PROLOGUE: SARS-CoV-2 is 'Unrestricted Bioweapon and the current pandemic a result of Unrestricted Biowarfare' latest scientific research reveals, confirming the findings of other honest scientists and uncovering the scientific fraud. 

When the first, instigated and clearly manipulated horror-news about the 'dangerous virus outbreak' in Wuhan China were irresponsibly spread by especially the Anglo-American, French and German mainstream-media, in what clearly has been proven now as a concerted and pre-mediated action following the narrative of the exercise "Event 201", almost all 'conservation' organizations were quickly lured to use the master-minded crisis for their own benefit and for fund-raising campaigns to support their own programmes - targeting the closure of wildlife markets, wet-markets in general and wildlife-trafficking. While each of these goals has its own merits per se, the solely conservation-minded organizations were not able to look beyond their fundraising plates, not realizing that their outcries were actually serving the pre-mediated narrative to spread fear - especially when then the less-loved bats were quickly identified as the "culprit". Even funding from BigPharma was accepted by the mainstream-conservationist to further the spin, like they did during the emerging HIV scare, blaming promiscuous Africans and vervet monkeys coming out of deforested areas as well as during the Ebola crisis, when already bats had been blamed, though the first outbreak of the patented strain was close to a CDC field lab. Only a few organizations working in the field of nature protection - like Bat Conservation International (BCI), Friends of Peoples close to Nature (fPcN) and ECOTERRA Intl. (ETI) - did not fall into that trap and maintained that the contagion - quickly dubbed SARS-CoV-2 - did NOT come from bats or any other wild animal traded in the horrific wet-markets of China, because the hard science did not proof the narrative. Those resisting the hype didn't get funding from the masterminds of the corona crisis, but at least they remained honest. And now it has been proven beyond any reasonable doubt that SARS-CoV-2 is a man-made and lab-produced contagion.

CONCLUSION: STOP any gain‐of‐function research as well as any contagion development research - including of all nano-technology components. Close all uncontrolled and especially all private BSL-4 laboratories, place the remaining BSL-4 labs under 100% independent international control and begin the long overdue process by an independent, international tribunal to fully investigate the SARS-CoV-2 event with the task to bring those guilty to justice. Whoever delays such tribunal proofs guilty for obstruction of justice.

Covid: Why bats are not to blame, say scientists

Short-nosed fruit bat, Thailand
Bats have been on Earth for more than 50 million years image copyright Science Photo Library

By Helen Briggs - 13. October 2020

Every now and then, Dr Mathieu Bourgarel seeks permission from the village elders to visit the sacred caves, bringing a gift to appease the spirits.

Donning mask, overalls, and three layers of gloves, he descends into the darkness, climbing down rope ladders and squeezing through the narrow chambers of caves.

The tell-tale odour of bats is everywhere, their excrement deposited in layers on the floor, like wading through fresh snow.

Occasionally, a bat is startled from sleep, wings brushing by as it takes flight.

People in this part of Zimbabwe call bats "winged dragons", "flying rats" or simply the "evil ones".

Like elsewhere in the world, the flying mammals are much misunderstood. For this wildlife ecologist, they're beautiful and incredible creatures. "They are fascinating," he says. "People are frightened of something they don't know."

Cave, Zimbabwe

The caves are home to colonies of small bats image copyright M Bourgarel/Cirad

Dr Bourgarel is a virus hunter for the French research institute, Cirad. Working with colleagues at the University of Zimbabwe he goes into the bat caves to collect samples and droppings from bats.

Back at the lab, the scientists extract and sequence the genetic material of bat viruses. They have already discovered different coronaviruses, including one in the same family as Sars and Sars-CoV-2.

The research is part of a worldwide effort to investigate the diversity and genetic make-up of the viruses that bats carry, providing the tools to react quickly, should people start to get sick.

"The local population frequently visits these bats' habitat, in order to collect guano to use as fertiliser for their crops. It is therefore essential to know the pathogens carried by the bats, because they could be transmitted to humans," says Dr Elizabeth Gori of the University of Zimbabwe.

Going into the cave

The scientists wear full personal protective equipment to enter the caves image copyright M Bourgarel/Cirad

Bat experts have launched a campaign, Don't Blame Bats, to dispel unfounded fears and myths about bats, which are threatening conservation. They say bats are some of the most misunderstood and undervalued animals on the planet.

Long the target of disdain, persecution and cultural prejudice, they have been blamed for a host of evils visited upon humans. And fears and myths about bats have only intensified in the time of Covid.

Facts about bats

  • Bats are the only mammal capable of true flight
  • Insect-eating bats may save US farmers $3.7bn each year by reducing crop damage
  • Hundreds of plant species rely on bats for pollination
  • Bats are under unprecedented threat from habitat destruction, climate change, hunting and other pressuresPresentational white space

The precise origin of the virus that has wreaked such havoc across the world has not been pinned down. But the vast majority of scientists agree that it crossed into humans from an animal species, most likely a bat. That doesn't mean bats are to blame; it's our increasing interference with these wild creatures that's at the root of the problem.

[N.B.: These last two lines are the preferred narrative by those who do not want to dig deeper, while it has become clear to all real scientists that SARS-CoV-2 is a man-made contagion constructed in a lab - see also the 3 scientific publications below.]

Outbreaks of emerging diseases have been linked to human destruction of nature. When forests or grasslands are razed to graze cattle, to grow soy or to build roads and settlements, wild animals are forced ever closer to humans and livestock, giving viruses an opportunity to jump ship.

"It is undeniable that bats, such as many other animal groups, present real risks as hosts for potentially dangerous diseases," says Ricardo Rocha of the University of Porto, Portugal.

But he points out that when you control for the number of bat species (a whopping 1,400 or more), the proportion of human-infecting viruses is similar to other groups, such as birds, domestic animals and rodents.

Forest loss, Borneo

Since 2000 Borneo has lost 20,000 sq miles of forest

Scientists estimate that three out of every four new or emerging infectious diseases in people come from animals. A warning of the dangers came in 2002, when the mysterious illness, Sars, emerged in China, killing almost 800 people around the world.

In 2017, researchers identified a colony of horseshoe bats living in remote caves in Yunnan province that harboured genetic pieces of the human Sars virus. They warned then that a similar disease could emerge again, and they were proved right.

But rather than blaming one species or another, we need to reassess our relationship with the natural world, says Dr Rocha. He points out that bats are vital for healthy ecosystems and human well-being.

Bats suppress insects that swarm over crops. They pollinate plants in the tropics, such as durian fruits. And they disperse the seeds of trees found in rainforests, helping in the fight against climate change.

Bats, Mexico

Bats emerge from a limestone cave in Mexico

It would be a "terrible outcome" if bats were demonised, since the spread of diseases from animals to humans is much more about humans encroaching into their domain than the other way around, says Dr David Robertson of the University of Glasgow. The antecedents of Sars-CoV-2 have likely been circulating in bats for decades, he says, with the ability to infect other animal species too.

There have been isolated reports of Covid-related backlash against bats, including actual or intended killings in Peru, India, Australia, China and Indonesia.

Scientists warn that a few misguided actions could have serious consequences for vulnerable bat species and even increase the risk of disease spillover.

