Document:Logistical and Technical Exploration into the Origins of the COVID-19 virus

From Wikispooks
Jump to navigation Jump to search
Report of a thorough investigation into the origins of the virus that caused the pandemic. Whilst the author is circumspect, the evidence presented points clearly to the virus being the product of laboratory engineering.

Disclaimer (#3)Document.png report  by Jonathan Jay Couey dated 31 January 2020
Subjects: 2020 coronavirus pandemic, COVID-19, SARS, Wuhan Institute of Virology, Zhengli Shi, Xing-Yi Ge, Johns Hopkins Center for Health Security, Fort Detrick, Porton Down
Source: Harvard to the Big House blog (Link)

An accessible and comprehensive YouTube summary of this report by its author, Jonathan Jay Couey, Professor of Neurobiology at the University of Pittsburgh’s Medical School, is available here. His takedown of Nature magazine’s recent article [1] which claims that COVID-19 definitely wasn’t from a lab, can be read here.

Author's Note

This report is the product of a collaboration between a retired professional scientist with dozens of peer-reviewed publications and 30 years of experience in genomic sequencing and analysis, who worked at the Theoretical Biology Division of the Los Alamos National Laboratory and later helped design several ubiquitous bioinformatic software tools, and a former NSA counterterrorism analyst. It considers whether the Wuhan Strain of coronavirus (COVID-19) is the result of naturally emergent mutations, against the possibility that it may be a bio-engineered strain – directly altered by genetic manipulation, subject to artificially-guided evolutionary selection [2], or both – and most likely released into the public by accident since China’s rate of occupational accidents is about ten-times higher than America’s, and some twenty-times more than Europe’s,[3] the only other regions with high-level virology labs.


4star.png 22 March 2020 Peter  A near conclusive case for COVID-19 being a laboratory engineered virus
  1. default:

★ Start a Discussion about this document
Logistical and Technical Exploration into the Origins of the Wuhan Strain of Coronavirus (COVID-19)


Raising the odds of an accidental release, researchers from China’s only BSL-4 lab in Wuhan were reported to have particularly sloppy field research methods, being both bled and peed on by local bats [4] that host coronaviruses remarkably similar to the Wuhan Strain COVID-19. And they’ve also been reported to smuggle used research animals out of their labs, selling them for cash on the street. [5] Perhaps unsurprisingly, in mid February the Chinese Ministry of Science sent out a directive to all its labs emphasizing the importance of carefully handling bio-infectious agents and alluding to slack oversight and past lapses, even mentioning coronaviruses specifically. [6]

Mistakes may have been precipitated by the need to quickly finish research that was being rushed for John HopkinsEvent 201 which was held in October 2019 and meant to gameplan the containment of a global pandemic. Research may also have been hurried due to deadlines before the impending Chinese New Year – the timing of these events point to increased human error, not a globalist conspiracy. Beijing has had four known accidental leaks of the SARS virus in recent years, [7] so there is absolutely no reason to assume that this strain of coronavirus from Wuhan didn’t accidentally leak out as well. This is unlikely to be a plot twist in one of the novels Tom Clancy wrote after he started mailing it in.

Simply and horribly, this is likely to become another Chernobyl or Fukushima – a catastrophic illustration of mankind’s hubris and intransigence clashing with Nature, as fate again reaps a once unimaginably tragic toll.

Given that this outbreak was said to begin in late December when most bat species in the region are hibernating [8] and the Chinese horseshoe bat’s habitat covers an enormous swath of the region containing scores of cities and hundreds of millions people, [9] the fact that this Wuhan Strain of coronavirus, denoted as COVID-19, emerged in close proximity to the only BSL-4 virology lab in China, which in turn was staffed with at least two Chinese scientists – Zhengli Shi and Xing-Yi Ge – both virologists who had previously worked at an American lab which had already bio-engineered an incredibly virulent strain of bat coronavirus – the accidental release of a bio-engineered virus from Wuhan’s virology lab cannot be automatically discounted, especially when the Wuhan Strain’s unnatural genomic signals are considered.

2 February 2020 UPDATE

A probable smoking pre-print has been released, by the National Natural Science Foundation of China:

“In summary, somebody was entangled with the evolution of 2019-nCoV coronavirus. In addition to origins of natural recombination and intermediate host, the killer coronavirus probably originated from a laboratory in Wuhan.” [4]

In a predictable turn, that article has been removed and both researchers have since deleted their profiles off of the ResearchGate site completely. Furthering the appearance of a cover-up, back on January 2nd, the Wuhan Institute of Virology’s director sent out a memo forbidding discussion of an “unknown pneumonia in Wuhan” after ordering the destruction of all related lab materials a day earlier, [10] making it abundantly clear that the Chinese government knew about this outbreak long before they took any steps to contain it, or made any public announcement.

