PreprintPDF Available

The Myth of the Blind Watchmaker

Preprints and early-stage research may not have been peer reviewed yet.
Preprint

The Myth of the Blind Watchmaker

Abstract

Although bearing the same title, this is essentially a new document. It surveys the relevant findings related to both the FCS & the HIV inserts, within the context of the early 2020 decision to minimize or censor scientific discussion, respectively. My purpose is not to answer the origin question-it is to show that regardless of the provenance of the virus itself, the result of the censorship had profound implications for both the short-term response and the long-term impact on global health [i.e. "long COVID"]. My Origin Research Reference Project, also on ResearchGate, contains a tab [tab 23] that lists more than 200 references related to this document - everything linked within the endnotes and much more.
The Myth of the Blind Watchmaker Summary 5/28/2022
© Charles H. Rixey, 2022 DRASTIC
The Myth of the Blind Watchmaker: A Legacy of Collateral Damage
Preface & Prologue
This summary has been placed on ResearchGate to serve as a record for posterity, in order to begin raising
awareness about the conclusions it contains. A fuller and more formal analysis will ultimately replace it, just as this
is replacing the initial 4-page document published on 4/9/2022.
Many will find the 4/9/2022 livestream
i
between Dr. Jonathan Couey and I very helpful for clarity on some
details; however, this updated version covers far more ground. A topical bibliography with more than 200
references
ii
is also available on ResearchGate. An unofficial companion article by Arkmedic
iii
from 4/10/2022
remains highly relevant.
This work remains, unequivocally, the most important thing I’ve ever written. It attempts merely to
synthesize the efforts of DRASTIC and numerous other independent researchers with whom I’ve collaborated
directly [the left-hand column below], as well as the outstanding research of those scientists who’ve fought against
the censorship and false narratives that obscured their findings:
Jonathan Couey Fernando Castro-Chavez
Johanna Deinert Angus Dalgleish
Kevin McCairn Richard Fleming
Rossana Segreto Luc Montagnier
Ah Khan Syed [pseud] Jean-Claude Perez
Jack Ward [pseud] Steven Quay
Dayou Zhang Birger Sorenson
Igor Chudov Walter Chesnut
My findings and conclusions on scientific censorship are based on several thousand hours of individual
research. The findings related to the HIV inserts in general, gp120, the furin cleavage site and other aspects of the
SARS-CoV-2 genome are the product of those listed above, or others referenced in the endnotes.
The implications are profound, and profoundly disturbing; the scale of the response to the first draft and
livestream has clearly shown me that my intuition about their importance was correct. I’ve published them here,
now, because the evidence has become so overwhelming that I can’t, in good conscience, withhold these
conclusions from the public. In short:
- Dr. Fauci & others knew, based upon the suspicious elements of the SARS-CoV-2 genome, that the
virus had almost certainly been manipulated
- They knew that such manipulations likely came from pseudovirus & insertion techniques very familiar
to US & Chinese viral vaccine & therapeutic/MCM programs
- They immediately took steps to censor and control public & scientific discussions related to the HIV
inserts and FCS, respectively; these actions are more properly viewed as obstruction of justice
- This had major implications for both the early response to the pandemic [FCS] and the long-term
impact on global public health [the HIV inserts and ‘Long COVID’ sequelae]
Without hesitation, I would testify under oath to the veracity of the evidence in support of these
conclusions. They involve implications that are horrific regardless of which scientists, from which country, may
have been responsible for creating SARS-CoV-2. I propose the list of questions that follows on behalf of the victims
of the COVID-19 pandemic, who cannot ask them themselves. I promise you, however, that all of them are waiting
to hear the answers.
Semper Fidelis,
Charles H. Rixey
The Myth of the Blind Watchmaker Summary 5/28/2022
© Charles H. Rixey, 2022 DRASTIC
1 week to slow the spread [of uncomfortable narratives]: 1/29/2020 2/4/2020
On January 31st, 2020, an 80-page book titled Analysis of Wuhan Coronavirus: Déjà vu was
published as a free download on Amazon’s Kindle service. This was the first English-language
publication to discuss the existence and implications of the FCS [the only prior reference was a Chinese
research paper published as a pre-print on 1/21/2020 to the ChinaXiv server]. Gallaher’s first mention of
the FCS came 2 days earlier, in a post on the Virology.org professional message board.
iv
Also on January 31st, a 9-page scientific article titled “Uncanny similarity of unique inserts in the
2019-nCoV spike protein to HIV-1 gp120 and Gag” was uploaded to the pre-print server bioRxiv. The
authors, a group of researchers from India, listed a set of 4 short segments they’d discovered within the
then-2019-nCoV spike protein’s genome that matched portions of HIV-1 the virus responsible for
AIDS. That same day, Trevor Bedford [an expert
in viral evolutionary dynamics]
v
began tweeting in
response
vi
to the paper’s claims, and Anthony Fauci
and Jeremy Farrar called for an emergency
teleconference to be held the next day a Saturday
with leading scientists & public officials from four
countries. By Monday afternoon, a second
teleconference had been held,
vii
with GOF-
implicated scientists, Trevor Bedford, Anthony
Fauci, Tom Inglesby, Gigi Gronvall and more
attending at the request of Kelvin Droegemeier, the
Presidential Science Advisor for President Trump
and the director of the White House Office of
Science & Technology Policy; the stated purpose of
the event was to “combat misinformation
viii
surrounding the origin of the 2019-nCoV virus.
One of the speakers was David “Chris”
Hassell, senior science advisor to Robert Kadlec,
Assistant Secretary for Preparedness & Response
[AS/PR] at the Department of Health & Human Services; Hassell was also the chair of the P3CO
oversight committee created in 2017 to review gain-of-function research involving Potential Pandemic
Pathogens. Together, this group reached the decision to construct a specific narrative, meant to silence
any inquiries that might travel down a path that implicated many of the most prominent virologists and
vaccinologists in the world.
