Undetectable Engineering Methods Used to Create SARS-CoV-2

Is the COVID-19 pandemic the result of a manmade virus? And, if so, what does that say about mankind’s ability to safely conduct gain-of-function experiments? “Gain-of-function” refers to experiments in which a pathogen is altered to give it new or added functionality, such as the ability to infect humans, when before it could not, or increased infectiousness or lethality, for example.

A decade ago, Dr. Anthony Fauci defended and promoted gain-of-function research on bird flu viruses, saying such research was worth the risk because it allows scientists to prepare for pandemics.¹

In reality, this kind of research does not appear to have improved governments’ pandemic responses at all. If anything, it’s a curious coincidence that the very viruses undergoing gain-of-function research are the ones causing pandemics.

As noted in the 2016 paper,² “Gain-of-Function Research: Ethical Analysis,” even if gain-of-function research does lead to improved and effective control measures, laboratory accidents or “malevolent action” in which souped-up pathogens are released can still result in casualties numbering in the millions.

The Controversy Surrounding Gain-of-Function Research

Gain-of-function research has been controversial since it started being openly discussed.³ As noted in the 2012 paper, “Rethinking Biosafety in Research on Potential Pandemic Pathogens”:⁴

“If accidentally released, mammalian-transmissible influenza A/H5N1 viruses could pose a greater threat to public health than possibly any other infectious agent currently under study in laboratories, because of such viruses’ likely combination of transmissibility and virulence to humans …

Such potential pandemic pathogens, as they have been called, jeopardize not only laboratory workers and their contacts, but also the wider population, who should be involved in assessments of when such risks are acceptable in the service of scientific knowledge that may itself bear major public health benefits.”

The U.S. put a moratorium⁵ on government funding of gain-of-function research into SARS, MERS and avian flu in 2014, following several biosafety lapses at federal research facilities.⁶ In a May 2016 paper in The Journal of Infectious Diseases, American scientists noted:⁷

“The recent safety lapses at the Centers for Disease Control and Prevention and the NIH that could have resulted in exposure to anthrax and smallpox, respectively, have diminished public confidence in the ability of even high-containment laboratories to mitigate the risk of accidental release of pathogens of potential harm …

Public tolerance of that risk may be the ultimate determinant of what types of research are allowed to proceed … As recent lapses at high profile laboratories have illustrated, there remains the potential that bacterial and viral strains can escape even the most secure environments.”

Again and again, scientists have called for public transparency, saying the public should be part of the decision process, seeing how our health is at stake and it’s our taxpayer money that’s being used to conduct this research.

As noted in a 2013 paper,⁸ “controllability of escape events is not guaranteed and, given the rapid increase of biosafety laboratories worldwide, this poses a serious threat to human health.” Advertisement

---

Funding Pause Didn’t Halt All Gain-of-Function Research

Twenty-one gain-of-function research projects were placed on hold when funding was paused,^9,10 but several were given special permission to continue,¹¹ including experiments on bat coronaviruses¹² at the Wuhan Institute of Virology in China, funded by the National Institute of Allergy and Infectious Diseases (NIAID), under Fauci’s leadership.

As noted in “A SARS-Like Cluster of Circulating Bat Coronaviruses Shows Potential for Human Emergence,” published in Nature Medicine in 2015 by Shi Zhengli-Li et.al.:¹³

“These studies were initiated before the U.S. Government Deliberative Process Research Funding Pause on Selected Gain-of-Function Research Involving Influenza, MERS and SARS Viruses. This paper has been reviewed by the funding agency, the NIH. Continuation of these studies was requested, and this has been approved by the NIH.”

Near the end of 2017, the moratorium was lifted,¹⁴ and new guidelines¹⁵ and review processes for gain-of-function research were issued but not made mandatory. According to a January 2020 Nature article,¹⁶ researchers are now pushing for greater public transparency when it comes to government’s funding of gain-of-function research. Whether or not that will actually happen remains to be seen:

“U.S. disease researchers are pushing the government to be more transparent about federally funded research that involves making pathogens more deadly or more transmissible.