Egyptian fruit bat

Some tropical fruit bats carry seeds inside them, carrying them far and wide

"A major concern is that many bat species are threatened with extinction, so even small instances of misguided violence could cause irreversible damage and have catastrophic flow-on effects for ecosystems that humans rely on," says Douglas MacFarlane of the University of Cambridge.

Bats have lived alongside humans for centuries, for mutual good. In the university city of Coimbra in Portugal, bats have occupied an 18th Century library for more than 300 years, feasting on insects that might otherwise destroy manuscripts. Visit at dusk and you might see them flit out of the library windows and swoop down over the steep cobbled streets.

Ricardo Rocha says we must remember that bats are an integral part of the complex natural webs that keep ecosystems healthy. "If there is a big take-home message from this unfortunate moment in history it's that making nature ill, makes us ill," he says.

Follow Helen on Twitter.


SARS-CoV-2 Is an Unrestricted Bioweapon: A Truth Revealed through Uncovering a Large-Scale, Organized Scientific Fraud


By Limeng Yan - The University of Hong KongShu KangJie GuanShanchang Hu - 20. August 2020 - 

reviewed, accepted and published October 2020

Abstract and Figures

Two possibilities should be considered for the origin of SARS-CoV-2: natural evolution or laboratory creation. In our earlier report titled "Unusual Features of the SARS-CoV-2 Genome Suggesting Sophisticated Laboratory Modification Rather Than Natural Evolution and Delineation of Its Probable Synthetic Route", we disproved the possibility of SARS-CoV-2 arising naturally through evolution and instead proved that SARS-CoV-2 must have been a product of laboratory modification. Despite this and similar efforts, the laboratory creation theory continues to be downplayed or even diminished. This is fundamentally because the natural origin theory remains supported by several novel coronaviruses published after the start of the outbreak. These viruses (the RaTG13 bat coronavirus, a series of pangolin coronaviruses, and the RmYN02 bat coronavirus) reportedly share high sequence homology with SARS-CoV-2 and have altogether constructed a seemingly plausible pathway for the natural evolution of SARS-CoV-2. Here, however, we use in-depth analyses of the available data and literature to prove that these novel animal coronaviruses do not exist in nature and their sequences have been fabricated. In addition, we also offer our insights on the hypothesis that SARS-CoV-2 may have originated naturally from a coronavirus that infected the Mojiang miners. Revelation of these virus fabrications renders the natural origin theory unfounded. It also strengthens our earlier assertion that SARS-CoV-2 is a product of laboratory modification, which can be created in approximately six months using a template virus owned by a laboratory of the People's Liberation Army (PLA). The fact that data fabrications were used to cover up the true origin of SARS-CoV-2 further implicates that the laboratory modification here is beyond simple gain-of-function research. The scale and the coordinated nature of this scientific fraud signifies the degree of corruption in the fields of academic research and public health. As a result of such corruption, damages have been made both to the reputation of the scientific community and to the well-being of the global community. Importantly, while SARS-CoV-2 meets the criteria of a bioweapon specified by the PLA, its impact is well beyond what is conceived for a typical bioweapon. In addition, records indicate that the unleashing of this weaponized pathogen should have been intentional rather than accidental. We therefore define SARS-CoV-2 as an Unrestricted Bioweapon and the current pandemic a result of Unrestricted Biowarfare. We further suggest that investigations should be carried out on the suspected government and individuals and the responsible ones be held accountable for this brutal attack on the global community. 2

Illustration of steps involved in the sequencing and assembly of coronavirus genomes. A. The normal process. B. A possible route of fabricating a viral genome by creating a genomic sequence first and obtaining raw sequencing reads guided by it. NGS: Next Generation Sequencing.

Illustration of steps involved in the sequencing and assembly of coronavirus genomes. A. The normal process. B. A possible route of fabricating a viral genome by creating a genomic sequence first and obtaining raw sequencing reads guided by it. NGS: Next Generation Sequencing.

Abnormal distribution of synonymous and non-synonymous mutations in Spike revealed by the comparison between RaTG13 and SARS-CoV-2. Synonymous and non-synonymous mutations are analyzed between closely related coronaviruses on large viral proteins: A. Spike (S), B. Orf1a, C. Orf1b, and D. Nucleocapsid

Abnormal distribution of synonymous and non-synonymous mutations in Spike revealed by the comparison between RaTG13 and SARS-CoV-2. Synonymous and non-synonymous mutations are analyzed between closely related coronaviruses on large viral proteins: A. Spike (S), B. Orf1a, C. Orf1b, and D. Nucleocapsid


Five amino acid mutations are observed in S2 (684-1273) in twenty randomly selected SARS-CoV-2 sequences. They are at positions 829, 1020, 1101, 1176, and 1191. GenBank accession number for each isolate is shown in the sequence's name following the country name.

Five amino acid mutations are observed in S2 (684-1273) in twenty randomly selected SARS-CoV-2 sequences. They are at positions 829, 1020, 1101, 1176, and 1191. GenBank accession number for each isolate is shown in the sequence's name following the country name.


Phylogenetic analysis of SARS-CoV-2 and representative viruses from the subgenus sarbecoronavirus. Figure redrew from Zhou et al 9 . Colored viruses were all reported after the COVID-19 outbreak.

Phylogenetic analysis of SARS-CoV-2 and representative viruses from the subgenus sarbecoronavirus. Figure redrew from Zhou et al 9 . Colored viruses were all reported after the COVID-19 outbreak.


Analysis of synonymous and non-synonymous mutations in S2 between RmYN02 and RaTG13. The abrupt change of trajectory of the non-synonymous mutation (red) curve and its subsequent flattening are observed.


Analysis of synonymous and non-synonymous mutations in S2 between RmYN02 and RaTG13. The abrupt change of trajectory of the non-synonymous mutation (red) curve and its subsequent flattening are observed.

Figures - uploaded by Limeng Yan

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DOI: 10.5281/zenodo.4073131.svg


Limeng Yan at The University of Hong Kong

Limeng Yan - The University of Hong Kong


Might SARS‐CoV‐2 Have Arisen via Serial Passage through an Animal Host or Cell Culture?

A potential explanation for much of the novel coronavirus’ distinctive genome

Karl Sirotkin 

Dan Sirotkin

First published: 12 August 2020


Despite claims from prominent scientists that SARS‐CoV‐2 indubitably emerged naturally, the etiology of this novel coronavirus remains a pressing and open question: Without knowing the true nature of a disease, it is impossible for clinicians to appropriately shape their care, for policy‐makers to correctly gauge the nature and extent of the threat, and for the public to appropriately modify their behavior. Unless the intermediate host necessary for completing a natural zoonotic jump is identified, the dual‐use gain‐of‐function research practice of viral serial passage should be considered a viable route by which the novel coronavirus arose. The practice of serial passage mimics a natural zoonotic jump, and offers explanations for SARS‐CoV‐2's distinctive spike‐protein region and its unexpectedly high affinity for angiotensin converting enzyme (ACE2), as well as the notable polybasic furin cleavage site within it. Additional molecular clues raise further questions, all of which warrant full investigation into the novel coronavirus's origins and a re‐examination of the risks and rewards of dual‐use gain‐of‐function research.

