U.S. Right to Know (USRTK), an investigative public health nonprofit group, has filed a lawsuit1 against the National Institutes of Health after the agency failed to respond to the USRTK’s July 10, 2020, Freedom of Information Act (FOIA) request. According to the NIH, records were withheld due to them being part of an ongoing legal investigation.
The USRTK’s lawsuit seeks access to nonexempt records of gain-of-function experiments relating to the COVID-19 pandemic from the Wuhan Institute of Virology and the Wuhan Center for Disease Control and Prevention, as well as the EcoHealth Alliance, which partnered with and funded the Wuhan Institute.2 According to the USRTK’s November 5, 2020 press release:3
“Today’s litigation against the NIH is one part of our efforts to try to uncover what is known about the origins of SARS-CoV-2, and the risks of biosafety labs and gain-of-function research, which seeks to augment the infectivity or lethality of potential pandemic pathogens. Since July, we have filed 36 state, federal and international public records requests about these subjects.”
Flawed Studies Form Base of Zoonotic Theory
USRTK is also concerned about new claims that PLOS Pathogens and Nature published key papers on the origin of SARS-CoV-2 despite being flawed. I discussed these disturbing findings in “Top Medical Journal Caught in Massive Cover-Up.” It appears data sets were changed without notices of correction being published.
November 9, 2020, USRTK published a series of emails4 they’d sent to the lead authors and editors of the papers in dispute. The questions raised5 by the responses they received “put in doubt the validity of these key studies,” USRTK writes. As noted by USRTK reporter Carey Gillam:6
“Chinese governmental authorities first promoted the idea that the source of the causal agent for COVID-19 in humans came from a wild animal in December. Chinese government-supported scientists then backed that theory in four separate studies submitted to the journals between February 7 and 18 …
The four papers in question are Liu et al.,7 Xiao et al.,8 Lam et al.9 and Zhang et al.10 The two that are currently being investigated by the journal editors are Liu et al and Xiao et al. In communications with the authors and journal editors of those two papers, USRTK has learned of serious problems with the publication of those studies, including the following:
• Liu et al. did not publish or share (upon being asked) raw and/or missing data that would allow experts to independently verify their genomic analyses.
• Editors at both Nature and PLoS Pathogens, as well as Professor Stanley Perlman, the editor of Liu et al., have acknowledged in email communications that they are aware of serious issues with these papers and that the journals are investigating them. Yet, they have made no public disclosure of the potential problems with the papers.
… The problems with the research papers raise ‘serious questions and concerns’ about the validity of the zoonotic theory overall, according to Dr. Sainath Suryanarayanan, a biologist and sociologist of science, and USRTK staff scientist.”
Why We Need to Know the Origin of SARS-CoV-2
In a November 3, 2020, PNAS opinion,11 Dr. David Relman — a microbiologist and professor of medicine, microbiology and immunology at Stanford12 — explains why it’s so important to identify the origin of SARS-CoV-2:
“SARS-CoV-2 is a betacoronavirus whose apparent closest relatives, RaTG13 and RmYN02, are reported to have been collected from bats in 2013 and 2019, respectively, in Yunnan Province, China. COVID-19 was first reported in December 2019 more than 1,000 miles away in Wuhan City, Hubei Province, China.
Beyond these facts, the ‘origin story’ is missing many key details, including a plausible and suitably detailed recent evolutionary history of the virus, the identity and provenance of its most recent ancestors, and surprisingly, the place, time, and mechanism of transmission of the first human infection.
Even though a definitive answer may not be forthcoming, and even though an objective analysis requires addressing some uncomfortable possibilities, it is crucial that we pursue this question. Preventing the next pandemic depends on understanding the origins of this one …
If we find more concrete evidence of a ‘spill-over’ event with SARS-CoV-2 passing directly from bat to human, then efforts to understand and manage the bat-human interface need to be significantly strengthened. But if SARS-CoV-2 escaped from a lab to cause the pandemic, it will become critical to understand the chain of events and prevent this from happening again.”
Relman goes on to review the top three contending origin hypotheses:
- The virus evolved in bats and then spread directly or via an intermediate host to humans through natural mechanisms
- SARS-CoV-2, or a recent ancestor, was collected from an infected animal and then either knowingly or accidentally propagated or genetically manipulated before accidental release
- SARS-CoV-2 was deliberately engineered through gain-of-function research on coronaviruses, and was intentionally released
As noted by Relman, we’ve thus far been unable to identify the immediate parent or parents of SARS-CoV-2, and this is a key piece of information needed to unlock the full puzzle. The two closest relatives — RaTG13 and RmYN02 — aren’t close enough to have mutated into SARS-CoV-2.