“They made a decision, almost a P.R. decision, that they were going to push one point of
view only” and suppress rigorous debate. They argued they did it in defense of science, but it
was antithetical to science.”
ix
- Robert Redfield, Director of the US CDC, 2018-2021 (from Eban, 2022)
The Myth of the Blind Watchmaker Summary 5/28/2022
© Charles H. Rixey, 2022 DRASTIC
“This is a tiny tiny sequence and in no way suggests engineering”
Trevor Bedford’s tweet [pictured above] of 2/1/2020 argued that “Insert 4 (QTNSPRRA) shares
GTNS with the bat virus RaTG13, while PRRA represents unique material in #nCoV2019. This is a tiny
tiny sequence and in no way suggests engineering.” It’s hard to overstate how disingenuous his statement
was, especially since the internet archive shows that Bedford had been active on the message board
during the period between Gallaher’s first post on 1/29/2020 and Bedford’s 2/1/2020 tweet.
The existence of the Furin Cleavage Site [FCS] couldn’t be suppressed, because its crucial role in
increasing the infectiousness of respiratory pathogens was widely understood
x
within the international
scientific community. However, the existence of the FCS was not highlighted by any of the scientists or
public health officials convened by Anthony Fauci and Jeremy Farrar on 2/1/20 until the final publication
of “The Proximal Origin of SARS-CoV-2” on 3/17/2020 in which the potentially unnatural origin of the
FCS was roundly rejected, and its relevance for infectivity [as compared to the ACE2 receptor] was
minimized.
Much of what has been done to combat the pandemic especially here in the United States has
been the opposite of what would’ve been recommended, if all of the information available to Dr. Fauci by
February 1st 2020
xi
been publicly known. Collateral damage from the decision to withhold this
information can be grouped into 6 primary topics:
1 & 2-COVID’s origin & Censorship of it:
Dr. Fauci and a few other senior scientists knew instantly that the discovery of HIV spike
inserts
xii
within the SAR-CoV-2 viral genome made it almost impossible for the virus to be natural;
xiii
mixing elements of HIV-1’s spike protein with CoV sequences and/or backbones
xiv
[or vice versa] has
been part of HIV-1/CoV vaccine research
xv
since at least 2006
xvi
[at least 2007 for the WIV
xvii
, and at least
as recently as 2018
xviii
]. They knew
xix
about the Furin cleavage site [FCS] the single biggest genomic
contributor to SARS-CoV-2’s ability to become a pandemic virus
xx
yet didn’t share that information
xxi
with the rest of the world, even though medical professionals in particular needed to be warned.
3 & 4-Non-Parmaceutical Interventions [NPI] & Early Treatments:
They suppressed early treatments that were already available including the very fusion
inhibitors implicated by the high homology [similarity]between the fusion peptides of HIV & SARS-like
coronaviruses
xxii
even after a pioneer in the field recommended their use so early in the outbreak.
xxiii
As
a career Marine in the field of CBRN defense, I know that early treatment & prophylaxis are vital for
WMD mitigation plans
xxiv
why wouldn’t this be the case during a pandemic?
5 & 6-Vaccine Development & Implications of the FCS/HIV Inserts:
The QTNSPRRA that encodes for the FCS forms the bookends of the HIV gp120 motif a
feature that may be the reason SARS-CoV-2 can infect human T-cells. Ignoring the need for early
research into the antigenic implications of the HIV inserts and ignoring the potential risks of including
the complete spike sequence within most SARS-CoV-2 vaccine prototypes, directly contributed to many
of the issues associated [or soon to be associated] with “Long COVID.
Continuing to suppress research and discussion that questions the viability of the mRNA platform
& prototypes given their partial epitope coverage and high recombination traits as well as the decade
of prior failed attempts to produce a vaccine that overcame these challenges, will only exacerbate the
Long COVID challenges.
The Myth of the Blind Watchmaker Summary 5/28/2022
© Charles H. Rixey, 2022 DRASTIC
The true legacy of Anthony Fauci the implications of censorship of
Intelligent Design
These questions are valid regardless of who created the SARS-CoV-2 virus, or for what purpose it was
created. The magnitude of their implications is such that simply refusing to answer them should itself be
considered obstruction of justice.
A) Key Questions & Considerations [sorted by topic]:
a. The origin of SARS-CoV-2
i. Why did Dr. Fauci react to the announced discovery of HIV-like inserts in the
2019-nCoV genome by immediately moving to neutralize the subject?
ii. He’d previously spent almost 4 decades being the world’s foremost advocate for
HIV-1/AIDS research why would he not embrace the challenge of a capstone
pandemic with an HIV connection?
iii. Especially now, when we’re learning about how SARS-CoV-2 can infiltrate the
immune system
xxv
[and so can his VRC-designed vaccines]?
iv. Why did the US intelligence community report called the Biden Report [both the
original announcement & the de-classified ‘full’ document] on the origin of the
SARS-CoV-2 virus make no mention of the CIA’s connections to EcoHealth
Alliance via the USAID, or the DEFUSE documents that were found stored
within a folder on JWICS, a shared, top-secret intelligence server?
v. Why did Anthony Fauci & Kelvin Droegemeier withhold highly relevant
information about gain-of-function research connections between the WIV & the
NIAID from President Trump’s administration, and potentially President Biden’s
as well?
b. Scientific censorship
i. Why did Anthony Fauci, Francis Collins & Jeremy Farrar immediately act to
curtail research
xxvi
[including pressuring the authors of Pradhan et al to withdraw
their paper] into the potential lab origin of SARS-CoV-2, despite their own
significant concerns?
ii. Why did Anthony Fauci & Kelvin Droegemeier the Presidential Science
Advisor withheld virtually everything from President Trump
xxvii
and his team
related to US-funded gain-of-function research being conducted with the Wuhan
Institute of Virology?
iii. Why was Bill Gallaher removed from any mention within Proximal Origin?
xxviii
His Déjà vu book was the only citation from the Virological.org version of
2/16/2020
xxix
that was removed from the final version, published on 3/17/20 in
Nature Communications.