These propaganda efforts have been bolstered by possible collusion from American scientists, some of which is detailed below – but also most notably by one Peter Daszak, who had been publishing papers on coronaviruses alongside the primary Chinese person-of-interest, Zhengli Shi, for years. [11] Perhaps most notably, Daszak is listed as a co-author in the paper first documenting the isolation of a coronavirus from a bat that targets the ACE2 receptor [12] – just like COVID-19 – research done in Wuhan’s virology lab and supervised by Zhengli Shi, and led by a second suspect Chinese researcher who you’ll meet below. At best, Daszak is perhaps acting as an unwitting agent of the Chinese government, but regardless holds an enormous conflict-of-interest. And if nothing else, it is wildly irresponsible to speak-out against the possibility that the virus got out of a lab when a natural origin has not been conclusively demonstrated. Daszak’s statement in The Lancet is either [13]incompetence, or is meant to be a smokescreen for the wanton hubris and greed that have fueled the gain-of-function research detailed below: As one possible related project which may have overlapped with this one, coronaviruses have been seen as a viable vector for an HIV vaccine for years [14] – a project with hundreds of millions of dollars dangling over it. [15]

And unfortunately Daszak is far from alone, there are countless “journalists” mindlessly regurgitating statements from the Chinese government and the WHO with no effort to fact-check whatsoever, as well as “scientists” whose real job is running PR for pharmaceutical and research companies who have spent weeks serving China by making extraordinarily misleading and overconfident statements to the public about the origins and capabilities of this virus. And it should be noted that in 2018, the esteemed scientific journal Nature – which has published numerous articles speciously claiming this virus is definitely natural – was revealed to have buckled to censorship demands from the Chinese government, killing over 1,000 articles to placate their Chinese partners. [16]

Many involved in this dissimulation are effectively acting as agents of a foreign government, and they have left most Americans entirely unprepared for the tragedy that’s beginning to occur in our nursing homes and hospitals. If the idea that just maybe this thing came from a lab had been part of the national dialogue from the start – wouldn’t everyone have been much more cautious and open to social distancing and other limitations once the need arose?

And so being an offshoot of this sort of vaccine program, possibly as a Red Team designed to build defenses and therapeutics against, is just one possible gain-of-function pursuit that would fit some of the unusual genomic and logistical picture below. Whether or not it was the exact target of the Wuhan lab’s genomic tinkering – the reality is millions of dollars of funding from multiple world governments have poured into this research, funding that’s dangled over these scientists as they’ve chased it like Icarus, this time not just risking their own lives – but hundreds of millions of others as well.

Subsequently, we are calling for an immediate end to dual-use gain-of-function research. [17]

Assembly of the first DNA virus from scratch

In 2002, Stony Brook first assembled a DNA virus from scratch, [18] building a polio-virus, and providing proof-of-concept for the creation, alteration, and manipulation of DNA-virus genomes. Two years prior, a separate team had already built an simpler RNA-virus from scratch – choosing to engineer a coronavirus from the ground up, and even swapping out its vital spike-protein genes to make it more infectious. And a generation earlier, artificially enhancing selection by intentionally infecting countless series of lab animals with different viruses is understood to have created the H1N1 Swine Flu. Its Franken-genome has a mysterious untraceable genetic parentage [19] and a “clear unnatural origin,” [20] and H1N1 became the poster-child for a moratorium against gain-of-function research – experimentation that seeks to increase a pathogen’s virulence, creating a more effective double-edged sword to counter and learn from. A ban that was in place for years, but was recently lifted by the American government. In the case of H1N1, it wasn’t a question of if it’d escaped from a research laboratory, only whether it’d been designed as part of a weapons system, or been part of a vaccine trial. [20]>


When a virus manages to infect a new species of host it’s known as a zoonotic jump, a process that generally takes months or even years to complete. The first stage is when a virus infects one individual in a new host species, which is typically a dead-end the first time it happens since there’s no way for the virus to be adapted to a different species’ biology. The second stage of a zoonotic jump is when the virus manages to move from the first new host into more hosts of the new species, which results in some temporary transmission in a localized area – these are known as endemics and generally fizzle out the first few times they happen as the virus adapts to its new host species, and mutations win or lose the survival battle. The final stage, the only time a zoonotic jump is considered complete, is when there’s sustained host-to-host transmission in the new species. These zoonotic jumps have some predictable characteristics, the primary one is that adapting to a new host inevitably requires mutations that weren’t optimal in the old host. And so the virus gets weakened as its initially attempting to jump into a new host species, which is why the above sequence of steps – one new host, a few new hosts that pass it among themselves temporarily, and then finally sustained transmission – takes at least several months if not years to play out, since a good bit of time is required for all three steps to occur. Viral trial-and-error is required for the virus to find the right mutations that will allow it to prosper in a new host species, it’s never been known to just happen magically all at once.

The improbability of the virus emerging naturally

And so assuming that COVID-19 emerged naturally in a matter of weeks in the middle of a massive urban metropolis the size of New York City, when the host population of bats was hibernating anyways, requires completely ignoring everything we know about how viruses transfer between species. Not only was Wuhan’s population not interacting with bats since they hardly interact with humans in urban situations to begin with, but any possible host bats were sleeping in their caves anyways. And not only would the circumstances of this transfer require rewriting the textbooks on zoonotic jumps if it occurred it all, but beyond that: supposedly not only did a zoonotic jump happen instantly without the necessary steps, but when it hit humans it was extraordinarily virulent from the start, something that’s supposed to take an extensive amount of time to ever happen as mutations go through selective trial-and-error. This trial-and-error takes time and is why viruses have never made a zoonotic jump and been instantly virulent in a new host species like COVID-19 has been in humans. Nothing we know about how viruses naturally make zoonotic jumps point to that happening here.

