The National
Institutes of Health have in recent years funded dangerous
gain-of-function research on bat coronaviruses at the biosafety level 4
(BSL4) laboratory in Wuhan, China
Gain of
function research refers to research in which pathogenicity or
transmissibility of pathogens is enhanced to make a pathogen more
dangerous to humans
To gain entry
into a cell, the virus must first bind to an ACE2 or CD147 receptor.
Next, the S2 spike protein subunit must be proteolytically cleaved.
Without this protein cleavage, the virus would be unable to enter
There are
several enzymes that cleave spike proteins, including plasmin, which
also degrades fibrin. When a blood clot is dissolved, a byproduct called
D-dimer is created, and many patients with serious COVID-19 infection
have elevated D-dimer, which is indicative of blood clots
Another protein
cleaver is furin, and the presence of a furin cleavage site on
SARS-CoV-2 is “the smoking gun” that proves SARS-CoV-2 was lab-created
Since the breakout of COVID-19, a
number of scientists have spoken out saying the virus does not appear
to have evolved naturally, and those suspicions are only getting
stronger.
As reported1
by Newsweek April 28, 2020, the National Institutes of Health (NIH)
has in recent years funded dangerous gain-of-function research on bat
coronaviruses at the biosafety level 4 (BSL4) laboratory in Wuhan,
China.
This research was backed by the National Institute for Allergy and Infectious Diseases (NIAID), led by Dr. Anthony Fauci, who is now heading up the White House pandemic response team. According to Newsweek:2
“In 2019, with the backing of NIAID, the National Institutes of
Health committed $3.7 million over six years for research that included
some gain-of-function work. The program followed another $3.7 million,
5-year project for collecting and studying bat coronaviruses, which
ended in 2019, bringing the total to $7.4 million.
Many scientists have criticized gain of function research, which
involves manipulating viruses in the lab to explore their potential for
infecting humans, because it creates a risk of starting a pandemic
from accidental release.”
As noted by GM Watch,3
“Bolstering the lab escape hypothesis in the eyes of the media is the
news that the U.S. Defense Intelligence Agency (DIA) has updated its
assessment of the origin of the COVID-19 virus SARS-CoV-2 to reflect that it may have been accidentally released from a lab in Wuhan due to ‘unsafe laboratory practices.’"
Unfortunately, mainstream media journalists are by and large
ignoring the long history of accidental releases of dangerous pathogens
from BSL3 and 4 laboratories. Journalist Sam Husseini discusses this
history in a May 5, 2020 article in Independent Science News.4
Mainstream media journalists clearly are also not asking enough
questions, or the right questions, about the origins of SARS-CoV-2. In
his May 4, 2020, video update (above), Chris Martenson,5
who has a Ph.D. in pathology, carefully details the science behind his
assertion that SARS-CoV-2 must have undergone laboratory manipulation.
The evidence he lays out is close to conclusive, and really would be
front-page news if unbiased journalism still existed.
What Is Gain of Function?
As explained by Martenson, gain of function research refers to
research in which the pathogenicity or transmissibility of pathogens is
enhanced. In other words, pathogens are manipulated in various ways to
make them deadlier, and/or allow them to infect humans with greater
ease. They also take viruses that are harmless to humans and conduct
experiments to make them transmissible to humans.
As noted by Martenson, while this kind of research is justified by
saying we need to know how viruses adapt and mutate so we can more
easily figure out how to combat them should they gain these functions
naturally, there’s not a shred of evidence suggesting we’ve learned
anything about how to combat SARS-CoV-2. If we’re not actually learning
how to treat illnesses through gain-of-function research, then why are
we doing it?
Advertisement
How Viruses Enter Your Cells
Martenson goes on to explain the two-stage process viruses use to
gain entry into your cells. This is important, as viruses can only
replicate by entering into and infecting a cell.
To gain entry, the virus must first bind to an ACE2 or CD147
receptor on the cell. Next, the S2 spike protein subunit must be
proteolytically cleaved (cut). Without this protein cleavage, the virus
would simply attach to the receptor and not get any further.
There are several enzymes that can do this job, including plasmin
and furin. Plasmin, which is present in your blood, also degrades
fibrin — plasma protein that can cause blood clots. When a blood clot
is dissolved, a byproduct called D-dimer is created.
As explained in “Might Enzymes Help Blood Clotting Associated With COVID-19?” many patients with serious COVID-19 infection have elevated D-dimer, which is indicative of blood clots.
Martenson also cites the review paper6
“Elevated Plasmin(ogen) as a Common Risk Factor for COVID-19
Susceptibility,” which found that COVID-19 patients who have
comorbidities that increase their susceptibility for the illness (i.e.,
those with high blood pressure, diabetes, coronary heart disease,
cerebrovascular illness, chronic obstructive pulmonary disease and
kidney dysfunction), tend to have elevated levels of plasmin.