1. This is despite the fact that Gallaher’s arguments regarding the origin of
the FCS and the SARS-CoV-2 virus itself were copied almost verbatim
from his book or the virological.org posts that discussed his findings.
iv. Why was Gallaher’s advice on therapeutics
xxx
ignored/suppressed?
xxxi
v. Censorship
xxxii
/Narrative
xxxiii
& Top 6 journals,
xxxiv
c. Non-pharmaceutical interventions [NPI’s]
i. Why did Anthony Fauci and the other attendees of the 2/1 teleconference not
warn the rest of the world of the existence
xxxv
and implications of the FCS?
ii. Why did Anthony Fauci continuously push back on President Trump’s travel ban
throughout the latter part of January, 2020, during this period of silence?
iii. Further, why has the aerosol
xxxvi
/airborne transmission
xxxvii
of the virus been
largely ignored by the WHO
xxxviii
and most public health agencies?
The Myth of the Blind Watchmaker Summary 5/28/2022
© Charles H. Rixey, 2022 DRASTIC
d. Early treatments
i. Why did Anthony Fauci, BARDA, AS/PR push Remdesivir but not other anti-
viral drugs; specifically fusion inhibitors,
xxxix
which had been invented in the US
xl
and showed strong potential
xli
in 2 decades’ worth of in silico,
xlii
in vitro
xliii
& in
vivo
xliv
studies on Class 1 viruses including HIV-1/2 and CoV’s?
ii. Robert Garry recently informed us that Vitamin D is critical for our T-Cell
response,
xlv
which is one of the bodily systems hit hardest
xlvi
during a severe
COVID-19 infection. [Why didn’t Anthony Fauci et al ever recommend/include
Vitamin D as a prophylactic/early treatment [or weight loss, exercise or healthier
diets]]?
iii. Why was Bill Gallaher’s note on the Chinese use of chloroquine
xlvii
[to block the
virus from using endosomal entry, especially in the lungs] during the Wuhan
outbreak never specifically addressed [pictured below]?
iv. Why was Remdesivir targeted for approval for the treatment of late-stage
COVID-19 infection, when its mechanism targets the virus itself which has
already inflicted its damage by that point in the infection? Ralph Baric & Mark
Denison who helped create and test it reiterated this point in February
2020.
xlviii
v. Why didn’t we look at antivirals besides Remdesivir? You know, like…. fusion
peptide inhibitors, for instance?
vi. Why issue an EUA for an FDA-approved medication like Hydroxychloroquine?
What was so dangerous about Drs. prescribing anything off-label?
vii. China had a potent pan-CoV inhibitor prior to the COVID-19 outbreak in Wuhan
[EK1, published on 4/1/2019]; they literally pointed this out several times in Jan-
Feb 2020, before announcing an even more effective fusion inhibitor [EK1C4] on
3/30/2020.
viii. Some have suggested that SARS-CoV-2 is a Live Attenuated Vaccine [LAV]
reverting to its original form, something seen with LAV’s with Dengue Fever.
However, that makes no sense why would China need an antidote for a
vaccine/vaccine trial?
e. Deformed Consent: Vaccine development
i. Why did the VRC drop the SARS-CoV-2 spike into their mRNA backbone
before its immunogenicity/risks were understood? Apart from the HIV inserts,
Bill Gallaher described 1 such immunosuppressive domain,
LQPRTFLLKYNENGTITDAVD, with similarity to strains of Ebola and
HIV1.
xlix
The Myth of the Blind Watchmaker Summary 5/28/2022
© Charles H. Rixey, 2022 DRASTIC
ii. Why did Dr. Fauci, the VRC, BARDA, and FDA remain silent about the poor
results of previous studies involving mRNA and other CoV vaccine attempts in
animals especially those of Ralph Baric?
l
iii. Why was the DoD forced to universally vaccinate our active-duty troops with a
partial-epitope-coverage
li
spike protein vaccine less than 3 years after DARPA
rejected
lii
a very similar proposal in bats?
liii
iv. Why were the vaccines mandated for many Americans just as evidence of escape
was emerging c. Fall 2021?
v. Why universally vaccinate ALL troops when the long-term effects of the mRNA
method are unknown much less the long-term antigenic effects of the SARS-
CoV-2 spike itself?
liv
Why risk the operational readiness of the entire American
military by transfecting all troops with a ‘leaky’ vaccine?
vi. Why are Dr. Fauci et al still silencing any discussion of the potential immune
suppression of the vaccines,
lv
and stalling the clinical trial data from Pfizer
lvi
et
al? The potential implications of massive immune damage
lvii
supersede any FDA
deliberations about follow-on booster shots.
f. Why is the QTNSPRRA sequence that contains the furin cleavage site so important and
so unique?
i. First, the insert should be viewed as two distinct 4 protein/12-nt segments, since
they actually form the book-ends of the full gp120;
lviii
the latter half is the PRRA
that is more commonly referred to as the “Furin cleavage site.” This particular
FCS motif cannot function without the QTQTNS that precedes it.
lix
ii. When viewed as a group, the full set of 4 HIV inserts appears to form a
functional gp120 sequence that can infect T-cells, thus being the worst possible
thing anyone could add to an mRNA transfection that can only stimulate
antibody responses. No other than the WIV itself just published a study
demonstrating t-cell infection by spike proteins;
lx
thus, the wild & vaccine spikes
teach our cells to literally manufacture spikes with HIV-like antigens. Why
would this be a desirable outcome for a transfecting coronavirus vaccine?
iii. Why would extra steps be taken to stabilize the immunogenic elements of the
spike, including QTNSPRRA, which serves as an SEB toxin
lxi
& contained the
FCS?
lxii
iv. Furthermore, why would so much faith be placed in the use of lipid nanoparticles
to convey spike proteins that already exhibited broad tropism
lxiii
via the FCS?
v. Why would a prion-like domain be conserved
lxiv
within the vaccine’s genome
lxv
at all? There is no reason to risk transfecting any part of any genome that could
trigger amyloidogenesis
lxvi
the creation and thus buildup of amyloid plaques
which drives the emergence of Parkinson’s Disease, Alzheimer’s Disease and
Creutzfeldt-Jakob Disease [colloquially referred to as Mad Cow Disease], etc.