It’s quite possible that there is more than one ancestral lineage. Recombination between different viruses is common both in nature and in laboratory research, and to determine which route the virus took, we need to identify the starting point. Relman’s opinion ends with the following comment:13
“A more complete understanding of the origins of COVID-19 clearly serves the interests of every person in every country on this planet. It will limit further recriminations and diminish the likelihood of conflict; it will lead to more effective responses to this pandemic, as well as efforts to anticipate and prevent the next one.
It will also advance our discussions about risky science. And it will do something else: Delineating COVID-19’s origin story will help elucidate the nature of our very precarious coexistence within the biosphere.“
Unfortunately, evidence suggests data scrubbing and cover-ups have already occurred, which makes establishing SARS-CoV-2’s origin all the more difficult. The question is, why was this done?
Was there a political purpose behind it? Was this a purposely engineered virus released to provide justification for the globalist “reset” plan? Was it an accidental release that was covered up to protect the future existence of dangerous gain-of-function research?
Indeed, pinpointing the virus’ origin is key to answering these important questions, and no one but the ones responsible for the attempted cover-up have anything to gain from shielding the public from the truth, whatever it might be.
I’ve written several articles about the various hypotheses surrounding the origin of SARS-CoV-2. Importantly, anomalies in its genetic structure lean toward it being a genetically manipulated virus, although the exact method remains unknown. What we do know is that there are many ways — including low-tech ones — in which a virus such as SARS-CoV-2 could have been created.
According to the August 2, 2020, paper14 “HIV Man-Manipulated Coronavirus Genome Evolution Trends,” written by Nobel Laureate professor Luc Montagnier and mathematician Jean Claude Perez, HIV/SIV sequences have been identified in a small localized region of SARS-CoV-2’s genome that allows the virus to infect human cells.
“This region has been ‘manipulated’ by humans,” the authors state, adding that since deletions in this region have been observed in COVID-19 patients, “we can expect a faster genetic evolution of the virus toward a less pathogenic strain lacking this human-made region.”
Montagnier, who received the Nobel Prize in medicine for his co-discovery of the HIV virus,15 has previously gone on record stating he believes SARS-CoV-2 was manipulated — as it has elements of HIV in its genome — and that it was likely released by accident.16,17
In an April 2020 interview with the French media outlet CNews,18 Montagnier stated he believes “the HIV sequence was inserted into the genome of the coronavirus in an attempt to make an HIV vaccine.” According to Montagnier and Perez, SARS-CoV-2’s master code “shows optimal spike PRRA site inserts” that are also shared with RaTG13.19,20
Again, RaTG13 is one of the most closely related viruses to SARS-CoV-2. It was discovered by the Wuhan Institute of Virology in 2013 after it was reported that six miners had contracted a mysterious viral infection that resulted in severe pneumonia. Three of the miners died. Montagnier and Perez write:21
“In the comparative analysis of both SPIKES genes of COVID-19 [i.e., SARS-CoV-2] and Bat RaTG13, we note two abnormal facts:
1. The insertion of 4 contiguous PRRA amino acids in the middle of SPIKE (then we show that this site was already an optimal cleavage site BEFORE this insertion).
2. An abnormal ratio of synonymous codons / non synonymous codons in the second half of SPIKE.
Finally, we show the insertion in this 1770 bases SPIKE region of a significant EIE [external informative element] from Plasmodium Yoelii and of a possible HIV1 EIE with a crucial Spike mutation.
Through the 14 facts relating to each of the 14 paragraphs of this article, everything converges towards possible laboratory manipulations, which contributed to modifications of the genome of COVID-19, but also, very probably much older SARS, with perhaps this double objective of vaccine design and of ‘gain of function’ in terms of penetration of this virus into the cell.”
A study22 posted on the preprint server bioRxiv July 21, 2020 also discussed the PRRA found both in the RaTG13 spike and the SARS-CoV-2 spike:
“Strikingly, insertion of PRRA into the raTG13 Spike selectively abrogated the usage of horseshoe bat and pangolin ACE2 but conferred usage of mouse ACE2 by the relevant pseudovirus to enter cells …
The implications of this finding are twofold: First, if SARS-CoV-2 and raTG13 share the same ancestor which originates from horseshoe bat, it is likely that acquisition of PRAA would render this bat ancestor virus less efficient infecting horseshoe bat, hence the virus would have to find a new host. Secondly, insertion of PRRA may have a previously unrecognized impact on Spike-ACE2 interaction …
Modeling SARS-CoV-2 Spike and mouse ACE2 interaction predicts that mouse ACE2 is unlikely to support entry, which has been widely verified in experiments …
Our findings, however, suggest raTG13 Spike may adopt a different conformation from SARS-CoV-2 Spike and the presence of PRRA may subtly modulate the binding of its RBD [receptor binding domain] to ACE2 of horseshoe bat, pangolin and mouse.