The H1N1 affair

Tinkering with viral genomes is not anything new, but is not something that has ever been fully embraced by the scientific community at large. About a decade ago, two separate research teams successful tweaked the genome of the H5N1 Bird Flu in just two spots and then passed it through ferrets until it became both airborne and pathogenic to mammals, creating a virus that “could make the deadly 1918 pandemic look like a pesky cold.” [21] This involved selecting for a mutation that allowed the virus to access a receptor that’s found in ferret lungs, and was alarming enough that the research was urged to be published without revealing the specific methods involved and data collected – however it appears that only the most technical details were left out, and most of the research is freely available. [22]

The Gain of Function research ban and its reinstatement

By 2015, conducting research that was met with an enormous amount of concern, scientists at UNC had successfully created a “chimeric, SARS-like virus” [23]by altering the viral genome of a Chinese bat coronavirus’s spike-protein genes – sequences that code for the spikes that poke out from surface of viruses and allow them to unlock entry into hosts, in this case making the bio-engineered coronavirus incredibly contagious. This research raised eyebrows since it was clearly gain-of-function research, a practice banned in America from 2014 until December 2017 when NIH lifted the ban, [24] specifically to allow research on this sort of virus. Looking at UNC’s gain-of-function research on coronavirus spike-proteins, which received its funding just before the ban was implemented and was only allowed to go forward following a special review, a virologist with the Louis Pasteur Institute of Paris warned: “If the [new] virus escaped, nobody could predict the trajectory.”

But then oddly, in late January right as the pandemic was blooming, Dr. Ralph Baric claimed in an interview that people should be more concerned with the seasonal flu [25] – despite having personally overseen the controversial engineering of a hyper-virulent strain of batty coronavirus just a few years back. Immediately discounting the burgeoning outbreak of an unknown coronavirus as a non-event seems particularly troubling for someone who’d trained two Chinese scientists on how to make hyper-virulent coronaviruses, especially when it’s hard to imagine that Dr. Baric was unaware his past colleagues were now working at the Wuhan Virology Lab, the epicenter of the outbreak. Highlighting the dissembling absurdity of this statement, based on reporting from Who: the Wuhan Strain COVID-19 appears to be thirty-four times more lethal than the seasonal flu. [26]

The BSL-4 Wuhan lab and the 'Wet Market'

Scientists have expressed concern about China’s ability to safely monitor this BSL-4 lab in Wuhan [27] since it opened in 2017:

“an open culture is important to keeping BSL-4 labs safe, and he questions how easy this will be in China, where society emphasizes hierarchy. ‘Diversity of viewpoint, flat structures where everyone feels free to speak up and openness of information are important.'”

This lab is at most 20 miles from the wet market where the virus had been assumed to have jumped from animal to human. However the idea that a Chinese lab could have a viral sample escape is well-documented – as mentioned, one lab in Beijing has had four separate incidents of the SARS virus leaking out accidentally. [7]

Notably, the first three known cases from early December had no contact with that market, [28] and roughly one-third of the initial exposed cohort had no direct ties to Wusan’s wild meat wet-market, [29] the original presumptive source of the virus. And in mid February, reporting indicated that COVID-19’s patient zero in fact had no connection at all with the wet-market. [30] This is reinforced by the fact Chinese research has also concluded that COVID-19 “may have begun human-to-human transmission in late November from a place other than the Huanan seafood market in Wuhan.” [31]

Zoological origins of the virus still unknown

Since its discovery, scientists have been unable to fully determine the zoological origins of COVID-19, it was initially thought to have passed through snakes, but now all that’s agreed upon is that it’s mostly bat in origin. This inability to derive an exact zoological source is exactly what would be expected if the virus had been artificially engineered to target humans as UNC already has, this doesn’t prove an artificial nature – but it is consistent with one. Although there has been speculation that pangolins may have been the missing vector, the only data about the pangolin virome wasn’t entered into NCBI’s system until late January, and couldn’t possibly have been collected any earlier than late September 2019, and doesn’t fully answer the vector question anyway. And further research examining the regions of the genome that best show genetic heritage indicated it was “very unlikely” that similarities between their spike-protein genomes of COVID-19 and pangolins, where they share the most similarities, was due to the virus passing through pangolins at all.

As explained in Nature, COVID-19’s Franken-genome combines a cornucopia of distinct genetic markers from each of the three other distinct branches of the coronavirus family tree, but is distinct enough from all of them that it in fact forms its own clade [32]. Along those same lines, a full-genome evolutionary analysis of COVID-19 published in The Lancet concluded, “recombination is probably not the reason for emergence of this virus” [8] since it seems that the Wuhan Strain isn’t a mosaic of previously known coronaviruses, but instead draws from distant, discrete parts of the coronavirus family tree – not how these viruses naturally evolve. Because even mixing and matching coronavirus genomes from every known zoological virus, scientists couldn’t find any possible combination that would explain those regions of the Wuhan Strain’s genome. The Lancet muses that a mysterious animal host could still be out there, however since they’ve already searched through every known possibility and been unable to find a match, another obvious explanation is that bio-engineering accounts for the inexplicable nucleotide signature of the Wuhan Strain’s genome

COVID-19 targets the ACE2 receptor

Early research found that COVID-19 targets the ACE2 receptor, [33] which seems to be distributed in roughly equal proportions across global populations, indicating that the Wuhan Strain was likely developed as part of a defensive gain-of-function project possibly linked to immunotherapy or vaccinations – never meant to leave the lab, but meant to serve as a Red Team to fight back against, not as an offensive weapon targeting one specific global population. But counter-intuitively, researchers have pointed out that the most critical sections of the COVID-19’s protein-spike genome don’t match the previously reported pattern that would be expected for optimal binding to the specific ACE2 receptors found only in humans and ferrets, [34] which indicates that these particular segments wouldn’t have been directly genetically engineered to increase virulence.