1. Can this amyloidogenesis be systemic? Is this related to the seemingly
irrational objection to Zinc, or to Vitamin D?
vi. The viral genome appears to be attempting to revert [de-attenuate] away from the
FCS & HIV inserts,
lxvii
further evidence that those mutations didn’t occur
naturally.
vii. Why does the region of the FCS match a reverse complement sequence
lxviii
from
Moderna, who partnered with the NIAID’s Vaccine Research Center [VRC] to
produce an mRNA vaccine?
viii. Why do the forward and reverse primers for PCR for SARS-CoV-2 match those
of Ralph Baric’s previous constructs
lxix
SARS-CoV-M15, SARS-CoV-Rs3367 &
SHC014-CoV-MA15?
The Myth of the Blind Watchmaker Summary 5/28/2022
© Charles H. Rixey, 2022 DRASTIC
ix. The virus gains the functions of an efficient FCS AND a potentially effective
antidote target with the appropriate peptide fusion inhibitor
lxx
[dozens of
proposed compounds, targeting various sequences of the SARS-CoV-2 spike
protein, have been developed or are currently being studied].
lxxi
In December,
Chinese scientists reported that their EK1C4 inhibitor also helps reduce the risk
of Antibody-Dependent Enhancement.
lxxii
x. As with previous coronaviruses, Antibody-Dependent Enhancement [ADE]
lxxiii
is
a realistic possibility, as Robert Malone himself also pointed out
lxxiv
in early
March of 2020.
xi. The FCS increases the ability of the virus to infect via the inhalation route, which
has the added benefit of lowering the bar for the size of the viral load needed for
an infectious dose.
lxxv
xii. Jean-Claude Perez & Luc Montagnier [who was awarded the 2008 Nobel Prize in
Physiology or Medicine for his discovery of the HIV-1 virus in 1983] showed
that the location of the PRRA insert within the SARS-CoV-2 genome was
already an optimal cleavage site BEFORE this insertion.
lxxvi
xiii. As oxygen levels decrease
lxxvii
[hypoxia] in the lungs, furin expression
increases,
lxxviii
which can contribute to rapid declines in patient disposition as a
snowball effect. This also plays a role in reducing the suppression of cancerous
cells.
lxxix
xiv. Even mild hypoxia [~10% reduction] was enough to allow SARS-CoV-2 to pass
through the Blood-Brain Barrier [BBB].
lxxx
xv. The existence of many arginine residues within a small region that contains the
FCS follows the pattern associated with the mechanism known as binding of cell
penetrating peptides.
lxxxi
The goal of building up a high cumulative positive
charge
lxxxii
is to enhance cell affinity towards the virus.
lxxxiii
SARS-CoV-2’s
ability to utilize the human sodium channel ENaC
lxxxiv
is unlikely to be fortuitous.
xvi. How would someone investigate a SARS-like CoV’s ability to infiltrate dendritic
cells via the DC-SIGN pathway, as stated in the DEFUSE proposal?
lxxxv
The
virus best known for utilizing this pathway is… HIV-1:
The Myth of the Blind Watchmaker Summary 5/28/2022
© Charles H. Rixey, 2022 DRASTIC
i
The DRASTIC Report with Charles Rixey: They added gp120 from HIV-1 and they have the antidote,” archived on Bitchute,
originally streamed on 4/9/2022 on GigaOhm Biological’s Twitch page.
ii
(PDF) 20220514 - The Myth of the Blind Watchmaker - Topical Bibliography.pdf (researchgate.net)
iii
Ah Kahn Syed, "Absolute proof: The Gp-120 sequences prove beyond all doubt that "COVID-19" was man-made," Substack,
4/10/2022.
iv
William R. & Andrew D. Gallaher, "Analysis of Wuhan Coronavirus: déjà vu [findings on 1/29, 1st edition on 2/1],"
Virological.org, 2/1/2020.
v
Trevor Bedford, Ph.D, from the Fred Hutchinson Institute website, 5/1/2022.
vi
Trevor Bedford, https://twitter.com/trvrb/status/1223337991168380928?s=20&t=GjdGSZ8PbXB7fTscIxLAGw,” Twitter,
1/31/2020.
vii
Charles Rixey, Who Watches The Watchmen? - Fauci's "Noble Lie" Exposed,” Zero Hedge, 7/24/2021.
viii
Volume 11 of Ralph Baric’s emails, Baric-Emails-2.17.21.pdf,” US Right-To-Know Biohazard FOIA collection, pages 115-
133, 2/17/2021.
ix
Katherine Eban, “Inside the Virus-Hunting Nonprofit at the Center of the Lab-Leak Controversy,” Vanity Fair, 3/31/2022.
x
Exchanges between Ralph Baric, Mark Denison, Philip Dormitzer & David Relman, et al. Session 5: Potential Benefits of GOF
Research II: Treatment and Response - YouTube,” YouTube, December 2014.
xi
House E&C Committee, "House Energy & Commerce Committee letter to NIH, January 2022," US House of Representatives,
1/12/2022.
xii
Prashant Pradhan et al, "Uncanny similarity of unique inserts in the 2019-nCoV spike protein to HIV-1 gp120 and Gag,"
bioRxiv, 1/30/2020.
xiii
Ah Kahn Syed, "Absolute proof: The Gp-120 sequences prove beyond all doubt that "COVID-19" was man-made," Substack,
4/10/2022.
xiv
Qiuying Huang et al, "Preparation of a Chimeric Armored RNA as a Versatile Calibrator for Multiple Virus Assays," Clinical
Chemistry, 7/1/2006.
xv
Vinu Arumugham, "Root cause of COVID-19? Biotechnology's dirty secret: Contamination. Bioinformatics evidence
demonstrates that SARS-CoV-2 was created in a laboratory…," Zenodo, 4/25/2020.