In other words, it’s this elevated plasmin that — at least in part —
puts these people at a higher risk for serious COVID-19 infection. In
his May 6, 2020, update below, Martenson discusses this clotting
problem encountered in many COVID-19 patients. As he points out,
COVID-19 is “really more of a blood disorder, a clotting disorder,”
than a normal lung infection.
Furin Cleavage Site Is the ‘Smoking Gun’
As mentioned, furin can also cut or cleave the S2 spike protein
subunit. Furin is a protein coding gene that activates certain proteins
by snipping off specific sections. As explained by Martenson, contrary
to other protein-cutting enzymes, furin is very specific about the
locations it cuts. What’s more, when arginine is present in the second
or third place of the protein sequence, then the efficiency of the
cleavage is magnified.
This, he says, is “the smoking gun” that proves SARS-CoV-2 was created in a lab. An excellent, well-written article7
in Medium also addresses this finding and explains why furin cleavage
sites are so important for determining whether SARS-CoV-2 is natural or
not.
In “Furin, a Potential Therapeutic Target for COVID-19,”8,9
Chinese researchers report that CoV-2 is the only coronavirus with a
furin cleavage site. Not even distant relatives of CoV-2 have it, and
the coronaviruses that do have it share only 40% of CoV-2’s genome. As
reported in this paper:10
“It was found that all Spike with a SARS-CoV-2 Spike sequence
homology greater than 40% did not have a furin cleavage site … including
Bat-CoVRaTG13 and SARS-CoV (with sequence identity as 97.4% and 78.6%,
respectively).
The furin cleavage site ‘RRAR’ in SARS-CoV-2 is unique in its
family, rendering by its unique insert of ‘PRRA.’ The furin cleavage
site of SARS-CoV-2 is unlikely to have evolved from MERS, HCoV-HKU1,
and so on.
From the currently available sequences in databases, it is
difficult for us to find the source. Perhaps there are still many
evolutionary intermediate sequences waiting to be discovered."
Mutation Cannot Explain Furin Site in SARS-CoV-2
According to these researchers, the furin cleavage site present in
SARS-CoV-2 “is unique in its family” and “is unlikely to have evolved.”
In other words, the virus must have been modified somewhere along the
way to give it a furin cleavage site, as there’s no apparent source for
this virus.
Put another way, there’s no coronavirus out there that is similar
enough that SARS-CoV-2 might have evolved or mutated from it.
Martenson does an excellent job of explaining this in his video, so I
strongly recommend watching it. Yuri Deigin also does this in his
Medium article,11 so if you prefer reading, you can review much of the same data there.
Importantly, both reveal how virologists claiming SARS-CoV-2 is a
natural bat coronavirus that jumped to pangolin and then to humans are
simply wrong, and the genetic sequence proves it. The furin cleavage
site PRRA found in SARS-CoV-2 is NOT found in either bats or pangolins,
so it could not have mutated through these animals.
The fact that this furin cleavage site is present in SARS-CoV-2 is
evidence that it has been inserted (opposed to mutated), and Martenson
provides an easy to understand illustration of the difference between a
mutation and an insert in his video. It is extremely unlikely that 12
new nucleotide base pairs would all of a sudden emerge from where there
was nothing before.
What About the Studies Saying It’s Natural?
Two studies heavily cited by mainstream media as evidence SARS-CoV-2
is a natural mutation that jumped from animal to human include a
February 3, 2020, Nature paper,12
which claims SARS-CoV-2 is a coronavirus of bat origin that then jumped
species. However, one of the authors of this paper, Shi Zhengli, was
involved in the weaponization of the SARS virus, and therefore has
reason to try to cover up any link to such research.
A second paper,13
published in Nature Medicine, March 17, 2020, offers “a perspective on
the notable features of the SARS-CoV-2 genome,” and discusses
“scenarios by which they could have arisen.” According to this paper,
“Our analyses clearly show that SARS-CoV-2 is not a laboratory
construct or a purposefully manipulated virus.”
However, even though they acknowledge SARS-CoV-2 has a polybasic
cleavage site (PRRA) that does not exist elsewhere, they fail to
explain how these 12 base pairs could have magically been inserted
naturally. As noted by Martenson, “whole inserts are not part of the
mutation pathway.”
Scientific Community Has Reason to Hide Origin
He goes on to cite several studies showing how scientists around the
world have been working on inserting cleavage sites to make
coronaviruses more virulent. Clearly, we have the capability to create
SARS-CoV-2, and scientists around the world have engaged in such
research for many years.
Martenson calls out leading virologist Michael Osterholm who, in a
March 10, 2020, interview with Joe Rogan, stated that “we could not
have crafted a virus like this to do what it’s doing; I mean we don’t
have the creative imagination or the skill set.”
Really? Published research shows we clearly have the technology,
know-how and “creative imagination” to create SARS-CoV-2, and Osterholm
simply cannot be ignorant of that fact.