Several disease researchers who attended a recent meeting to discuss transparency around such studies say the U.S. government should offer a public explanation when it approves such ‘gain-of-function’ experiments, disclose who made the decision to fund them and make a broad public announcement when a study begins. Others argued that greater transparency could make it harder to approve necessary research.

The debate over how much to disclose about such work is revving up because the government is preparing to revisit rules that guide gain-of-function research — especially with regard to their communication to the public.”

SARS-CoV-2 — Engineered or Not?

Because of the heavily censored media, any quick online search will easily lead you to believe that there’s no evidence of SARS-CoV-2 being an engineered virus, but mounting evidence points directly to that being a reality.

What some experts point to as “smoking gun” evidence for it being a manmade virus are the Antiviral Research paper,¹⁷ “The Spike Glycoprotein of the New Coronavirus 2019-nCoV Contains a Furin-Like Cleavage Site Absent in CoV of the Same Clade,” published in April 2020, and “Furin, a Potential Therapeutic Target for COVID-19,”^18,19 posted in February 2020.

According to these papers, SARS-CoV-2 is the only coronavirus with a furin cleavage site. Not even distant relatives of SARS-CoV-2 have it, and the coronaviruses that do have it share only 40% of SARS-CoV-2’s genome.^20,21

While neither of these papers makes any claims about how this gain-of-function might have come about, others have pointed out that this novel function couldn’t possibly have arisen naturally. I summarized Chris Martenson’s²² and Yuri Deigin’s²³ reviews of these findings in “The Smoking Gun Proving SARS-CoV-2 Is an Engineered Virus.”

Logic Behind Manmade Claims

An anonymous — possibly Chinese — researcher has also discussed the scientific evidence supporting the claim that SARS-CoV-2 is a manmade virus in a blog called Nerd Has Power. The anonymous blogger, who refers to him or herself as “a nobody scientist,”²⁴ points out there appears to be a concerted effort to promote the idea that SARS-CoV-2 is a natural occurrence.

“Not nearly as much literature or other forms of substantial writing have been put out to describe or argue for the other possibility — this virus is man-made,” the blogger states in a March 15, 2020, post.²⁵

He or she then goes on to explain the importance of the S1 and S2 spike sections of a given virus, and details significant changes found in the S1 portion of the SARS-CoV-2 spike protein, “which dictates which host a coronavirus targets.” According to the blogger:²⁶

“… the details of these differences and the way the human and the bat viruses differ from each other here in S1, in my and many other people’s eyes, practically spell out the origin of the Wuhan coronavirus — it is created by people, not by nature.”

The reason people are suspicious of the origin of SARS-CoV-2, the blogger states, is in large part due to the virus’ genome, i.e., its genetic sequence, compared to related coronaviruses. While genetic sequences can be compared using either gene sequences or protein sequences, when it comes to viruses, the sequence you choose makes little difference, as the entire genome “is practically translated into proteins.”

Using the protein sequence for his or her comparison, the blogger explains that since SARS-CoV-2 is only 86% identical to the SARS coronavirus, it could not have evolved from SARS. Yet, it’s oddly similar to the bat coronaviruses ZC45 and ZXC21, sharing 95% of the genome of either of these two, and certain proteins are 100% identical.

“The nucleocapsid is 94% identical. The membrane protein is 98.6% identical. The S2 portion (2nd half) of the spike protein is 95% identical. However, when it comes to the S1 portion (1st half) of the spike protein, the sequence identity suddenly drops to 69%.

This pattern of sequence conservation, between either of the closely related bat coronaviruses and the Wuhan coronavirus, is extremely rare and strange!” the blogger states, adding:²⁷

“This is extremely rare because natural evolution typically takes place when changes (mutations) occur randomly across the whole genome. You would then expect the rate of mutation being more or less the same for all parts of the genome.”

SARS-CoV-2 Unlikely To Be the Result of Recombination

While an evolutionary event known as recombination can account for this discrepancy, the blogger explains why recombination is “practically impossible” in the case of SARS-CoV-2:²⁸

“Importantly, to go from such ancestor to the Wuhan coronavirus, one combination event is not enough. What has to happen is that recombination has to take place twice during the evolution of the Wuhan coronavirus.