xvi
Richard Fleming, Is COVID-19 a Bioweapon? A scientific & forensic investigation, 9/7/2021.
xvii
Zheng-Li Shi et al, "Difference in Receptor Usage between Severe Acute Respiratory Syndrome (SARS) Coronavirus and
SARS-Like Coronavirus of Bat Origin," Journal of Virology, 12/12/2007.
xviii
Yu Jie, “The modification of vaccinia virus based on EEV egress related genes for potential application as vaccine vector,” a
dissertation submitted to the University of the Chinese Academy of Sciences, 6/1/2018. In this dissertation, the env protein of
HIV-1 was inserted into a vaccinia virus backbone, producing a strong immune response in vitro and in vivo.
xix
leopold-nih-foia-anthony-fauci-emails.pdf
xx
Vineet Menachery et al, “Furin Cleavage Site Is Key to SARS-CoV-2 Pathogenesis,BioRxiv, 8/26/2020.
xxi
Zheng-Li Shi et al, "ACE2-independent infection of T lymphocytes by SARS-CoV-2," Signal Transduction & Targeted
Therapy, 3/11/2022.
xxii
Yossef Kliger & Erez Levanon, "Cloaked similarity between HIV-1 and SARS-CoV suggests an anti-SARS strategy," BMC
Microbiology, 6/1/2003.
xxiii
https://virological.org/t/analysis-of-wuhan-coronavirus-deja-vu/357/4
xxiv
See numerous unclassified but restricted US & NATO Joint Publications on CBRN defense, mitigation, hazard prediction,
consequence management, etc [I am well-versed in the technical aspects of these publications, as a former Instructor &
Curriculum Developer at the United States Marine Corps CBRN School in Fort Leonard Wood, Missouri.
xxv
Zheng-Li Shi et al, "ACE2-independent infection of T lymphocytes by SARS-CoV-2," Signal Transduction & Targeted
Therapy, 3/11/2022.
xxvi
Charles Rixey, Glenn Beck & Jason Buttrill, “Crimes or Cover-Up? Exposing the World’s Most Dangerous Lie,” The Blaze
TV, 11/17/2021.
xxvii
Charles Rixey, Glenn Beck & Jason Buttrill, “Crimes or Cover-Up? Exposing the World’s Most Dangerous Lie,” The Blaze
TV, 11/17/2021.
xxviii
Kristian G Andersen et al, "The proximal origin of SARS-CoV-2," Nature Medicine, 3/17/2020.
xxix
Kristian Andersen, “The Proximal Origin of SARS-CoV-2 - SARS-CoV-2 coronavirus / nCoV-2019 Evolutionary History -
Virological,” Virological.org post, 2/16/2020.
xxx
William R. & Andrew D. Gallaher, "Analysis of Wuhan Coronavirus: déjà vu [findings on 1/29, 1st edition on 2/1],"
Virological.org, 2/1/2020.
xxxi
In Déjà vu, Gallaher described fusion peptide inhibitors, protease inhibitors, chloroquine to protect the endosomal pathway in
lung cells, potential immunosuppressive portions of the SARS-CoV-2 spike protein that should be avoided in any vaccines, etc.
xxxii
Charles Rixey, “Gaslight of the Gods, part II: A 13% 'Consensus' of implicated scientists censored science - & then us - to
protect themselves,” Prometheus Shrugged, 3/28/2022.
xxxiii
Charles Rixey, “Gaslight of the Gods, part III: The Architects of COVID-19 #Consensuship,” Prometheus Shrugged,
4/1/2022.
xxxiv
Charles Rixey, “Ignoble Lies & Inconvenient Truths: Scientific collusion on COVID-19 comes from the top,” Prometheus
Shrugged, 8/14/2021.
The Myth of the Blind Watchmaker Summary 5/28/2022
© Charles H. Rixey, 2022 DRASTIC
xxxv
Li Xin et al, "A furin cleavage site was discovered in the spike protein of the 2019 nCoV," Chinese Journal of
Bioinformatics, 1/21/2020.
xxxvi
Robert Garry et al, “Persistence of Severe Acute Respiratory Syndrome Coronavirus 2 in Aerosol Suspensions,” Emerging
Infectious Diseases, 9/26/2020.
xxxvii
Evidence for lack of transmission by close contact and surface touch in a restaurant outbreak of COVID-19,” Journal of
Infection, 5/29/2021.
xxxviii
Webinar: The Science of COVID-19 Aerosol Transmission An Interview with Dr. Jose-Luis Jimenez,
https://youtu.be/bnEpEHWN1Ew,” YouTube, 4/6/2021.
xxxix
Peptide-Based HIV Entry Inhibitors | SpringerLink
xl
Bill Gallaher & Robert Garry, SARS Press Release,” Virology.net, 5/1/2003.
xli
Xinling Wang et al, "Pan-coronavirus fusion inhibitors as the hope for today and tomorrow," Protein & Cell, 1/9/2021.
xlii
Khadijeh Ahmadi et al, "Enfuvirtide, an HIV-1 fusion inhibitor peptide, can act as a potent SARS-CoV-2 fusion inhibitor: an
in silico drug repurposing study," Journal of Biomolecular Structure & Dynamics, 1/13/2021.
xliii
Hongzhou Lu, “Drug treatment options for the 2019-new coronavirus (2019-nCoV) (jst.go.jp),” BioScience Trends,
1/28/2020.
xliv
Huihui Chong et al, "A Lipopeptide HIV-1/2 Fusion Inhibitor with Highly Potent In Vitro, Ex Vivo, and In Vivo Antiviral
Activity," Journal of Virology, 5/12/2017.
xlv
Jay Kolls & Robert Garry, "Role of the T cell vitamin D receptor in severe COVID-19," Nature Immunology, 12/20/2021.
xlvi
Sonia Andre et al, "T cell apoptosis characterizes severe Covid-19 disease," Nature Cell Death & Cell Differentiation,
1/22/2022.
