSH3 in spike is a genetic toxin.

Either way it needs to be designated a toxin itself, anything producing this toxin must be labeled a toxic substance, and
Informed Consent has to be provided.
Please let me know how we make this happen.
If there is genuine controversy between the federal and state government on this issue then I will need to speak with the
VDH Liaison to Attorney General Miyares please.
Have a Blessed Day!
Anthony Pena
757-814-9885
EXHIBIT E
7/13/22, 12:22 PM Gmail - Long COVID
Long COVID
covid19-questions-VDH, rr <covid19-questions@vdh.virginia.gov> Tue, Jun 21, 2022 at 12:23 PM

To: fwdquestionshere@gmail.com
Dear Mr. Pena,
Thank you for your email to the Virginia Department of Health.
We agree with your comment that the SARS-CoV-2 spike protein is closely related to the cause of Long COVID. COVID-
19 infection itself and Long COVID are not considered “healthcare-associated infections.” Types of healthcare-associated
infections that are reportable to VDH are outlined on the Healthcare-Associated Infections and Antimicrobial Resistance
Program website. Healthcare facilities are required to report individual cases of COVID-19 as discussed in this letter.
The Spike protein-related document that you attached has important information detailing (1) the growing awareness of
the importance of Long COVID and (2) the many risks of spike proteins of SAR-CoV-2 viruses sticking out like a crown (or
corona) on the outside coat of those countless viruses that freely circulate when people have COVID-19. This risk is
highlighted on the bottom of page 13 of the article with the statement that “Free S1 particles play a role in the
pathogenesis of the disease.”
On page 21 of the article is a statement that says “For some reason, CDC refers to the spike protein as harmless.”
However, CDC and others note that the natural spike proteins sticking out of the surface of the SARS-CoV-2 viruses are
potentially harmful because they can link up with the cells’ ACE-2 receptors and then begin infecting cells. However, after
vaccination, the pieces of spike proteins produced in immunity cells do not stick out of their cells in the same way. They
do not form the “crown” that is the source of the Coronavirus name. Instead, they are embedded on the surface of the
walls of these cells in a way that prevents them from interacting with the ACE-2 cell receptors, but still allows the
lymphocytes and other cells of the immune system to recognize them as foreign spike proteins. Because they are foreign
proteins, the body then begins to produce antibodies and other forms of immunity that would act against viral spike
proteins if they show up during an infection on the outside of SARS-CoV-2 virus.
Finally, the best way to prevent Long COVID is (1) to stay up to date with COVID-19 vaccination and (2) to take whatever
other COVID-19 prevention steps (for example, masking, avoiding poorly ventilated spaces, etc.) that are appropriate for
your community’s COVID-19 level and for your personal COVID-19 risk.
We hope this information is helpful.
EXHIBIT F
7/19/22, 3:40 PM Gmail - Long COVID
Long COVID
Anthony Pena <fwdquestionshere@gmail.com> Mon, Jul 18, 2022 at 11:08 AM

To: "covid19-questions-VDH, rr" <covid19-questions@vdh.virginia.gov>, grace.akol@vdh.virginia.gov,
dwight.flammia@vdh.virginia.gov, delgdavis@house.virginia.gov
The statement that “Free S1 particles play a role in the pathogenesis of the disease.” appears to be ignored even though
it is known to be the causative agent of Long Covid... S1 is a biologic toxin
I am still unaware of how introducing more of a causative agent of a coronavirus disease disabling sequelae improves the
conditions of the patient long-term. 🤷‍♂️
"after vaccination, the pieces of spike proteins produced in immunity cells do not stick out of their cells in the same way." -
if spike proteins are being produced in immunity cells then this would create an autoimmune disorder...
"They do not form the “crown” that is the source of the Coronavirus name. Instead, they are embedded on the surface of
the walls of these cells in a way that prevents them from interacting with the ACE-2 cell receptors" - What biological
guarantee can anyone make to what any protein artificially expressed on the surface of any cell, may, or may not interact
with? None... this also ignores the fact ACE2 may be expressed internally...
"the body then begins to produce antibodies and other forms of immunity that would act against viral spike proteins" - This
is overly simplistic.
Part 3 of the attached document provides a better scope of physiological and immunological consequences, as well as
clinical results, as a result of artificially creating toxic spike proteins with synthetic "stabilized" mRNA via Lipid-
nanoparticles in patients every six months for a strain of public health threat no longer in natural circulation -
https://fwdquestionshere.com/2022/07/11/part-3-all-about-the-vaccine/
It would appear, physiologically, the most important step to preventing COVID-19 disease is to prevent the Spike protein
from being "activated" once TMPRSS2 cleaves S1 from S2 which is known to be the main driver in pathogenesis...
Spike Protein is a biologic toxin, and I will need Informed Consent of such for any substance creating it in my body.
[Quoted text hidden]
AFIC - S1 Spike; Complete - 7.12.2022.pdf
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Pena V VDH W/ Exhibits A - F - Declaratory Judgement