1 Introduction

To date, the origins of SARS‐CoV‐2 remain in doubt, and its behavior enigmatic: It has been reported that “the virus acts like no microbe humanity has ever seen.”[1]Although based on sequence analysis many prominent virologists and other eminent scientists have concluded that the novel coronavirus causing the current pandemic was not designed or manipulated in a laboratory and was the result of a natural zoonotic jump,[2] this assertion fails to fully account for all possible origins of two unique genomic characteristics found in SARS‐CoV‐2, and ignores the long history of serial passage as a method to manipulate viral genomes. The long‐standing practice of serial passage is a form of gain‐of‐function research that forces zoonosis between species, and requires the same molecular adaptations necessary for a natural zoonotic jump to occur within a laboratory, leaving the same genetic signatures behind as a natural jump but occurring in a much shorter period of time.

The genetic signatures in question includes two distinctive features possessed by SARS‐CoV‐2's spike‐protein: the unique sequence in the receptor binding domain (RBD), a region known to be critical for SARS‐CoV‐2's utilization of human angiotensin converting enzyme (ACE2), which is the cell surface receptor used by both SARS‐CoV and SARS‐CoV‐2 for fusion with target cells and subsequent cell entry. The second feature is the presence of a polybasic furin cleavage site, which is also known as a multibasic cleavage site (MBS)—a four amino acid insertion with limited sequence flexibility—within the coronavirus's novel spike‐protein, that is not found in SARS‐CoV or other lineage B coronaviruses. This furin cleavage site, which is poly or multibasic by definition since its composed of multiple basic amino acids, is an important virulence feature observed to have been acquired by fusion proteins of avian influenza viruses and Newcastle Disease Virus either grown under experimental conditions or isolated from commercial animal farms—settings that mimic the conditions of serial laboratory passage. In fact, no influenza virus with a furin cleavage site has ever been found in nature,[3] and it is a feature that has been thoroughly investigated in the literature since it appears to allow the influenza viruses that carry it to establish a systemic multiorgan infection using different cell types including nerve cells,[3] is correlated with high pathogenicity, and also plays a key role in overcoming the species barrier.[4] More generally, despite the fact that not all serially passed viruses have demonstrated an increase in pathogenicity, the fact remains that every highly pathogenic avian influenza virus, defined by having a furin cleavage site, has either been found on commercial poultry farms that create the pseudo‐natural conditions necessary for serial passage, or created in laboratories with gain‐of‐function serial passage experiments.[3]

Although they only emerge under artificial conditions in influenza viruses, these furin cleavage sites are found within several branches of the coronavirus family tree. However SARS‐CoV‐2 is the only lineage B coronavirus found with one, and the only other coronaviruses known to have them are only at most 60% identical to this novel coronavirus.[5] An intriguing clinical correlate is that furin cleavage sites within influenza viruses are associated with lymphopenia in infected mice, and with neurological conditions following replication in the brains of ferrets,[6]both of which are clinical manifestations observed in hospitalized patients infected by SARS‐CoV‐2 and suffering from COVID‐19.[1] This indicates that furin cleavage sites may be an example of the convergent evolution that dominates virus–host interactions, since viral proteins evolve convergently and often accumulate many of the same linear motifs that mediate many functionally diverse biophysical interactions in order to manipulate complex host processes.[7] It is possible that this novel coronavirus gained its furin cleavage site through recombination in an intermediate host species, however there are also two laboratory processes that may have imbued SARS‐CoV‐2 with its furin cleavage site which will be discussed below.

Without incorporating the historical and biological implications of serial viral passage either through lab animals in vivo or through cell cultures in vitro, it is impossible to comprehensively evaluate whether SARS‐CoV‐2 is the result of a laboratory leak or a natural zoonotic jump. Moreover, despite the published consensus being that SARS‐CoV‐2 arose naturally, because these publications universally ignore the scenario of the widely used practice of laboratory serial passage, this latter scenario deserves a thorough investigation. Especially since serial passage through a live animal host simply forces the same molecular processes that occur in nature to happen during a zoonotic jump, and in vitro passage through cell culture mimics many elements of this process—and neither necessarily leaves any distinguishing genetic traces.

2 The History of Viral Serial Passage

The dual‐use gain‐of‐function research tool of serial passage was first applied to a strain of H1N1 Swine Flu, a variant of the pandemic influenza virus that was genetically modified before it either leaked out of a Soviet lab or was introduced as part of an attenuated vaccine trial in 1977. Although no one has ever taken responsibility for the introduction of this virus, it would become the first known example of a virus created by serial passage leaving a lab, which was later determined due to its inexplicable genetic distance from any known sister strain.[8] This extra distance would be expected since serial passages artificially accelerates genetic divergence between taxa, resulting in the accumulation of genetic distance at a much faster rate than it occurs in a natural setting.

Then in 1979, just 2 years after the introduction of this modified H1N1 Swine Flu, a different Soviet lab leaked weaponized anthrax out through an improperly maintained exhaust filter, and Soviet authorities convincingly blamed the deaths on contaminated local meat. This cover up withstood a formal inquiry conducted in 1986, and was not revealed to be a fabrication until 1992, when an analysis of dispersion patterns revealed that the victims were not those working with the supposedly contaminated meat, but instead all lived downwind from the Sverdlovsk weapons lab and its improperly maintained exhaust vent. Therefore, there is a history of denying laboratory leaks on the commercial meat industry that dates back about 40 years, an effective excuse that provided the Soviets with an alibi that held up for nearly 2 decades.

The Soviet strain of serially passaged H1N1 Swine Flu was likely being developed as part of a vaccine program, one of the humane goals of gain‐of‐function research that exist alongside riskier and more troublesome ones like developing bioweapons. Its emergence ignited the debate between the risks and rewards of dual‐use gain‐of‐function research—causing it to became the poster virus for the dangers this protocol posed.[8]

This debate would largely fade in the decades that followed, until two separate teams used genetic manipulation followed by serial passage between ferrets to create mammal‐transmissible H5N1 Bird Flu strains of influenza virus in 2011 that had the gain‐of‐function of being transmissible by aerosol. The first team was led by Dr. Ron Fouchier and conducted at the Erasmus Medical Center in the Netherlands, and demonstrated that as few as five mutations prior to serial passage were sufficient to create a modified strain of the H5N1 Bird Flu that could be transmitted by aerosol while remaining highly lethal.[9] The creation of this highly virulent strain that was said by a reporter to be able to “make the deadly 1918 pandemic look like a pesky cold,”[10] and was contentious enough to cause the scientists working on them to prepare for a media storm[11]—a storm that rolled in on the back of a second similar experiment.

Instead of only tweaking the H5N1 Bird Flu in a few places before serial passage, Dr. Yoshihiro Kawaoka of the Universities of Tokyo and Wisconsin used genetic engineering to combine genes from the H1N1 Swine Flu as well as the H5N1 Bird Flu to create a chimeric virus that was then serially passed through ferrets, creating another airborne virus with potentially pandemic properties.[12] Both experiments created a modified genome that appeared to be the result of natural, albeit accelerated, selection since the process of serial passage forces the mutations selected for in natural zoonotic jumps, and masks the direct genetic engineering done on the viruses. These experiments were viewed by many as being sufficiently dangerous that they should not be published,[13] however they were both eventually released with certain methodological and sequence details left out.