xlvii
Gallaher & Gallaher, 2020.
xlviii
Mark Denison, Ralph Baric, and Alan Embry, “NVAC l February 2020 l Day 1, Pt 3: Coronavirus Presentations,” The
National Vaccine Advisory Council meeting, Day 1 on YouTube, 2/13/2020.
xlix
Gallaher highlighted 1 particular potentially immuno-suppressive peptide in Déjà vu, on page 39:
LQPRTFLLKYNENGTITDAVD.
l
Ralph Baric et al, "SARS-like WIV1-CoV poised for human emergence," PNAS, 1/20/2016.
li
Charles Rixey, PREEMPTive Spike: Scientific support for mandates is built upon a known false premise,” Prometheus
Shrugged, 10/6/2021.
lii
DRASTIC, "PREEMPT - DRASTIC'S Analysis of the DEFUSE Rejection Letter," DRASTIC, 9/20/2021.
liii
PREEMPT_HR00111880017_Notes_v1_b.docx
liv
Rossana Roncato et al, “Lipid rafts as viral entry routes and immune platforms: A double-edged sword in SARS-CoV-2
infection?Molecular & Cell Biology of Lipids 6/1/2022.
lv
Stephanie Seneff et al, "Innate immune suppression by SARS-CoV-2 mRNA vaccinations: The role of G-quadruplexes,
exosomes, and MicroRNAs," Food & Chemical Toxicology, 4/15/2022.
lvi
FDA Begins Releasing Pfizer COVID Vax Documents
lvii
Official U.S. Government data suggests Fully Vaccinated Americans are developing AIDS,” The Expose, 5/8/2022.
lviii
Jean-Claude Perez & Luc Montagnier, "COVID-19, SARS and Bats Coronaviruses Genomes Unexpected Exogeneous RNA
Sequences," OSF Pre-Prints, 4/25/2020.
lix
Menachery et al, "QTQTN motif upstream of the furin-cleavage site plays key role in SARS-CoV-2 infection and
pathogenesis," bioRxiv, 12/17/2021
lx
Zheng-Li Shi et al, "ACE2-independent infection of T lymphocytes by SARS-CoV-2," Signal Transduction & Targeted
Therapy, 3/11/2022.
lxi
Mary Hongying Cheng, et al, "Superantigenic character of an insert unique to SARS-CoV-2 spike supported by skewed TCR
repertoire in patients with hyperinflammation," PNAS, 9/28/2020.
lxii
B. Coutard et al, "The spike glycoprotein of the new coronavirus 2019-nCoV contains a furin-like cleavage site absent in CoV
of the same clade," Antiviral Research, 2/10/2020.
lxiii
Rossana Roncato et al, “Lipid rafts as viral entry routes and immune platforms: A double-edged sword in SARS-CoV-2
infection?Molecular & Cell Biology of Lipids 6/1/2022.
lxiv
Judith White et al, Structures & Membranes of Viral Membrane Fusion Proteins,” Critical Reviews in Biochemical &
Molecular Biology, 5/1/2009.
lxv
Richard Fleming, Is COVID-19 a Bioweapon? A scientific & forensic investigation, 9/7/2021.
lxvi
Shin be Oh et al, “Associative Interactions among Zinc, Apolipoprotein E, and Amyloid-β in the Amyloid Pathology,”
International Journal of Molecular Sciences, 1/25/2020.
lxvii
Richard Fleming, “BASES2021 SARS CoVd2 Gain of Function Research Violations of Law,” YouTube, 7/16/2021 [minute
56].
lxviii
Ah Khan Syed, “How to BLAST your way to the truth about the origins of COVID-19,” Substack, 12/28/2021.
lxix
Richard Fleming, “BASES2021 SARS CoVd2 Gain of Function Research Violations of Law,” YouTube, 7/16/2021 [minute
59].
lxx
Shuai Xia et al, "Peptide-Based HIV Entry Inhibitors," Advances in Experimental Medicine & Biology, 4/11/2022.
lxxi
Qiaoshuai Lan et al, “Coronavirus Entry Inhibitors,” Virus Entry Inhibitors, 4/13/2022.
The Myth of the Blind Watchmaker Summary 5/28/2022
© Charles H. Rixey, 2022 DRASTIC
lxxii
Zai Wang et al, ACE2 can act as the secondary receptor in the FcγR-dependent ADE of SARS-CoV-2 infection,” iScience,
1/21/2022.
lxxiii
Jiong Wang & Martin Zand, "The potential for antibody-dependent enhancement of SARS-CoV-2 infection: Translational
implications for vaccine development," Journal of Clinical & Translational Science, 4/13/2020.
lxxiv
Darrell Ricke & Robert Malone, “Medical Countermeasures Analysis of 2019-nCoV and Vaccine Risks for Antibody-
Dependent Enhancement (ADE),” SSRN, 3/2/2020.
lxxv
Nancy Leung, “Transmissibility and transmission of respiratory viruses,” Nature Reviews Microbiology, 3/22/2021.
lxxvi
Jean-Claude Perez & Luc Montagnier, “HIV man-manipulated coronavirus genome evolution trends,” Zenodo, 8/5/2020.
lxxvii
Elisabeth Braun & Daniel Sauter, Furin‐mediated protein processing in infectious diseases and cancer, Clinical &
Translational Medicine, 8/5/2019.
lxxviii
Stephanie McMahon et al, "Hypoxia-enhanced Expression of the Proprotein Convertase Furin Is Mediated by Hypoxia-
inducible Factor-1," Journal of Biological Chemistry, 12/15/2004.
lxxix
Dominique Arsenault et al, "Hypoxia enhances cancer cell invasion through relocalization of the proprotein convertase furin
from the trans‐golgi network to the cell surface," Journal of Cellular Physiology, 4/18/2011.
lxxx
Iqra Pervaiz et al, Assessing the effects of COVID‐19‐induced hypoxia and ACE2 signaling on the human blood‐brain
barrier in‐vitro,” The FASEB Journal, 5/13/2022.