In summary, we showed that spike proteins from all three viruses, SARS-CoV-2, bat CoV raTG13, and CoV-pangolin/GX, have the potential to mediate entry using ACE2 from multiple animal species besides human. The PRRA insertion selectively allows SARS-CoV-2 to infect human lung cell line Calu-3 and unexpected altered dependence of raTG13 Spike on ACE2 of three species.”
Is SARS-CoV-2 the Result of Passage Through Transgenic Mice?
This leads us to yet another possibility, namely that the SARS-CoV-2 virus might be the result of RaTG13 (or another close ancestor virus) being passed through transgenic mice equipped with human ACE2 receptors.
As reported by The Jackson Laboratory,23 structural differences between the mouse ACE2 and the human ACE2 proteins make regular lab mice unsuitable for research relating to SARS-CoV-2, as the virus cannot readily infect them.
However, there are transgenic mice that express human ACE2. The first of these transgenic mice, known as K18-hACE2, were developed in 2007. Other transgenic mice with human ACE2 have been created since then. At least two recent studies have shown that transgenic mice with human ACE2 are easily infected and killed by SARS-CoV-2:
- The first, published in the July 8, 2020, issue of Cell Host & Microbe found transgenic mice with human ACE2 of all ages had far higher viral loads in the lungs, trachea and brain than wild-type mice. While none died, older transgenic mice infected with SARS-CoV-2 came down with pneumonia and had elevated cytokines. The virus was found to produce “productive infection” both via intranasal and intragastric infection.24
- The second, published in the July 9, 2020, issue of the journal Cell found SARS-CoV-2 infected HFH4-hACE2 transgenic mice, causing death. The infection was primarily localized to the lungs, causing interstitial pneumonia similar to that seen in COVID-19 patients. Low levels of viral RNA were also found in the eyes, heart and brain in a small number of animals.25
In response26 to questions for a July 31, 2020 Science article, Wuhan Institute of Virology coronavirus researcher Dr. Shi Zhengli stated that:27,28
“We performed in vivo experiments in transgenic (human ACE2 expressing) mice and civets in 2018 and 2019 in the Institute’s biosafety laboratory. The viruses we used were bat SARSr-CoV close to SARS-CoV …
The results suggested that bat SARSr-CoV can directly infect civets and can also infect mice with human ACE2 receptors. Yet it showed low pathogenicity in mice and no pathogenicity in civets. These data are being sorted and will be published soon”.
So, in summary, Zhengli admits experiments were done on transgenic mice using a bat-derived SARS-related coronavirus, which closely resembles SARS-CoV, in 2018 and 2019. (SARS-CoV is the virus responsible for severe acute respiratory syndrome (SARS), that broke out in 2003.)
Could this be the missing intermediate species that explains why SARS-CoV-2 is so well-adapted to infecting humans via the ACE2 receptor? It’s still too early to tell, but it’s a possibility. Of course, this does not exclude the possibility that other engineering methods were also used.
Foxes Guard the Henhouse
After months of stonewalling, investigative commissions are now being launched,29,30 ostensibly to get to the bottom of SARS-CoV-2’s origin. Whether they will actually unearth the truth or simply bury it deeper remains to be seen, but based on key members’ clear conflicts of interests, it doesn’t look promising.
For example, The Lancet’s COVID-19 Commission is being led by Dr. Peter Daszak.31 Not only has Daszak already spoken out about his conviction that the virus is natural and shunned theories to the contrary, as the president of the EcoHealth Alliance he’s also deeply conflicted from a business standpoint, seeing how EcoHealth Alliance received grants from the NIH for coronavirus research that was then subcontracted to the Wuhan Institute of Virology.
Daszak has every reason to make sure SARS-CoV-2 ends up being declared natural, because if it turns out to be a lab-creation, his own livelihood as a scientist is at stake. It would be naïve to believe that safeguarding the continuation of dangerous gain-of-function research wouldn’t be a powerful motivator to preserve the zoonotic origin narrative.