In the years that followed, gain‐of‐function serial passage through ferrets was used to increase the virulence of the H7N1 Bird Flu as well as allowing for its aerosol transmission without first introducing any mutations.[14] Additionally, the H1N1 Bird Flu was also found to become airborne and increase in virulence after in vivo passage through swine.[1516] And although serial passage in the laboratory does not invariably increase viral pathogenicity, highly pathogenic influenza viruses all contain furin cleavage sites,[16] which only emerge after serial passage in laboratories or pseudo‐naturally on commercial animal farms.

The process of sequential passage through animal hosts or cell cultures leaves a genome that appears natural and not purposefully manipulated since it effectively mimics the natural process of zoonosis, and leaves a genome that appears to be the result of natural selection so long as its relationship to related strains of virus is ignored. However, the artificial generations added by forced serial passage creates the artificial appearance of evolutionary distance, which was the characteristic of the H1N1 Swine Flu Soviet leak in the 1970s that lead researchers to conclude it had been constructed in a lab, and is exactly what is found with SARS‐CoV‐2, which is distant enough from any other virus that it has been placed in its own clade.[17]

2.1 Serial Passage and Its Molecular Signatures

Although serial passage mimics many of the natural zoonotic processes that occur during a natural zoonotic jump, because serial passage artificially condenses a natural phenomenon into a small temporal window, some subtle differences can be found. In addition to the inexplicable genetic distance from its sister strains, which screams out for an intermediate relative to complete the phylogenetic picture, SARS‐CoV‐2 has a remarkably strong affinity for spike‐protein binding to ACE2—some 10–20 times higher than SARS‐CoV's.[18] That affinity may have emerged after mutational events either in an intermediate natural host or after a zoonotic jump into humans that theoretically could have occurred earlier than the first documented infection, which would give it time to increase that significantly. So logically, it could also have emerged via selection after serial passage through laboratory cell cultures or laboratory animals as well. And regarding the second distinctive feature found in the novel coronavirus: If other viruses have been observed to acquire furin cleavage sites by passage under experimental laboratory conditions, then such a mechanism is theoretically possible for SARS‐CoV‐2 as well.[2]

In the case of influenza viruses like those mentioned above, their gain‐of‐function furin cleavage sites are thought to be a result of two different molecular processes. The first is either nucleotide insertions or substitutions that are able to be rescued and then eventually selected for due to the high multiplicity of infection found in serial passage protocols.[19] And the second is the recombination of multiple viral RNAs inside a host cell,[20] which may also include additional viruses introduced through accidental laboratory co‐infections.

Unlike influenza viruses, serial passage through ferrets has not been recorded in the literature for coronaviruses. However, since several branches of coronavirus have furin cleavage sites, a molecular pathway for their emergence must exist and may reemerge during serial passage. Several factors weigh into the probability that coronaviruses can gain furin cleavage sites following serial passage: The frequency of evolutionary motifs meant to deal with virus–host interactions that are often shared between viruses, the observations that when the infectious bronchitis coronavirus (IBV) coronavirus is serially passed through chickens it developed notable mutations along its spike‐protein genes,[21] and the fact that when a lineage A bovine coronavirus was subject to in vitro serial passage through cell lines, a 12‐nucleotide insert found within only a small minority of the pooled viruses spike‐protein region was strongly selected for and quickly emerged as the dominate strain.[22] These findings all point to the possibility that SARS‐CoV‐2 may have gained its furin cleavage site the same way influenza viruses do—through the in vivo serial passage between the live hosts that presents the immune challenges and intense selective pressure necessary for the recombination and mutations that lead to its emergence to occur. And just like influenza viruses are only able to preserve their furin cleavages in artificial environments since the heightened virulence they impart kills their hosts before they can propagate in a natural setting, based on the known taxonomy lineage B coronaviruses do not appear to be able to support furin cleavages in nature.

There is no doubt that the acquisition of the furin cleavage site was one of the key adaptations that enable SARS‐CoV‐2 to efficiently spread in the human populations compared to other lineage B coronaviruses, and provides a gain‐of‐function.[23] In addition to the possibility of obtaining a furin cleavage site through natural recombination in a secondary host or through serial passage either in a laboratory or on a commercial farm, one could have been spliced directly into the novel coronavirus's backbone in a laboratory using classic recombinant DNA technology that has been available for nearly 20 years. This allows for the removal of the restriction site junctions that are the telltale sign of direct genetic manipulation and permits reassembly without introducing nucleotide changes—creating a virus without any evidence of manipulation using the aptly named “No See'm technology.”[24] So although the entire spike‐protein RBD was not assembled from scratch, it is certainly plausible that the 12‐nucleotide‐long furin cleavage site could have been spliced directly into SARS‐CoV‐2. Furin cleavages already have been successfully spliced into other coronaviruses, including the IBV,[25] and even into SARS‐CoV, where it increased cell‐to‐cell fusion in in vitro experiments that only examined only the spike‐protein's function, which would presumably heighten its infectivity in vivo.[26]

Moreover, when a furin cleavage site was introduced to the IBV coronavirus spike‐protein via recombination, just like influenza viruses hosting this feature, it appeared to impart it with increased lethality as well as inflict neurological symptoms that had never previously been reported in studies of the murine IBV coronavirus.[25] The presence of this cleavage site also increased damage to the respiratory and urinary systems, paralleling SARS‐CoV‐2 systemic multiorgan symptoms—especially reports that infection with the novel coronavirus not only targets the lungs where it binds to ACE2 receptors, but also the entire cardiovascular system,[27] the nervous system,[28] and our kidneys as well.[29] It might be more than a coincidence that the Vero cells often used in serial passage are derived from kidney epithelial cells extracted from African green monkeys, which have ACE2 receptors very similar to those found in humans and would be shared by the humanized mice that are also used for serial passage research.

2.2 Natural Origin, or Gain‐of‐Function Lab Escape?

Gain‐of‐function research on bat‐borne coronaviruses has been ongoing for nearly a decade everywhere from the University of North Carolina to the Wuhan's Institute of Virology, which is supported by related facilities such as Wuhan's Center for Disease Control and Prevention as well as Wuhan University. A coronavirus that targets the ACE2 receptor like SARS‐CoV‐2 was first isolated from a wild bat in 2013 by a team out of Wuhan. This research was funded in part by EcoHealth Alliance,[30] and set the stage for the manipulation of bat‐borne coronavirus genomes that target this receptor and can become airborne. Many more viruses have been collected in Wuhan over the years, and one research expedition captured as many as 400 wild viruses,[31] which were added to a private repository that has since grown to over 1500 strains of virus,[32] meaning that the Wuhan Center for Disease Control and Prevention has a massive catalogue of largely undisclosed viruses to draw from for experiments. And in subsequent years, EcoHealth Alliance received funding for project proposals outlining gain‐of‐function research to be done in Wuhan, hoping to use cell cultures and humanized mice as well as “[spike]‐protein sequence data, infectious clone technology, in vitro and in vivo infection experiments and analysis of receptor binding”[33] to manipulate bat coronavirus genomes—all of which are consistent with the wet‐work that would be needed to engineer this novel coronavirus in a laboratory. But for whatever reason, the Wuhan Institute of Virology has refused to release the lab notebooks of its researchers, which are ubiquitous in even the simplest laboratories and are expected to be meticulously detailed given the sensitive and delicate work that takes place in BSL‐4 research labs intent on documenting their intellectual property, despite the fact that these notebooks would likely be enough to exonerate the lab from having any role in the creation of SARS‐CoV‐2.[34]