lxxxi
Birger Sørensen, Angus Dalgleish & Andres Susrud, "Biovacc-19: A candidate vaccine," QRB Discovery, 6/2/2020.
lxxxii
From Birger Sorenson et al (2020): “The co-receptor dependent phagocytic general method of action of SARS-CoV-2
appears to be specifically related to cumulative charge: please refer to SARS-CoV-2 peaks above pI = 8.24 (Fig.5) compared to
human SARS-CoV (Fig. 4). These basic domains partly inserted and partly substituted amino acids explain the salt bridges
formed between the SARS-CoV-2 spike and its co-receptors on the cell membrane. Indeed, these data suggest that the infectivity
of SARS-CoV-2 is best explained by this cumulative charge associated with these basic charged domains, enabling extra salt
bridges to attach to membrane components as well as to the membrane itself.”
lxxxiii
Angus Dalgleish et al, "The evidence which suggests that this is no naturally evolved virus," Minerva, 7/2/2020.
lxxxiv
Praveen Anand et al, “SARS-CoV-2 strategically mimics proteolytic activation of human ENaC,” eLife, 5/26/2020.
lxxxv
PREEMPT Volume 1 no ESS HR00118S0017 EcoHealth Alliance DEFUSE.
ResearchGate has not been able to resolve any citations for this publication.
Article
Full-text available
SARS-CoV-2 induced marked lymphopenia in severe patients with COVID-19. However, whether lymphocytes are targets of viral infection is yet to be determined, although SARS-CoV-2 RNA or antigen has been identified in T cells from patients. Here, we confirmed that SARS-CoV-2 viral antigen could be detected in patient peripheral blood cells (PBCs) or postmortem lung T cells, and the infectious virus could also be detected from viral antigen-positive PBCs. We next prove that SARS-CoV-2 infects T lymphocytes, preferably activated CD4 + T cells in vitro. Upon infection, viral RNA, subgenomic RNA, viral protein or viral particle can be detected in the T cells. Furthermore, we show that the infection is spike-ACE2/TMPRSS2-independent through using ACE2 knockdown or receptor blocking experiments. Next, we demonstrate that viral antigen-positive T cells from patient undergone pronounced apoptosis. In vitro infection of T cells induced cell death that is likely in mitochondria ROS-HIF-1a-dependent pathways. Finally, we demonstrated that LFA-1, the protein exclusively expresses in multiple leukocytes, is more likely the entry molecule that mediated SARS-CoV-2 infection in T cells, compared to a list of other known receptors. Collectively, this work confirmed a SARS-CoV-2 infection of T cells, in a spike-ACE2-independent manner, which shed novel insights into the underlying mechanisms of SARS-CoV-2-induced lymphopenia in COVID-19 patients.
Article
Full-text available
Severe SARS-CoV-2 infections are characterized by lymphopenia, but the mechanisms involved are still elusive. Based on our knowledge of HIV pathophysiology, we hypothesized that SARS-CoV-2 infection-mediated lymphopenia could also be related to T cell apoptosis. By comparing intensive care unit (ICU) and non-ICU COVID-19 patients with age-matched healthy donors, we found a strong positive correlation between plasma levels of soluble FasL (sFasL) and T cell surface expression of Fas/CD95 with the propensity of T cells to die and CD4 T cell counts. Plasma levels of sFasL and T cell death are correlated with CXCL10 which is part of the signature of 4 biomarkers of disease severity (ROC, 0.98). We also found that members of the Bcl-2 family had modulated in the T cells of COVID-19 patients. More importantly, we demonstrated that the pan-caspase inhibitor, Q-VD, prevents T cell death by apoptosis and enhances Th1 transcripts. Altogether, our results are compatible with a model in which T-cell apoptosis accounts for T lymphopenia in individuals with severe COVID-19. Therefore, a strategy aimed at blocking caspase activation could be beneficial for preventing immunodeficiency in COVID-19 patients.
Article
Full-text available
It is unknown whether antibody-mediated enhancement (ADE) contributes to the pathogenesis of COVID-19, and the conditions for ADE needs to be elucidated. We demonstrated that without inducing an ACE2-independent ADE on Raji cells, the neutralizing antibody CB6, a mouse anti-S1 serum and convalescent plasma induced ADE on cells expressing FcγRIIA/CD32A and low levels of endogenous ACE2. ADE occurred at sub-neutralizing antibody concentrations, indicating that unneutralized S protein was required for ADE. The enhanced infectivity of 614G variant was higher than that of 614D wildtype in the presence of antibodies, further suggesting that ADE may be influenced by virus strains with different ACE2 binding affinity. Finally, knockdown of ACE2 or treatment with a fusion-inhibition peptide EK1C4 significantly reduced ADE. In conclusion, we identified an ADE mechanism mediated by neutralizing antibodies against SARS-CoV-2. ACE2 may act as a secondary receptor required for the antibody- and FcγR-mediated enhanced entry of SARS-CoV-2.
Preprint
Full-text available
In 2019, the 2019 novel Coronavirus (2019-nCoV) has caused the pneumonia outbreak in Wuhan (a city of China). In our previous study, the analytical results showed that both 2019-nCoV and SARS coronavirus belongs to Betacoronavirus subgroup B (BB coronavirus), but have large differences. The most important finding was that the alternative translation of Nankai CDS could produce more than 17 putative proteins, which may be responsible for the host adaption. The genotyping of 13 viruses using the 17 putative proteins revealed the high mutation rate and diversity of betacoronavirus. The present study for the first time reported a very important mutation in the Spike (S) proteins of BB coronavirus. By this mutation, 2019-nCoV acquired a cleavage site for furin enzyme, which is not present in the S proteins of all other BB coronavirus (e.g. SARS coronavirus) except the Mouse Hepatitis coronavirus (MHV). This mutation may increase the efficiency of virus infection into cells, making 2019-nCoV has significantly stronger transmissibility than SARS coronavirus. Because of this mutation, the packing mechanism of the 2019-nCoV may be changed to being more similar to those of MHV, HIV, Ebola virus (EBoV) and some avian influenza viruses, other than those of all other BB coronavirus (e.g. SARS coronavirus) except the Mouse Hepatitis coronavirus (MHV). In addition, we unexpectedly found that some avian influenza viruses acquired a cleavage site for furin enzyme by mutation as 2019-nCoV. Further studies of this mutation will help to reveal the stronger transmissibility of 2019-nCoV and lay foundations for vaccine development and drug design of, but not limited to 2019-nCoV.