In one occasion, the ancestor bat coronavirus would have to acquire, through recombination with a SARS-like coronavirus, the precise short segment of S1 that is responsible for human ACE2 interaction …

In another occasion, the ‘improved’ bat coronavirus would further swap in a furin-cleavage site through recombination with yet another coronavirus that carries a furin-cleavage site between its S1 and S2 of spike.

Also, again, given the overall high sequence identity (95%) between the bat coronaviruses and the Wuhan coronavirus, it is reasonable to believe that these two diverged from each other fairly recently. Therefore, both recombination events must have taken place fairly recently as well.

Now, we know that SARS crossing over to infect human is a very rare event. To have another SARS-like sequence exist in nature so that the ancestor bat coronavirus can do recombination with is a very unlike event.

Not to mention that this SARS-like virus must have a spike that binds ACE2 the same way as SARS and yet the piece of S1 that is most critical for binding ACE2 would differ with that of SARS spike only at non-essential sites.

On top of that, furin-cleavge site has not been observed in any beta coronaviruses in the same lineage so far. Although similar furin-cleavage sites have been observed in other coronaviruses, none of them contains the same exact sequence.

Therefore, the chance that the furin-cleavage site in the Wuhan coronavirus was obtained through recombination with another furin-cleavage-site-containing coronavirus is very low. Now, what are chances for both of these next-to-impossible recombination events to take place? My answer is NO CHANCE.”

S1 Spike Portion Has Undergone Strange Changes

As explained in “The Smoking Gun Proving SARS-CoV-2 Is an Engineered Virus,” (hyperlinked earlier), viruses use a two-step process to gain entry into your cells. First, the S1 portion of the spike protein must bind to an ACE2 receptor.

Next the S2 subunit must be proteolytically cleaved (cut). Without this protein cleavage, the virus would simply attach to the receptor and not get any further. Furin is one of the enzymes that can do that.

Discussing the S1 portion of the spike, the part responsible for the virus’ ability to bind to the host receptor (in this case the ACE2 receptor), the blogger notes:²⁹

“Whether or not a particular ‘lock’ can be opened by a specific ‘key’ is decided exclusively by this S1 part of spike. In other words, S1 of a coronavirus dictates which host(s) or cells the virus can infect. Now you may be able to appreciate what I call extremely strange.

While everything else of the Wuhan coronavirus remains almost identical to the two bat coronaviruses, the S1 portion, which dictates which host a coronavirus targets, has changed significantly from the two bat coronaviruses to the Wuhan coronavirus.”

The following graphic shows the genetic sequence of SARS-CoV-2’s spike proteins compared to five other relevant coronaviruses, including the Wuhan-Hu-1 virus, isolated from the current pandemic, along with 2019-nCov_USA-AZ1. The remaining four are two bat coronaviruses and two SARS coronaviruses.

The horizontal orange lines demarcate the segment that determines the viruses’ ability to interact with the human ACE2 receptor. The green lines indicate the furin-cleavage site that is only found in the coronaviruses isolated during the current pandemic.

According to the blogger:³⁰

“The Wuhan coronavirus, while being almost identical to their bat relatives (ZC45 and ZXC21) everywhere else, has somehow ‘inherited’ the critical, short piece from SARS spike to replace the incompetent piece in the bat coronavirus spike.

As a result of this miraculous ‘replacement’ in S1 — all key residues preserved and many non-essential residues changed, the Wuhan coronavirus has practically ‘acquired’ the ability to infect humans, something its closest bat relatives do not have. Could natural evolution achieve something this precise and, at the same time, this deceptive? …

Let’s move on to appreciate magic trick #2. Please look at the region marked by two green lines … Here only the Wuhan coronaviruses contain an additional piece, SPRRA.

Importantly, this added piece allows the spike protein to be readily cleaved by a host protease enzyme — furin, a desirable property known to produce more infectious viruses in the case of influenza. Note that no beta coronaviruses in the same lineage … except this new Wuhan coronavirus, contain such a furin-cleavage site.”

No Proof SARS-CoV-2 Emerged Naturally

According to a 2020 paper³¹ in the journal Nature Medicine, “The Proximal Origin of SARS-CoV-2,” the virus is the result of natural mutation and selection in bats, pangolins and/or human hosts.