Although it does not prove a laboratory origin, another gain‐of‐function experiment demonstrates one possible step along the way to engineering SARS‐CoV‐2: the synthetic reconstruction of the SARS coronavirus to impart this virus with a high affinity for ACE2. This involved isolating a progenitor coronavirus from civets and then serially passing it through mammalian ACE2 receptor‐expressing cells—serial passage through host cell lines instead of entire hosts, which imparted a strong affinity for ACE2,[35] and another novel strain of coronavirus that was also presumably airborne. A few years after this study, more gain‐of‐function research was performed that involved the creation of a chimeric bat‐borne coronavirus by directly manipulating the bat coronavirus spike‐protein gene,[36] which created a coronavirus so virulent that it evoked the following dire warning from Simon Wain‐Hobson, a virologist with the Pasteur Institute in Paris: “If the [new] virus escaped, nobody could predict the trajectory.”[37]

Although SARS‐CoV‐2's efficient solution for ACE2 binding has been accurately described as something that could not be intentionally engineered nucleotide‐by‐nucleotide,[2] it could well be selected for after serial passage through ferrets or cell cultures in a lab. The only origin for the SARS‐CoV‐2 spike‐protein RBD that the sequence data excludes is the deliberate manufacturing and introduction of the entire SARS‐CoV spike‐protein RBD sequence to create SARS‐CoV‐2. Otherwise, there are no genetic data to distinguish among natural and engineered possibilities at the present time.

2.3 Ferreting Out the Signs of Serial Passage

Curiously, studies examining SARS‐CoV‐2's infectivity in ferrets found that it spreads readily among them, and also appears airborne in that animal model.[38]This lends support to the idea that ferrets may have been used for serial passage since viruses typically take a significant many months if not years to acclimate enough to spread at all among any new species, nonetheless become airborne, which requires further mutations.

This relationship was further supported by reports out of the Netherlands that the novel coronavirus had spread among thirteen different mink farms there, and also to at least one farm in Denmark[39] and to another in Spain where 87% of the mink were infected.[40] Minks are a closely related subspecies of ferret that can produce fertile offspring together, and so the fact that not only did the virus spread to fifteen different farms in three countries, but also appears to have spread from minks into farm workers[41] indicates that accidental commercial serial passage through minks could have played a role in its creation, as an alternative to laboratory ferrets. Nevertheless, regardless of where any possible serial passage occurred, the fact that SARS‐CoV‐2 spreads from humans to minks and then back to humans demonstrates a high affinity for both species, despite neither nominally being a natural reservoir. Further support for the possibility that serial passage through lab ferrets or throughout mink farms played a role in the genesis of this novel coronavirus is provided by a preprint that notes the obvious ease with which it passes through the air between ferrets, since SARS‐CoV‐2 was transmitted through the air to three out of four indirect recipient ferrets monitored for airborne passage of the novel coronavirus.[42] It seems reasonable to think that SARS‐Cov‐2's apparent affinity for ferrets and minks should lead to an investigation of mink farms in the Hubei province were the novel coronavirus was discovered, since a viable pathway for its emergence could be infected bats defecating on commercial mink farms, which would loosely parallel the emergence of MERS‐CoV from herds of camels following putative fecal contamination by local bats.[43]

The prospect that serial passage through lab animals or on commercial farms may have played a role in the creation of SARS‐CoV‐2 is also raised by an April 2020 preprint, which appears to have been retracted after Chinese authorities implemented the censorship of any papers relating to the origins of the novel coronavirus.[44] This paper found that coronaviruses that target the ACE2 receptor bind with ferret cells more tightly than any other species except the tree shrew, which only scored about 2% higher. Tree shrews have also been used for serial viral passage, and have been promoted as a preferable animal host for laboratory experimentation since they are cheaper, smaller, easier to handle, and closer to humans evolutionarily and physiologically than ferrets.[45] However, one does not exclude the other as a possible host, and a recent preprint examining SARS‐CoV's binding affinity in humans raises additional questions about its initial emergence. It found that the novel coronavirus appears to be far more adapted to human ACE2 receptors than those found in bats, which is unexpected given that bats are the virus's assumed source, and which lead the lead research to observe that SARS‐CoV‐2 was perfectly adapted to infect humans since its first contact with us, and had no apparent need to for any adaptive evolution at all.[46]

Although the novel coronavirus also appears to have a high affinity for the pangolin ACE2 receptor,[47] phylogenetic analysis of the neutral sites that best determine shared heritage[48] and a distinctive amino acid sequence both indicate that pangolins are unlikely to have served as an intermediate host,[47] so this affinity is likely due to the convergent motifs that often mark viral evolution and not shared heritage. The unexpected immediate affinity for humans was also reflected by another preprint, which observed that SARS‐CoV‐2 appeared just as adapted to humans at the very start of its epidemic as SARS‐CoV was in the latest stages of its emergence,[49] an unexpected finding since viruses are expected to mutate substantially as they acclimate to a new species.[50] SARS‐CoV‐2's muddled origins are made even more Gordian by a study published March 2018 that examined people who live in villages about a kilometer away from bat caves. This study revealed that only 2.7% of those villagers had antibodies indicating any past exposure to bat coronaviruses. The authors also sampled people living in Wuhan, and found no evidence of exposure to SARS‐CoV‐like coronaviruses at all.[51]

This means there is very little serological evidence of any exposure to these coronaviruses even in Chinese villagers living in close proximity to bat caves, and at the epicenter of the current outbreak—no previous exposure was found at all. These data do not support the idea that SARS‐CoV‐2 was circulating in humans prior to the outbreak began in Wuhan in the early winter or fall of 2019, making a zoonotic jump even more unlikely since natural jumps leave wide serological footprints in their new host populations as early variants of a prospective virus make limited and unsuccessful jumps into individuals of the new host species, a trial‐and‐error that must occur before mutations that allow adaptation to a new host species are selected.[50] However these results do not rule out a much earlier jump into humans somewhere outside Hubei province, an alternative that is awaiting empirical support.

Taken together, the available evidence does not point definitively toward a natural origin for SARS‐CoV‐2, rather, much of it is more consistent with what would be found if the novel coronavirus had arisen from serial passage of a “precursor” progenitor virus in a lab, or from bats infecting a commercial mink farm somewhere in China, which would also provide the conditions for serial passage. However, more evidence is required before a conclusive judgement can be made one way or the other.

Further research around SARS‐CoV‐2's affinity to ferrets and minks, as well as other possible intermediate hosts seems warranted, and certainly the examination of all past gain‐of‐function serial passage research by the scientific community at large should occur to determine what other definitive genomic signatures serial passage leaves besides the creation of furin cleavage sites, in case more of those can be found in this novel coronavirus. Two additional unique genomic signature are already being researched, as one preprint indicates that SARS‐CoV‐2 possesses a genomic region not found in other coronaviruses that appears to cloak the novel coronavirus from white blood cells, a characteristic also found with HIV.[52] And the second preprint identifies a region on the spike‐protein gene found in no other bat‐borne coronavirus that is nearly identical to superantigenic and neurotoxic motifs found in some bacteria, which may contribute to the immune overreaction that leads to the Kawasaki‐like multisystem inflammatory syndrome in children, and cytokine storms in adults.[53] Given the unique traits found in SARS‐CoV‐2 and all the open questions there still are around its emergence, until either a natural or laboratory origin is conclusively demonstrated both avenues should be robustly investigated by the scientific community.