And yet this is exactly what researchers looking to design something for a “safe” vaccine candidate to target would engineer, and doesn’t rule out a scenario where the virus was passed through a series of ferrets. The research team in fact notes that its spike “appears to be the result of selection on human or human-like ACE2 permitting another optimal binding solution to arise,” [34] failing to directly mention that the only other human-like receptors are found in ferrets – which have frequently been used for years in vaccine trials for viruses with this sort of protein-spike, [35] and is exactly how the H5N1 Bird Flu virus was altered to make it airborne. And so the Wuhan Strain’s unique affinity for the human ACE2 receptor, which a pre-print reports to be 10 to 20 times greater than SARS, [36] may be the exact type of vaccine-related accident that led to the moratorium on gain-of-function research in the first place and caused scientists to unsuccessfully call for the research around H5N1 to be partially sealed-off.

COVID-19 transmissable before host shows symptoms

The Wuhan Strain of coronavirus, COVID-19, appears to be transmissible even before its host shows any symptoms at all, making temperature-scanning at airports ineffective since hosts appear to be contagious for about a week before any symptoms emerge. This is in stark contrast with SARS, whose hosts weren’t contagious until they were symptomatic, allowing for its relatively quick containment. This chart is not from a peer-reviewed source but was claims to capture the comparative rates of infections between recent outbreaks. [37]A recent pre-print now gives COVID-19 a rating of R4, [38] meaning each host passes the virus on to four new victims, a rate significantly higher than any past global viral outbreak.

The successful end results of the aforementioned bat coronavirus bio-engineering research at UNC that was critiqued for being too risky in 2015, was published the following year and described the successful bio-engineering of a highly-virulent coronavirus derived from bats which was achieved by tinkering with its spike-protein genes. [39] In this paper, researcher #8 is listed as one “Zheng-li Shi” who’s listed as being attached to the “Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.

Zhengli Shi

Zhengli Shi seems to have returned to Wuhan at some point since 2016, specifically to the Wuhan Institute of Virology’s Disease Engineering Technical Research Center, [40] since she then appears in this September 2019 paper on the human behaviors most likely to lead to bat-borne coronavirus exposure in southern China, and also in the paper claiming that this coronavirus was bat in origin, [41] which was peculiarly submitted in coordination with the announcement of the outbreak. [42] Very, very peculiarly. She also appears in this pending preprint on the current outbreak of COVID-19 [43], just a small sample of the dozens of coronavirus-related papers she’s published over a three decade career.

Not only does Zhengli Shi provide a direct chain of expertise tying the already successful bio-engineering of a virulent bat-based coronavirus at UNC directly to the BSL-4 virology lab in Wuhan, but back in January 2014 she’d received a $665,000 grant from NIH for a study titled The Ecology of Bat Coronaviruses and the Risk of Future Coronavirus Emergence (NIAID R01 AI1 10964) as well as $559,500 more from USAID for a study titled Emerging Pandemic Threats PREDICT_2China (Project No. AID-OAA-A-14-00102). Beyond this American funding specifically into viral diseases zoonotically transferring from animals to humans which would slipped in just before the ban, over the years she’s also received around $3 million in grants to study these zoonotic viruses from China and other countries, and has served on the editorial board of several virological research magazines. More of her research into the intersection of coronaviruses like the Wuhan Strain and their epidemic potential was funded by the U.S. Department of Defense, the U.S. Threat Reduction Agency, and U.S. Biological Defense Research Directorate of the Naval Medical Research Center.

And so a scientist who’s been prolifically involved with studying the molecular interaction of coronaviruses and humanity, spending decades and millions of dollars, and having even helped build a hyper-virulent coronavirus from scratch at UNC – just so happens to be working at the only BSL-4 virology lab in China that also just so happens to be at the epicenter of an outbreak involved a coronavirus that’s escaping zoological classification, and has other unnatural characteristics that will be discussed below.

Xing-Yi Ge

Another Chinese virologist, Xing-Yi Ge, appears as an author on the 2016 UNC paper and is also attached to the lab in Wuhan. Previously in 2013, he’d been the very first scientist to successfully isolated a SARS-like coronavirus from bats which targets the ACE2 receptor [44], just like our present virus, the Wuhan Coronavirus COVID-19 uses. And it turns out that sections of the Wuhan Strain’s ACE2 receptor’s genes are unique: they’re almost identical to SARS’s spike-protein genes – despite the fact that almost none of the two coronavirus’s genomes are similar anywhere else at all [45]. Beyond that, although the Wuhan Strain’s spike-protein genome differs from SARS in four out of the five most important genomic spots that determine binding to the ACE2 receptor, [46] they surprisingly don’t effect the protein-spike’s shape. And in an even bigger coincidence, these four spots also code for the outside region of the spike that allows entry into cells, and do not effect it either – allowing the Wuhan Strain to still use the ACE2 receptor to unlock cells while possibly gaining additional capabilities. The odds that this concordance was bio-engineered into the virus are several orders of magnitude more likely than for this to randomly have evolved in nature, and is exactly the sort of process used to make the H5N1 Bird Flu airborne and highly pathogenic.