Another source you may want to look over is the Project Evidence webpage,14
which lists more information pointing toward a lab-created SARS-CoV-2
than I could possibly cover here. A summary of the evidence can be
found toward the bottom of the page under “Conclusion.”
Naturally, there must be people in the scientific community who
would now want to cover up any link to such research. Would you want to
be responsible for creating, funding or having any association
whatsoever with a virus responsible for a pandemic that has killed
people, destroyed the world economy and put people out of work around
the globe?
Would you want to be found guilty of violating the Biological
Weapons Anti-Terrorism Act of 1989, the punishment for which goes up to
and includes life in prison? The Biological Weapons Anti-Terrorism Act
of 1989 states:15
“Whoever knowingly develops, produces, stockpiles, transfers,
acquires, retains, or possesses any biological agent, toxin, or delivery
system for use as a weapon, or knowingly assists a foreign state or any
organization to do so, shall be fined under this title or imprisoned
for life or any term of years, or both. There is extraterritorial
Federal jurisdiction over an offense under this section committed by or
against a national of the United States.”
Other Experts Challenge Natural Evolution Claims
Martenson is far from alone in his belief that SARS-CoV-2 was genetically manipulated. An April 27, 2020, GM Watch article16
features professor Stuart Newman, who also believes “genetic
engineering may have been involved at some point in the virus’
history.”
According to Newman, a professor of cell biology and anatomy at New
York Medical College and editor-in-chief of the journal Biological
Theory, the argument used to deny that SARS-CoV-2 is a laboratory
construct in the March 17, 2020, Nature Medicine paper mentioned earlier
(which stated “Our analyses clearly show that SARS-CoV-2 is not a
laboratory construct or a purposefully manipulated virus”) actually
points to the exact opposite.
GM Watch writes:17
“As Adam Lauring, an associate professor of microbiology,
immunology and infectious diseases at the University of Michigan
Medical School, has noted,18
Andersen’s paper argues that, ‘the SARS-CoV-2 virus has some key
differences in specific genes relative to previously identified
coronaviruses — the ones a laboratory would be working with. This
constellation of changes makes it unlikely that it is the result of a
laboratory 'escape.’’
But Professor Newman says19
that this is totally unconvincing because “The ‘key differences’ were
in regions of the coronavirus spike protein that were the subject of
genetic engineering experiments in labs around the world (mainly in the
U.S. and China) for two decades’ …
In an email interview with GMWatch, Newman … amplified this
speculation by noting, ‘The Nature Medicine paper points to variations
in two sites of the spike protein of the new coronavirus that the
authors claim must have arisen by natural selection in the wild.
However, genetic engineering of one of these sites, the ACE2
receptor binding domain, has been proposed since 2005 in order to help
generate vaccines against these viruses (see this paper20).
It is puzzling that the authors of the Nature Medicine commentary did
not cite this paper, which appeared in the prominent journal Science …
The second site that Andersen et al. assert arose by natural
means, a target of enzyme cleavage not usually found in this class of
viruses, was in fact introduced by genetic engineering in a similar
coronavirus in a paper21 they do cite. This was done to explore mechanisms of pathogenicity.’
Newman said that he does not believe that these changes were
deliberately introduced to increase the pathogenicity of any single
strain, but that SARS-CoV-2 may have had genetically engineered
components in its history before being inadvertently introduced into the
human population.”
There Are Many Ways to Manipulate Pathogens
Those who claim the lack of “fingerprints” in the genetic code of
SARS-CoV-2 is evidence of natural evolution also fail to take into
account methods that do not leave clearly identifiable traces. As noted
by Dr. Meryl Nass (my interview with her will be posted May 24):22
“Prior to genetic engineering techniques being developed (1973)
and widely used (since late 1970s), more ‘primitive’ means of causing
mutations, with the intention of developing biological weapons, were
employed …
They resulted in biological weapons that were tested,
well-described, and in some cases, used … These methods can result in
biowarfare agents that lack the identifiable signature of a microbial
agent constructed in a lab from known RNA or DNA sequences.
In fact, it would be desirable to produce such agents, since it
would be difficult to prove they were deliberately constructed in a
lab. Here are just a few possibilities for how one might create new,
virulent mutants:
Exposing microorganisms to chemical or radiological agents that
cause high mutation rates and selecting for desired characteristics
Passaging virus through a number of lab animals or tissue cultures
Mixing viruses together and seeking recombinants with a new mix of virulence factors”
In my opinion, the strongest pieces of evidence so far all point
toward SARS-CoV-2 being a laboratory creation. As Martenson asserts,
the presence of furin cleavage sites23
makes a clear case for this, as this section of genetic code wouldn’t
just emerge by itself by way of natural mutation. How it got released,
however, is anyone’s guess.
No comments:
Post a Comment