3 Conclusions and Outlook

The history of gain‐of‐function research is one of science's most significant and troubling, especially since the Nuremberg Code, research scientists’ Hippocratic Oath, dictates that experiments that could endanger human life should only occur if the potential humanitarian benefits significantly outweigh the risks.[54] It seems ill‐advised to rule out the possibility that gain‐of‐function techniques such as serial passage may have played a role in the creation of SARS‐CoV‐2 until more definitive data are collected, and when the Center for Arms Control and Non‐Proliferation has calculated that the odds that any given potential pandemic pathogen might leak from a lab could be better than one in four.[55]

The release of the H1N1 Swine Flu in 1977 first initiated the discussion about the moral and physical hazards involved with dual‐use gain‐of‐function research, and it was the creation of extraordinarily virulent H5N1 Bird Flu strains—using the same technique of serial passage through an animal host in a lab—that contributed to the NIH imposing a moratorium on dual‐use gain‐of‐function research from 2014 until 2017, after which it was relaxed explicitly to allow influenza strains as well as coronaviruses to be studied. This moratorium was meant to limit “the potential to create, transfer, or use an enhanced potential pandemic pathogen.”[56] However, just as an increased pace of research into influenza vaccines increased the odds that a leak would occur leading up to the 1977 release of H1N1 Swine Flu, which is the most often cited as originating from a laboratory leak,[8] it would follow that an increased pace of research into coronaviruses over the past few years would have increased the odds that a lab leak of one would occur; after all, these viruses were pinpointed back in 2006 as a viable vector for an HIV vaccine[57] and research into a pan‐coronavirus vaccine has been ongoing for decades.

And whether or not gain‐of‐function research is determined to have played a role in SARS‐CoV‐2's emergence, the fact that it creates opportunities for pandemic viruses to leak out of labs calls for a re‐examination of the moratorium against this practice, because the emergence of this novel coronavirus has demonstrated that the international public health community is not prepared to handle the leak of a pandemic virus. Furthermore, none of the gain‐of‐function research conducted since 2014 has provided humanity with any tools at all to fight back against the ongoing pandemic caused by this novel coronavirus.


The authors would like to thank Philip Murphy M.D. for encouragement and helpful suggestions.

Conflict of Interest

The authors declare no conflict of interest.

And that shows the real problem, which is also highlighted by the unbelievably sloppy handling of contagions in the USA since many years:

BIOWEAPON SCARE: CDC halts research in Army labs

Alarm rasied over mishandled bioweapons.

Following the concern of live anthrax shipments from the Army lab in Utah, another Pentagon laboratory has been flagged due to suspected improper handling, mislabeling and shipment of other potentially dangerous agents of bioterrorism. Research moratorium has already been ordered on all bioweapon pathogens and viruses. Final results on tests are expected by the end of the month.


By Hannah Marfil - 14. September 2015

MUNTINLUPA, PHILIPPINES (Catholic Online) - USA Today reports The Centers for Disease Control and Prevention (CDC) had concerns on the handling of specimens derived from potentially dangerous bioterror weapons following last month's inspection at the Edgewood Chemical Biological Center in Maryland.

Sloppy safety practices since the anthrax scare last May have been flagged, but bioterror agents are suspected to have been shipped live, which introduces a lot of risks. 

Army spokesman Dov Schwartz said there has been no danger found on those who had handled the vials. The real risk is to scientists who handle specimens that come with inaccurate "death certificates," indicating the pathogen is not infectious when the reality is that they are still alive.

Two of the more serious pathogens to have been mislabeled are the Venezuelan equine encephalitis virus and Eastern equine encephalitis virus, which can cause rare but fatal illnesses that include brain inflammation. 

Concerns also extend to the Yersinia pestis, the plague-causing bacteria which is said to be responsible to the Black Death in 14th Century Europe. Millions of people died due to the illnesses brought about by the pathogen which can be treated by antibiotics today. 

The CDC explained that the plague can still kill about 11 percent of those infected despite modern-day antibiotics. The bacteria was found in the non-infectious store in the lab, but was found to be mislabeled by the CDC upon inspection.

"Anthrax being mishandled is disconcerting enough, but now the mishandling also includes other potentially dangerous viruses including plague. The committee has zero tolerance for these widespread mishaps and will continue working to ensure that the Department corrects these failures so that the nation's bioterrorism response efforts are not hampered further," said chairman of the House Energy and Commerce Committee Fred Upton, R-Mich., and Frank Pallone, R-NJ, through a joint statement released Thursday.

CDC lab regulators refused questions but admitted, "CDC has identified a number of transfers of concern involving multiply organisms."

Army Secretary John McHugh ordered the research moratorium on September 2 following the discovery of anthrax bacteria on the floors of two rooms at the Utah facility.


While in 2015 at least something came to light, the incident in mid 2019 in Ft. Dettrick, Maryland, USA, that led to the temporary closure of the BSL-4 facility, is still shrouded in secrecy.

Laboratory accidents actually happen: In the past few years there have been investigations into systemic problems with laboratories all over the world, including the U.S. and the United Kingdom. In August, the U.S. Army Medical Research Institute of Infectious Diseases was shut down, and it remains so as part of an ongoing review. Laboratory accidents in the United States, including the accidental shipping of H5N1 avian influenza to a U.S. Department of Agriculture lab and the exposure of approximately 75 U.S. Centers for Disease Control and Prevention workers to anthrax, led to a funding pause on certain kinds of “gain of function studies” that result in the creation of new “potential pandemic pathogens” with enhanced virulence and transmissibility.

But is not enough to just temporarily stop funding. Such facilities and the 'gain-of-function'-work must stop forever.


COVID-19 Is 'Unrestricted Bioweapon': Whistleblower Releases Second Paper Alleging 'Large-Scale, Organized Scientific Fraud'

By Tyler Durden - 08.  October 2020

Li-Meng Yan, A Chinese virologist (MD, PhD) who worked in a WHO reference lab and fled her position at the University of Hong Kong, has published a second co-authored report, alleging that SARS-CoV-2, the virus which causes COVID-19, was not only created in a Wuhan lab, it's an "unrestricted bioweapon" which was intentionally released.

"We used biological evidence and in-depth analyses to show that SARS-CoV-2 must be a laboratory product, which was created by using a template virus (ZC45/ZXC21) owned by military research laboratories under the control of the Chinese Communist Party (CCP) government," reads the paper.

SARS-CoV2 is a product of laboratory modification, which can be created in approximately six months using a template virus owned by a laboratory of the People's Liberation Army (PLA). The fact that data fabrications were used to cover up the true origin of SARS-CoV 2 further implicates that the laboratory modification here is beyond simple gain-of-function research.

The scale and the coordinated nature of this scientific fraud signifies the degree of corruption in the fields of academic research and public health. As a result of such corruption, damages have been made both tot he reputation of the scientific community and to the well-being of the global community.