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Pena V VDH W/ Exhibits A - F - Declaratory Judgement

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IN THE CIRCUIT COURT OF THE CITY OF RICHMOND

VERIFIED PETITION AT LAW FOR DECLARATORY JUDGMENT

COMES NOW, before this Honorable Court, Anthony Pena, pro se in

triformis, Executive Director, American Foundation for Informed Consent, a

Virginia limited liability company, and pursuant to the provisions of §8.01-184

JURISDICTION AND VENUE

declaratory judgments pursuant to Virginia Code § 8.01-184.

2. See also Va. Code § 8.01-186 (authorizing further relief based on a

decree “whenever necessary or proper”).

3. Venue is appropriate under Va. Code § 8.01-261(2) because this is an

action “against one or more officers of the Commonwealth in an official capacity,”

each of whom has official offices in Richmond, Virginia.

4. Petitioner, Anthony Pena, pro se in triformis, Executive Director,

American Foundation for Informed Consent, a Virginia limited liability company

5. Respondent, Virginia Department of Health (VDH)

6. Respondent, Dr. Colin Greene, in his official capacity as State Health

7. There is a justiciable controversy as to whether VDH must provide

Informed Consent as outlined in Va. Code. § 32.1-162.16 and § 32.1-162.18 for

trials (i.e. Human Research).

8. That an actual controversy exists is further demonstrated

requirements for informed consent processes for non-research use of any

9. There is also justiciable controversy as to whether or not the S1

Americans with Disabilities Act (ADA), as well as inducing other sequelae

appearing under 12VAC5-90-80. List of diseases that shall be reported:

*Coronavirus infection, severe; Hepatitis, other acute viral; *Unusual occurrence

of disease of public health concern.

10. That an actual controversy exists is further demonstrated by VDH

11. On August 15, 2021, Governor Northam Announce[d] COVID-19

for waiting is over.”

12. The mandatory nature of participation in human research entailed in

13. On January 20th, 2022, Governor Younkin declared a temporary state

of emergency in EO-11 and concurrently announced his COVID-19 VACCINE

MARSHALL PLAN FOR VIRGINIA.

14. Currently, all publicly-available COVID vaccines have only

approval. Comirnaty, while approved, is NOT being distributed in the US.

15. Vaccines authorized under EUA require complete and voluntary

informed consent, meaning “providing policies allowing knowing and voluntary

agreement, without undue inducement or any element of force, fraud, deceit,

duress, or other form of constraint or coercion, of a person who is capable of

16. In the case of Human Research, which applies to all publicly-available

COVID vaccines, the “basic elements of information necessary to such consent”

(Basic Elements) shall include:

1. A reasonable and comprehensible explanation to the person

of the proposed procedures or protocols to be followed, their

purposes, including descriptions of any attendant discomforts,

and risks and benefits reasonably to be expected;

2. A disclosure of any appropriate alternative procedures or

therapies that might be advantageous for the person;

3. An instruction that the person may withdraw his consent and

discontinue participation in the human research at any time

without prejudice to him;

4. An explanation of any costs or compensation which may

accrue to the person and, if applicable, the availability of third

party reimbursement for the proposed procedures or protocols;

5. An offer to answer and answers to any inquiries by the

person concerning the procedures and protocols.

of informed consent required as defined in § 32.1-162.16 provided by any agency’s

(DHRM, VDH, DOLI, etc.) ministerial response to the Governor’s discretionary

executive actions, orders, or directives.

Marshall Plan for Virginia.

VDH Denied Informed Consent

21. Following notification of a decision on SCV# 211184, Plaintiff set to

Long Covid. (Exhibit A)

Coronavirus infection, severe; Hepatitis, other acute viral; Unusual occurrence