Antibody-dependent enhancement

Numerous videos purportedly from inside hospitals in Wuhan depict a crisis that is far greater than the numbers released by China to date. There is widespread but unverified online reporting that Wuhan crematoriums have been running 24/7, which is consistent with a recent peer-reviewed study that claims that as of January 25, Wuhan had over 75,000 infections when the official number was just 761 [47]. Chinese language social media also reflects a sense of panic and desperation that is highly discordant with the numbers being released by the Chinese government. Who, notably, are refusing any direct assistance from the American CDC. (Evidence that China is vastly downplaying this pandemic’s severity: Example 1. Example 2. Example 3. Example 4. Example 5. Example 6.)

Some of the dystopian carnage creeping across China may be due to the fact that much of China’s population may have already been exposed to coronavirus infection via SARS or other less notorious strains, which would allow the Wuhan Stain COVID-19 to use antibody-dependent enhancement (ADE) to much more efficiently enter into cells [48], and then become much more virulent since this enhancement hijacks the body’s preexisting immune response to coronavirus infections and allows easier entry. However whether or not people have been exposed to a coronavirus infection before, once it’s been circulating in a population for long enough the Wuhan Strain may be able to reinfect its own past hosts and use this molecular hijacking on antibodies left from its own previous infection to become far more virulent, regardless of whether or not someone has been exposed to other coronaviruses before COVID-19. And early reporting from Chinese doctors indicates that re-infections of the Wuhan Strain are far more lethal than the first [49]. More evidence that ADE is occurring is its much higher affinity for the ACE2 receptor and far higher viral loads compared to SARS – both of these may be due at least in part to ADE allowing COVID-19 to much more efficiently bind to and enter cells. And another hint that the Wuhan Strain may be using ADE to more effectively attack its host is the fact that it seems to be targeting its host’s neurological systems, which is explored in depth below. A final clue is the fact that children seem to be far less effected by the Wuhan Strain COVID-19, a phenomenon that’s found in Dengue Fever, which is one of the classic examples for ADE.

Similarity to HIV

Another peculiar characteristic is COVID-19’s similarities 31 January 2020HIV. And so although another since-retracted pre-print noted several very short genomic sequences in COVID-19’s spike-protein gene that look far more similar to sequences found in HIV than to other coronaviruses [50] – critics quickly pointed out that the shared homology didn’t reach statistical significance. However a closer look at the data reveals that there were a few small shared genomic segments that, despite being physically separated from each other along each strand of DNA, all worked together to code for the Wuhan Strain’s protein-spike’s crucial receptor binding site. Something that is highly unlikely to have happened by chance. And despite most of its protein-spike being shared with SARS, these substituted segments weren’t shared at all – nor were they found in any other coronavirus. One possible but likely reason for these HIV-like segments is that they were meant to be epitopes, or molecular flags meant to mark intruders for a vaccine to target – meaning the Wuhan Strain was built as a monster for a specific vaccine to hunt. It is mathematically possible for this to happen in nature – but only in a ten-thousand bats chained to ten-thousand Petri dishes and given until infinity sense. Alternatively, this pattern could also be produced by infecting a room full of ferrets with a bespoke coronavirus and sifting through the wreckage for your genomic needle. [51]

Critics have brushed off the Wuhan Strain’s shared homology with HIV as statistically insignificant, however clinical reporting indicates that the Wuhan Strain may be using this shared HIV homology to attack CD4 immune cells just like HIV does, as an unusually high percentage of patients are showing low white blood cell counts, [52] especially the sickest ones. This pathogenicity may well be due to the unique HIV-live genomics of the Wuhan Strain, as one white-paper by LSU’s professor emeritus of Microbiology, Immunology, and Parasitology who’s also a Harvard-educated virologist with a PhD in Microbiology and Molecular Genetics notes: “This is the first description of a possible immunosuppressive domain in coronaviruses… The three key [mutations] common to the known immunosuppressive domains are also in common with the sequence from [the spike-protein]. While coronaviruses are not known for general immunosuppression of the style shown by HIV-1, this does not rule out immunosuppression at the site of active infection in the lung, which would prolong and potentially worsen infection at that site.” And early research has indicated that this unique region may make COVID-19 up to 1,000 times more likely to bind to human cells than SARS, [53] which could be due to either this homology or to ADE, or some combination of these or other factors.

Even more troubling, a peer-reviewed study noted that one particular part of the Wuhan Strain’s spike-protein genome also wasn’t found in any of its relatives, “and may provide a gain-of-function to [COVID-19] for efficient spreading in the human population.” [54] And according to that paper, this particular type of furin cleavage site makes similar viruses both more pathogenic and more neurotoxic. Additionally, this particular type of cleavage site is a hallmark of being passed through a series of animal hosts in a lab. [55] Evidence for the Wuhan Strain’s neurotoxicity arrived in late February, in a published paper which notes that “the most characteristic symptom of COVID‐19 patients is respiratory distress, and most of the patients admitted to the intensive care could not breathe spontaneously.” [56] Combined with the observation that “some COVID‐19 patients also showed neurologic signs such as headache, nausea and vomiting,” this paper asserts that since SARS was found heavily concentrated in the brainstems of its autopsied victims, COVID-19 is also probably crossing the blood-brain barrier and killing its victims not just via pneumonia, but also by causing neurological respiratory failure. Indicating that ADE may be occurring, but at a much faster rate than nature allows since reinfections of Dengue Fever that use ADE typically have years pass between them.