The report also claims that the RaTG13 virus which Wuhan "Batwoman" Dr. Zhengli Shi and colleagues say they obtained in bat feces in 2013 (and which is 96% identical to SARS-CoV-2), is fraudulent and also man made.

Since its publication, the RaTG13 virus has served as the founding evidence for the theory that SARS-CoV-2 must have a natural origin. However, no live virus or an intact genome of RaTG13 have ever been isolated or recovered. Therefore, the only proof for the “existence” of RaTG13 in nature is its genomic sequence published on GenBank.

The report goes on to say that the RaTG13 genome could easily be fabricated, and that "an entry on GenBank, which in this case is equivalent to the existence of an assembled viral genomic sequence and its associated sequencing reads, is not a definitive proof that this viral genome is correct or real," and that the process for sequencing DNA itself "leaves room for potential fraud."

If one intends to fabricate an RNA viral genome on GenBank, he or she could do so by following these steps: create its genomic sequence on a computer, have segments of the genome synthesized based on the sequence, amplify each DNA segment through PCR, and then send the PCR products (may also be mixed with genetic material derived from the alleged host of the virus to mimic an authentic sequencing sample) for sequencing.The resulted raw sequencing reads would be used, together with the created genomic sequence, for establishing an entry on GenBank. Once accomplished, this entry would be accepted as the evidence for the natural existence of the corresponding virus. Clearly, a viral genomic sequence and its GenBank entry can be fabricated if well-planned.


RaTG13 has 'multiple abnormal features,' according to the report. For starters, it's claimed that it was a fecal sample - yet just 1.7% of the raw sequencing reads are bacterial, when fecal swab samples are typically 70-90% bacterial. Second, the genomic sequence for RaTG13 contains segments of non-bat origin, including fox, flying fox, squirrels and other animals.

What's more, China destroyed all evidence of RaTG13. "No independent verification of the RaTG13 sequence seems possible because, according to Dr. Zhengli Shi,the raw sample has been exhausted and no live virus was ever isolated or recovered. Notably, this information was known to a core circle of virologists early on and apparently accepted by them."


Meanwhile, another coronavirus which shares a '100% nucleotide sequence identity with RaTG13' - RaBtCoV/4991 - on a 'short, 440-bp RNA-dependent RNA polymerase gene segment.'

RaBtCoV/4991 was allegedly discovered by Shi and colleagues in 2012 and published in 2016, and colleagues have been asking if it's the same virus as RaTG13.

Given the 100% identity on this short gene segment between RaBtCoV/4991 and RaTG13,the field has demanded clarification of whether or not these two names refer to the same virus. However,Dr. Shi did not respond to the requestor address this question for months. The answer finally came from Peter Daszak, president of EcoHealth Alliance and long-term collaborator of Shi, who claimed that RaBtCoV/4991 was RaTG1327.

Three suspicious facts

First, it makes no sense that 'Batwoman' Shi and her team wouldn't have conducted whole genome sequencing of RaBtCoV/4991 before 2020, as it was suspected in the deaths of miners who suffered from severe pneumonia after clearing out bat droppings in a Chinese mineshaft.

Given the Shi group’s consistent interests in studying SARS-like bat coronaviruses and the fact that RaBtCoV/4991 is a SARS-like coronavirus with a possible connection to the deaths of the miners, it is highly unlikely that the Shi group would be content with sequencing only a 440-bp segment of RdRpand not pursue the sequencing of the receptor-binding motif (RBM)-encoding region of the spike gene. In fact, sequencing of the spike gene is routinely attempted by the Shi group once the presence of a SARS-like bat coronavirus is confirmed by the sequencing of the 440-bp RdRpsegment25,32, although the success of such efforts is often hindered by the poor quality of the sample.

"Clearly, the perceivable motivation of the Shi group to study this RaBtCoV/4991 virus and the fact that no genome sequencing of it was done for a period of seven years (2013-2020) are hard to reconcile and explain."

Meanwhile, genomic sequencing of RaTG13 was conducted in 2018.

Second, why did Shi delay publication on RaTG13 until 2020 when it's got a Spike protein that can bind with human ACE2 receptors?

...if the genomic sequence of RaTG13 had been available since 2018, it is unlikely that this virus, which has a possible connection to miners’ deaths in 2012 and has an alarming SARS-like RBM, would be shelfed for two years without publication. Consistent with this analysis, a recent study indeed proved that the RBD of RaTG13(produced via gene synthesis based on its published sequence) was capable of binding hACE2

Third, there has been no follow-up work on RaTG13 by Shi's group.

Upon obtaining the genomic sequence of a SARS-like bat coronavirus, the Shi group routinely investigate whether or not the virus is capable of infecting human cells. This pattern of research activities has been shown repeatedly. However, such a pattern is not seen here despite that RaTG13 has an interesting RBM and is allegedly the closest match evolutionarily to SARS-CoV-2

Direct genetic evidence proving RaTG13 is fraudulent

Yan's group closely examined the sequences of specific spike proteins for relevant viruses - specifically comparing mutations, and found that the spike genes of SARS-CoV-2 and RaTG13 do not contain evidence of natural evolution when compared to other coronaviruses which naturally evolved.

A logical interpretation of this observation is that SARS-CoV-2 and RaTG13 could not relate to each other through natural evolution and at least one must be artificial.If one is a product of natural evolution, then the other one must be not. It is also possible that neither of them exists naturally. If RaTG13 is a real virus that truly exists in nature, then SARS-CoV-2 must be artificial.


It is highly likely that the sequence of the RaTG13 genome was fabricated by lightly modifying the SARS-CoV-2 sequence to achieve an overall 96.2% sequence identity. During this process, much editing must have been done for the RBM region of the S1/spike because the encoded RBM determines the interaction with ACE2 and therefore would be heavily scrutinized by others.

The paper concludes: All fabricated coronaviruses share a 100% amino acid sequence identity on the E protein with ZC45 and ZXC21

Evidence herein clearly indicates that the novel coronaviruses recently published by the CCP-controlled laboratories are all fraudulent and do not exist in nature. One final proof of this conclusion is the fact that all of these viruses share a 100% amino acid sequence identity on the E protein with bat coronaviruses ZC45 and ZXC21, which, as revealed in our earlier report1, should be the template/backbone used for the creation of SARS-CoV-2. Despite its conserved function in the viral replication cycle, the E protein is tolerant and permissive of amino acid mutations. It is therefore impossible for the amino acid sequence of the E protein to remain unchanged when the virus has allegedly crossed species barrier multiple times (between different bat species, from bats to pangolins, and from pangolins to humans). The 100% identity observed here, therefore, further proves that the sequences of these recently published novel coronaviruses have been fabricated.

Unrestricted bioweapon?

Yan notes that while it's not easy for the public to accept that SARS-CoV-2 is a bioweapon due to its relatively low lethality, it indeed meets the criteria of a bioweapon.

In 2005, Dr. Yang specified the criteria for a pathogen to qualify as a bioweapon:

  1. It is significantly virulent and can cause large scale casualty.
  2. It is highly contagious and transmits easily, often through respiratory routes in the form of aerosols. The most dangerous scenario would be that it allows human-to-human transmission.
  3. It is relatively resistant to environmental changes, can sustain transportation, and is capable of supporting targeted release.