Article
Full-text available
Outbreaks from zoonotic sources represent a threat to both human disease as well as the global economy. Despite a wealth of metagenomics studies, methods to leverage these datasets to identify future threats are underdeveloped. In this study, we describe an approach that combines existing metagenomics data with reverse genetics to engineer reagents to evaluate emergence and pathogenic potential of circulating zoonotic viruses. Focusing on the severe acute respiratory syndrome (SARS)-like viruses, the results indicate that the WIV1-coronavirus (CoV) cluster has the ability to directly infect and may undergo limited transmission in human populations. However, in vivo attenuation suggests additional adaptation is required for epidemic disease. Importantly, available SARS monoclonal antibodies offered success in limiting viral infection absent from available vaccine approaches. Together, the data highlight the utility of a platform to identify and prioritize prepandemic strains harbored in animal reservoirs and document the threat posed by WIV1-CoV for emergence in human populations.
Article
Full-text available
Hypoxia is a common tumorigenesis enhancer, mostly owing to its impact on gene expression of many angiogenic and invasion-related mediators, some of which are natural substrates for the proprotein convertase furin. Analysis of furin promoters revealed the presence of putative binding sites for hypoxia-inducible factor-1 (HIF-1), a transcription complex that plays a pivotal role in cellular adaptation to hypoxia. In fact, we demonstrate herein that the levels of fur mRNA, encoding furin, are remarkably increased upon hypoxic challenge. Cotransfection of a HIF-1α dominant negative form in wild-type (WT) cells or transfection of a furin promoter-reporter gene in HIF-1-deficient cells indicated the requirement of HIF-1 for furin promoter activation by hypoxia. Direct HIF-1 action on the furin promoter was identified as a canonical hypoxia-responsive element site with enhancer capability. The hypoxic/HIF-1 regulation of furin correlated with an increased proteolytic activation of the substrates membrane-type 1 matrix metalloproteinase and transforming growth factor-β1. Our findings unveil a new facet of the physiological consequences of hypoxia/HIF-1, through enhanced furin-induced proteolytic processing/activation of proproteins known to be involved in tumorigenesis.
Article
Peptides derived from the C-terminal heptad repeat (CHR) region of the human immunodeficiency virus type 1 (HIV-1) fusogenic protein gp41 are potent viral entry inhibitors, and currently, enfuvirtide (T-20) is the only one approved for clinical use; however, emerging drug resistance largely limits its efficacy. In this study, we generated a novel lipopeptide inhibitor, named LP-19, by integrating multiple design strategies, including an N-terminal M-T hook structure, an HIV-2 sequence, intrahelical salt bridges, and a membrane-anchoring lipid tail. LP-19 showed stable binding affinity and highly potent, broad, and long-lasting antiviral activity. In in vitro studies, LP-19 efficiently inhibited HIV-1-, HIV-2-, and simian immunodeficiency virus (SIV)-mediated cell fusion, viral entry, and infection, and it was highly active against diverse subtypes of primary HIV-1 isolates and inhibitor-resistant mutants. Ex vivo studies demonstrated that LP-19 exhibited dramatically increased anti- HIV activity and an extended half-life in rhesus macaques. In short-term monotherapy, LP-19 reduced viral loads to undetectable levels in acutely and chronically simian-human immunodeficiency virus (SHIV)-infected monkeys. Therefore, this study offers an ideal HIV-1/2 fusion inhibitor for clinical development and emphasizes the importance of the viral fusion step as a drug target.
Emerging Infectious Diseases, 9/26/2020. xxxvii Evidence for lack of transmission by close contact and surface touch in a restaurant outbreak of COVID-19
  • Robert Xxxvi
  • Garry
xxxvi Robert Garry et al, "Persistence of Severe Acute Respiratory Syndrome Coronavirus 2 in Aerosol Suspensions," Emerging Infectious Diseases, 9/26/2020. xxxvii Evidence for lack of transmission by close contact and surface touch in a restaurant outbreak of COVID-19," Journal of Infection, 5/29/2021. xxxviii Webinar: The Science of COVID-19 Aerosol Transmission An Interview with Dr. Jose-Luis Jimenez, https://youtu.be/bnEpEHWN1Ew," YouTube, 4/6/2021. xxxix Peptide-Based HIV Entry Inhibitors | SpringerLink xl Bill Gallaher & Robert Garry, "SARS Press Release," Virology.net, 5/1/2003.
Enfuvirtide, an HIV-1 fusion inhibitor peptide, can act as a potent SARS-CoV-2 fusion inhibitor: an in silico drug repurposing study
  • Wang Xli Xinling
xli Xinling Wang et al, "Pan-coronavirus fusion inhibitors as the hope for today and tomorrow," Protein & Cell, 1/9/2021. xlii Khadijeh Ahmadi et al, "Enfuvirtide, an HIV-1 fusion inhibitor peptide, can act as a potent SARS-CoV-2 fusion inhibitor: an in silico drug repurposing study," Journal of Biomolecular Structure & Dynamics, 1/13/2021. xliii Hongzhou Lu, "Drug treatment options for the 2019-new coronavirus (2019-nCoV) (jst.go.jp)," BioScience Trends, 1/28/2020.
SARS-like WIV1-CoV poised for human emergence
  • Ralph Xlix
  • Baric
xlix Ralph Baric et al, "SARS-like WIV1-CoV poised for human emergence," PNAS, 1/20/2016.