And it should be noted that SARS – much ballyhooed as a close relative to the Wuhan Strain – didn’t notably effect white blood cell counts. [57] Additionally, clinical treatment guides published online in late January by established Chinese medical sources [58] note the progressive reduction of white blood cells, as well as the importance of monitoring this decline. And reporting from Thailand indicates that adding a cocktail of two different anti-HIV drugs to the typical flu treatment regime seemed to effectively knock back the Wuhan Strain. [59] Additionally, one of the only autopsies performed outside of China to date found that the deceased had a severely depleted white blood cell count. [60] These lowered counts may come from this shared similarity with HIV, or it could also be the result of ADE as well, since this phenomenon primarily targets white blood cells for its hijackings and may help explain why consecutive infections are so lethal. [61]

In a highly concerning turn, scientists have noted that the Wuhan Strain can have a “striking” short term rate of mutation [62] which doesn’t indicate an artificial origin but captures the unique threat posed by this coronavirus regardless of its providence, since a faster mutation rates makes it more likely this virus can dodge testing and neutralize vaccines. Something there is already early evidence for. [63] Further concerning are reports out of China that even patients who appear cured still harbor COVID-19 in their system, [64] and although the full implications of this are not yet known – none of them are good.

A worst-possible mutation rate scenario

One of the worst possible scenarios for COVID-19’s mutation rate would be if it falls into the Goldilocks range that would allow it to form mutant viral swarms: [65] too many mutations will cause a virus to eventually implode, not enough allows host immune systems to catch-up, but if things are just right mutant swarms can form and spread across host populations, burrowing into host nervous systems and causing permanent neurological damage. Mutant swarms form when a virus produces mutationally-damaged copies of itself inside a host, some of which aren’t infectious but find their way into the nervous system where they burrow in causing damage, and others that combine with complimentary broken copies inside host cells to produce working infectious copies of the virus. So a host can not only become crippled with neurological issues, but also still be producing infectious copies of the virus. And it seems as if COVID-19 has many characteristics that indicate the potential to form mutant swarms: the “striking” mutation rate mentioned above and the fact a second widespread mutated strain seems to have already emerged in Washington State with many other isolated strains reported elsewhere, crossing between species is another factor and a dog in Hong Kong appears to have tested positive, the fact that the Wuhan Strain can infect not only the respiratory tract but feces as well – multi-organ involvement is an important contributor to viral swarms, [66] and finally the markedly viral load rate of COVID-19 compared to SARS – SARS produced a viral load several times lower which decreased over time, while COVID-19 produces a “very high” viral load [67] that appears to increase over time and can peak several orders of magnitude higher than SARS was measured to reach. [68] And alarming evidence that this phenomenon is occurring emerged from a Chinese pre-print which noted that over one-third of the roughly 200 patients studied has some neurological symptoms, with nearly half of the most severe patients exhibiting neurological issues. [69] And further evidence for the possibility of both mutant swarms and ADE is witnessed by a study published in Lancet, which notes that the case fatality rate in Wuhan could actually be as high as 20% – [70] the outbreak’s epicenter would be expected to have the highest rates of both phenomena as different of the Wuhan Strain infected and reinfected overlapping hosts.

Another exceptional and atypical trait of the Wuhan Strain COVID-19 is that not only does it form its own clade, it’s calculated to have diverged from SARS and its other sister coronaviruses some 260 years ago. [71] And yet in all that time, while it every other branch of the coronavirus tree was busy branching-off into countless variants, [72] if it emerged naturally, COVID-19 somehow spent a quarter of a millennium as the lone known example of its clade, somehow not mutating into related lineages in all that time. Another simpler explanation is that this apparent hereditary distance and genetic uniqueness is just the result of being altered in a lab. And although two distinct strains of COVID-19 have been identified, there’s no reason to believe this mutational differentiation happened before contact with humans in the winter of 2019. Additionally, when neutral sites, the specific points in the genome which most reliably show evolutionary change, were examined: COVID-19 looks even more evolutionarily distant from any of its possible relatives, [73] which would make sense if all that evolutionary distance was gained by artificially accelerated generational turn-over in a lab.

Also giving credence to the idea that the Wuhan Strain was bio-engineered is the existence of a patent application registered to a scientist from Wuhan that looks to modulate a coronavirus’ spike-protein genes [74] – the precise region altered by Zhengli Shi at UNC to make a hyper-virulent strain of coronavirus, and whose alteration and adaptation would explain the Wuhan Strain’s unusual behavior as discussed above.

And curiously, the head of Harvard’s Chemistry Department, Dr. Charles Lieber, was arrested in the midst of this outbreak on charges that he’d been accepting millions of dollars in bribes from the Chinese government. [75] According to his charging documents, Dr. Lieber first went to the Wuhan University of Technology (WUT), in November 2011 to participate in a nanotechnology forum, which was when he was recruited into a bribery scheme that would net him several million dollars to “establish a research lab and conduct research at WUT,” which became known as ” Joint Nano Key Laboratory,” as well as mentor and advocate for graduate students. By 2015, Dr. Lieber appeared to be fairly intimately involved with what seemed to begin as simply a nanotechnology lab, but now had shifted to involve biology as well, since he described visiting the lab multiple times per year “as we try to build up the nano-bio part of the lab.” Whether or not this nano-bio part of the Nano Key Laboratory is related to Wuhan’s BSL-4 virology lab isn’t clear, however if the Wuhan Strain was bio-engineered, technology classified as “nano-bio” would’ve almost certainly played a role.