The authors claim two key characteristics of the virus as evidence of natural evolution: the absence of a previously used virus backbone, and the slightly imperfect way in which the virus binds to human cells.

Based on computer modeling data, the virus is not perfectly constructed, and this, they claim, is “strong evidence that SARS-CoV-2 is not the product of purposeful manipulation.” In other words, their argument is that scientists would have followed the sequences indicated by computer modeling, and since the virus doesn’t have the computer predicted amino acid sequence, it must have arisen spontaneously. A May 20, 2020, GM Watch article³² points out:

“However, the London-based molecular geneticist Dr. Michael Antoniou commented that this line of reasoning fails to take into account that there are a number of laboratory-based systems that can select for high affinity RBD variants that are able to take into account the complex environment of a living organism.

This complex environment may impact the efficiency with which the SARS-CoV spike protein can find the ACE2 receptor and bind to it. An RBD selected via these more realistic real-world experimental systems would be just as ‘ideal,’ or even more so, for human ACE2 binding than any RBD that a computer model could predict.

And crucially, it would likely be different in amino acid sequence. So the fact that SARS-CoV-2 doesn’t have the same RBD amino acid sequence as the one that the computer program predicted in no way rules out the possibility that it was genetically engineered.”

Undetectable Methods of Genetic Engineering Have Been Used

GM Watch also highlights Dr. Richard Ebright’s critique of that Nature Medicine paper. Ebright, an infectious disease expert at Rutgers University, points out that U.S. and Chinese researchers have genetically engineered bat coronaviruses using methods that “leave no sign or signature of human manipulation.” According to GM Watch:³³

“Ebright flagged up a scientific paper³⁴ published in 2017 by WIV [Wuhan Institute of Virology] scientists, including Shi Zhengli, the virologist leading the research into bat coronaviruses, working in collaboration with Peter Daszak of the U.S.-based EcoHealth Alliance.

Funding was shared between Chinese and U.S. institutions, the latter including the U.S. National Institutes of Health and USAID. The researchers report having conducted virus infectivity experiments where genetic material is combined from different varieties of SARS-related coronaviruses to form novel ‘chimeric’ versions.

This formed part of their research into what mutations were needed to allow certain bat coronaviruses to bind to the human ACE2 receptor — a key step in the human infectivity of SARS-CoV-2. The WIV scientists did this, Ebright points out, ‘using ‘seamless ligation’ procedures that leave no signatures of human manipulation.'”

Interestingly, “The Proximal Origin of SARS-CoV-2,”³⁵ does not include seamless ligation in its review of genetic engineering methods that could have been used. This, despite the fact that researchers experimenting with bat coronaviruses at WIV were using this very method.

Equally interesting is Daszak’s comments in the video above about how over 100 SARS coronaviruses have been found, some of which can enter human cells and cause disease in human mouse models — and are untreatable and cannot be protected against with vaccines!

“A group of scientists from the University of North Carolina in the USA, with the WIV’s Shi Zhengli as a collaborator, published a study³⁶ in 2015 describing similar experiments involving chimeric coronaviruses, which were also created using standard undetectable genetic engineering techniques,” GM Watch writes.³⁷

“Commenting on Andersen and his team’s omission of these methods from their article³⁸ in Nature Medicine, Dr. Antoniou told us, ‘This shows that these authors’ conclusions about whether genetic engineering could have been involved are not justified by the available evidence.'”

Antoniou tried submitting a letter to Nature Medicine pointing out these omissions, but the journal refused to publish it, saying his counterarguments don’t advance or clarify understanding of the original article. You can find Antoniou’s letter at the bottom of GM Watch’s article.³⁹

Yet another way you can alter a virus in a laboratory — without genetic engineering — is by culturing the virus in cells that have the human ACE2 receptor.

Over time, the virus can thereby adapt and gain the ability to bind to that receptor. This technique, highlighted by Nikolai Petrovsky, a researcher at the College of Medicine and Public Health at Flinders University in South Australia, was reviewed by Live Science in an April 18, 2020, article.⁴⁰ – Mercola.com