All of the above have been met bySARS-CoV-2: it has taken hundreds of thousands lives, led to numerous hospitalizations, and left many with sequela and various complications; it spreads easily by contact, droplets, and aerosols via respiratory routes and is capable of transmitting from human to human, the latter of which was initially covered up by the CCP government and the WHO and was first revealed by Dr. Li-Meng Yan on January 19th, 2020 on Lude Press; it is temperature-insensitive (unlike seasonal flu) and remains viable for a long period of time on many surfaces and at 4°C (e.g. the ice/water mixture).

What's more, COVID-19 spreads asymptomatically, which "renders the control of SARS-CoV-2 extremely challenging."

"In addition, the transmissibility, morbidity, and mortality of SARS-CoV-2 also resulted in panic in the global community, disruption of social orders, and decimation of the world’s economy. The range and destructive power of SARS-CoV-2 are both unprecedented."

"Clearly,SARS-CoV-2 not only meets but also surpasses the standards of a traditional bioweapon. Therefore, it should be defined as an Unrestricted Bioweapon."


Tyler Durden


Bats are not to blame for coronavirus. Humans are

By Nick Paton Walsh and Vasco Cotovio - 20. March 2020

(CNN) Reclusive, nocturnal, numerous -- bats are a possible source of the coronavirus. Yet some scientists concur they are not to blame for the transfer of the disease that's changing daily life -- humans are.

Zoologists and disease experts have told CNN that changes to human behavior -- the destruction of natural habitats, coupled with the huge number of fast-moving people now on Earth -- has enabled diseases that were once locked away in nature to cross into people fast.

Scientists are still unsure where the virus originated, and will only be able to prove its source if they isolate a live virus in a suspected species -- a hard task.

But viruses that are extremely similar to the one that causes Covid-19 have been seen in Chinese horseshoe bats. That has led to urgent questions as to how the disease moved from bat communities -- often untouched by humans -- to spread across Earth. The answers suggest the need for a complete rethink of how we treat the planet.

Bats are a possible source of the coronavirus, but some scientists say humans are to blame for the spread of the disease.

Bats are a possible source of the coronavirus, but some scientists say humans are to blame for the spread of the disease.

Bats are the only mammal that can fly, allowing them to spread in large numbers from one community over a wide area, scientists say. This means they can harbor a large number of pathogens, or diseases. Flying also requires a tremendous amount of activity for bats, which has caused their immune systems to become very specialized.

"When they fly they have a peak body temperature that mimics a fever," said Andrew Cunningham, Professor of Wildlife Epidemiology at the Zoological Society of London. "It happens at least twice a day with bats -- when they fly out to feed and then they return to roost. And so the pathogens that have evolved in bats have evolved to withstand these peaks of body temperature."

Cunningham said this poses a potential problem when these diseases cross into another species. In humans, for example, a fever is a defense mechanism designed to raise the body temperature to kill a virus. A virus that has evolved in a bat will probably not be affected by a higher body temperature, he warned.

But why does the disease transfer in the first place? That answer seems simpler, says Cunningham, and it involves an alien phrase that we will have to get used to, as it is one that has changed our lives -- "zoonotic spillover" or transfer.

"The underlying causes of zoonotic spillover from bats or from other wild species have almost always -- always -- been shown to be human behavior," said Cunningham. "Human activities are causing this."

When a bat is stressed -- by being hunted, or having its habitat damaged by deforestation -- its immune system is challenged and finds it harder to cope with pathogens it otherwise took in its stride. "We believe that the impact of stress on bats would be very much as it would be on people," said Cunningham.

"It would allow infections to increase and to be excreted -- to be shed. You can think of it like if people are stressed and have the cold sore virus, they will get a cold sore. That is the virus being 'expressed.' This can happen in bats too."

Pathogens that have evolved in bats can withstand a high body temperature, so a human fever will not work as a defense mechanism.

Pathogens that have evolved in bats can withstand a high body temperature, so a human fever will not work as a defense mechanism.

In the likely epicenter of the virus -- the so-called wet-markets of Wuhan, China -- where wild animals are held captive together and sold as delicacies or pets, a terrifying mix of viruses and species can occur.

"If they are being shipped or held in markets, in close proximity to other animals or humans," said Cunningham, "then there is a chance those viruses are being shed in large numbers." He said the other animals in a market like that are also more vulnerable to infection as they too are stressed.

"We are increasing transport of animals -- for medicine, for pets, for food -- at a scale that we have never done before," said Kate Jones, Chair of Ecology and Biodiversity at University College London.

"We are also destroying their habitats into landscapes that are more human-dominated. Animals are mixing in weird ways that have never happened before. So in a wet market, you are going to have a load of animals in cages on top of each other."

Kate Jones, Chair of Ecology and Biodiversity at University College London, said increasing transport of animals and habitat destruction meant animals were mixing in ways they never had before.

Kate Jones, Chair of Ecology and Biodiversity at University College London, said increasing transport of animals and habitat destruction meant animals were mixing in ways they never had before.

Cunningham and Jones both pointed to one factor that means rare instances of zoonotic spillover can turn into global problems in weeks. "Spillovers from wild animals will have occurred historically, but the person who would have been infected would probably have died or recovered before coming into contact with a large number of other people in a town or in a city," said Cunningham.

"These days with motorized transport and planes you can be in a forest in central Africa one day, and in a city like central London the next."

Jones agreed. "Any spillover you might have had before is magnified by the fact there is so many of us, and we are so well connected."

There are two simple lessons, they say, that humanity can learn, and must learn fast.

First, bats are not to blame, and might actually help provide the solution. "It's easy to point the finger at the host species," said Cunningham.

"But actually it's the way we interact with them that has led to the pandemic spread of the pathogen." He added that their immune systems are poorly understood and may provide important clues. "Understanding how bats cope with these pathogens can teach us how to deal with them, if they spillover to people."

The cause of "zoonotic spillover,"  or transfer from bats or other wild species, is almost always human behavior, says Professor Andrew Cunningham from the Zoological Society of London.

The cause of "zoonotic spillover," or transfer from bats or other wild species, is almost always human behavior, says Professor Andrew Cunningham from the Zoological Society of London.

Ultimately diseases like coronavirus could be here to stay, as humanity grows and spreads into places where it's previously had no business. Cunningham and Jones agree this will make changing human behavior an easier fix than developing a vastly expensive vaccine for each new virus.

The coronavirus is perhaps humanity's first clear, indisputable sign that environmental damage can kill humans fast too. And it can also happen again, for the same reasons.

"There are tens of thousands [of viruses] waiting to be discovered," Cunningham said. "What we really need to do is understand where the critical control points are for zoonotic spillover from wildlife are, and to stop it happening at those places. That will be the most cost-effective way to protect humans."

Jones said viruses "are on the rise more because there are so many of us and we are so connected. The chance of more [spillovers into humans] happening is higher because we are degrading these landscapes. Destroying habitats is the cause, so restoring habitats is a solution."

The ultimate lesson is that damage to the planet can also damage people more quickly and severely than the generational, gradual shifts of climate change.

"It's not OK to transform a forest into agriculture without understanding the impact that has on climate, carbon storage, disease emergence and flood risk," said Jones. "You can't do those things in isolation without thinking about what that does to humans."


Nick Paton Walsh 2018

Nick Paton Walsh 

\Vasco Cotovio