Given the above facts, either:

  • A coronavirus spontaneously mutated and jumped to humans at a wet market or deep in some random bat cave which just so happened to be 20 miles from China’s only BSL-4 virology lab, a virus with an unusually slippery never-before-seen genome that’s evading zoological classification, that may be as much as twenty-times more contagious than SARS and whose spike-protein region which allows it to enter host cells holds an unique HIV-like signature with the concomitant clinical response, that somehow managed to infect its patient zero who had no connection to this market, and then be so fined-tuned to humans that it’s gone on to create the single greatest public health crisis in Chinese history with approaching 100 million citizens locked-down or quarantined – also causing Mongolia to close its border with its largest trading partner for the first time in modern history and Russia to ban Chinese citizens from entry into their country. [76]


  • Chinese scientists failed to follow correct sanitation protocols possibly while in a rush leading up to an international virological conference and during their boisterous holiday season, something that had been anticipated since the opening of the BSL-4 lab and has happened at least four times previously, and accidentally released this bio-engineered Wuhan Strain – likely created by scientists researching immunotherapy regimes against bat coronaviruses, who’ve already demonstrated the ability to perform every step necessary to bio-engineer the Wuhan Strain COVID-19 – into their population, and now the world. As would be expected, this virus appears to have been bio-engineered at the spike-protein genes which was already done at UNC to make an extraordinarily virulent coronavirus. Chinese efforts to prevent the full story about what’s going on from getting out [77] are because they want the scales to be even since they’re now facing a severe pandemic and depopulation event. No facts point against this conclusion.

An immediate international moratorium on all dual-use gain-of-function research must be instated and all existing experimentation must be autoclaved, only greed and hubris have ever been served by attempting this type of genetic manipulation. Humanity does not need a vaccine against HIV derived from a coronavirus, nor do we need to be tinkering with genetic material that holds the potential to wipe a significant percentage of us off the face of the Earth.

Failure to embrace such a ban may effectively become a death sentence for our species, assuming we aren’t already on our last mile.


Sign the petition to end gain-of-function research here

Medium user @siradrianbond provided all information regarding Dr. Zheng-li’s extensive grant funding.


  1. The proximal origin of SARS-CoV-2
  2. Gain function flu studies
  4. a b Origins of 2019-NCoV XiaoB Res
  5. Don’t buy China’s story: The coronavirus may have leaked from a lab - New York Post 22 February 2020
  6. Coronavirus ‘lab leakage’ rumors spreading - Asia Times 17 February 2020
  7. a b How deadly pathogens have escaped the lab — over and over again - Vox 20 March 2019
  8. a b Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding - The Lancet 22 February 2020
  9. Big Eared Horseshoe Bat Range - Wikipedia
  10. Twitter post @jenniferatntd 17 February 2020
  11. Google search - peter daszak" "zhengli shi"
  12. Isolation and characterization of a bat SARS-like coronavirus that uses the ACE2 receptor - Nature 30 October 2013
  13. Scientists ‘strongly condemn’ rumors and conspiracy theories about origin of coronavirus outbreak - Science 19 February 2020
  14. Towards a Coronavirus-Based HIV Multigene Vaccine = ResearchGate June 2006
  15. Bill Gates Predicts An HIV Vaccine By 2030 - Bloomberg 23 January 2015
  16. An Unacceptable Breach of Trust - Inside HigherEd 3 October 2018
  17. Reinstate the global moratorium on "gain-of-function" research
  18. Poliovirus Baked From Scratch - Science 11 July 2002
  19. On the Origin of the H1N1 (A/USSR/90/77) Influenza Virus = Microbiology Society 1 October 1981
  20. a b The Reemergent 1977 H1N1 Strain and the Gain-of-Function Debate - American Society for Microbiology
  21. Should scientists self-censor their H5N1 research - Dallas Morning News
  22. Airborne transmission of influenza A/H5N1 virus between ferrets. - PubMed 22 June 2012
  23. Lab-Made Coronavirus Triggers Debate - The Scientist 16 November 2016
  24. NIH Lifts Funding Pause on Gain-of-Function Research - The NIH Director 19 December 2017
  25. Tweet by David R Martinez - 29 January 2020
  26. WHO Announces Coronavirus Mortality Rate Has Jumped to 3.4 Percent National Review 3 March 2020
  27. Inside the Chinese lab poised to study world's most dangerous pathogens - Nature 23 February 2017
  28. How China’s Coronavirus Is Spreading — and How to Stop It - Foreign Policy 26 January 2020
  29. Wuhan seafood market may not be source of novel virus spreading globally - Science 26 Jan 2020
  30. First coronavirus patient had NO connection to Wuhan seafood market - so did the disease start elsewhere? - Daily Mail 18 February 2020
  31. Decoding the evolution and transmissions of the novel pneumonia coronavirus (SARS CoV 2) using whole genomic data - ChinaXIV 21 February 2020
  32. Functional assessment of cell entry and receptor usage for SARS-CoV-2 and other lineage B betacoronaviruses = Nature Microbiology 24 February 2020
  33. Genomic and protein structure modelling analysis depicts the origin and infectivity of 2019-nCoV, a new coronavirus which caused a pneumonia outbreak in Wuhan, China - bioRxiv
  34. a b The Proximal Origin of SARS-CoV-2 - Scripps Research Institute November 2019
  35. Animal models for SARS and MERS coronaviruses - HHS Public Access 9 June 2015
  36. Coronavirus up to 20 times more likely than SARS to bind to human cells, study suggests - South China Morning Post18 February 2020
  37. Comparative rates of infection chart
  38. Estimating the effective reproduction number of the 2019-nCoV in China - medRiv 11 January 2020
  39. SARS-like cluster of circulating bat coronavirus pose threat for human emergence - HHS Public Access 21 December 2015
  40. Twitter post about Zhengli Shi appointment - 12 February 2020
  41. A pneumonia outbreak associated with a new coronavirus of probable bat origin - Nature 3 February 2020
  42. Jennifer Zeng Twitter post - 12 February 2020
  43. Discovery of a novel coronavirus associated with the recent pneumonia outbreak in humans and its potential bat origin
  44. solation and characterization of a bat SARS-like coronavirus that uses the ACE2 receptor - Demantic Scholar 2013
  45. Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding - The Lancet 22 February 2020
  46. Evolution of the novel coronavirus from the ongoing Wuhan outbreak and modeling of its spike protein for risk of human transmission - Science China Life Sciences Vol 63 Issue 3
  47. The real number of coronavirus cases is more than 75,000, according to a scientific model that says the outbreak will double in size every 6.4 days = Business Insider 1 February 2020
  48. Molecular Mechanism for Antibody-Dependent Enhancement of Coronavirus Entry - Journal of Virology 2015
  49. Chinese doctors say Wuhan coronavirus reinfection even deadlier - Taiwan News 14 February 2020
  50. Uncanny similarity of unique inserts in the 2019-nCoV spike protein to HIV-1 gp120 and Gag - bioRxiv
  51. Ferret models of viral pathogenesis - ScienceDirect May 2015
  52. Scientific Puzzles Surrounding the Wuhan Novel Coronavirus - The Epoch Times 2 March 2020
  53. Coronavirus far more likely than Sars to bond to human cells due to HIV-like mutation, scientists say - South China Morning Post 27 February 2020
  54. The spike glycoprotein of the new coronavirus 2019-nCoV contains a furin-like cleavage site absent in CoV of the same clade - ScienceDirect Vol 176 April 2020
  55. Generation of a Highly Pathogenic Avian Influenza A Virus from an Avirulent Field Isolate by Passaging in Chickens - Journal of Virology 2001
  56. The neuroinvasive potential of SARS‐CoV2 may play a role in the respiratory failure of COVID‐19 patients - Journal of Medical virology 27 February 2020
  57. [ Role of lopinavir/ritonavir in the treatment of SARS: initial virological and clinical findings ] - Thorax BMJ Joutrnals Vol 59 Issue 3
  58. Scientific Puzzles Surrounding the Wuhan Novel Coronavirus - The Epoch Times 3 February 2020
  59. Cocktail of flu, HIV drugs appears to help fight coronavirus: Thai doctors - Physicians Weekly 3 February 2020
  60. Pathological findings of COVID-19 associated with acute respiratory distress syndrome - The Lancet - Respiratory Medicine 18 February 2020
  61. Model of antibody-dependent enhancement of dengue infection - Scitable - Nature Education
  62. ‘Striking’ coronavirus mutations found within one family cluster, Chinese scientists say - South China Morning Post 3 February 2020
  63. Scientists Warn: You Can Catch Coronavirus More Than Once - Neoscope 22 March 2020
  64. Coronavirus: Traces of virus found in patients who have recovered - New Zealand Herald 21 February 2020
  65. How Mutant Viral Swarms Spread Disease - Scientific American 14 September 2015
  66. Emergence and Transmission of Arbovirus Evolutionary Intermediates with Epidemic Potential - ScienceDirect 11 June 2014
  67. Viral load of SARS-CoV-2 in clinical samples - The Lancet 24 February 2020
  68. Clinical progression and viral load in a community outbreak of coronavirus-associated SARS pneumonia: a prospective study - The Lancet 24 May 2003
  69. Neurological Manifestations of Hospitalized Patients with COVID-19 in Wuhan, China: a retrospective case series study - medRxiv 25 February 2020
  70. Real estimates of mortality following COVID-19 infection - The Lancet 1 March 2020
  71. Analysis of Wuhan Coronavirus: Deja Vu - 29 January 2020
  72. Genetic Characterization of Betacoronavirus Lineage C Viruses in Bats Reveals Marked Sequence Divergence in the Spike Protein of Pipistrellus Bat Coronavirus HKU5 in Japanese Pipistrelle: Implications for the Origin of the Novel Middle East Respiratory Syndrome Coronavirus - Journal of Virology
  73. On the origin and continuing evolution of SARS-CoV-2 - National Science Review 3 March 2020
  74. Coronal virus genetic engineering protein and use thereof - Europe PMC 27 December 2005
  75. Harvard chemistry chief’s arrest over China links shocks researchers - Nature 3 February 2020
  76. Russia Bans Chinese citizens from entering the country - BNO Newsroom twitter post 18 February 2020
  77. Another bombshell - Jennifer Zeng twitter post 16 February 2020