More and more people are starting to take an interest in issues that have already been raised by 'wappies'. The 'With today's knowledge' argument is also increasingly being used, 'they couldn't have known that then'. There is also the Lab Leak theory, for which FOI (or FOIA) documents have now provided additional evidence. In the heated discussion of the last few weeks, I sometimes feel like in a time vortex: there is excitement about things that we really (could) have known for a long time. I therefore reread this translation of the book published in May 2021 article by Nicholas Wade, whether I remembered that correctly. It's a lot of text, but if you've read this, you'll be wondering, just like me: why all the additional evidence, that consternation, that consternation...? Is the time finally ripe for it? I myself have fragments that I find significant Bolded.

The Origins of COVID: Have Humans or Nature Opened Pandora's Box in Wuhan?

ThroughNicholas Wade| 5 May 2021

Introduction

The COVID-19 pandemic has disrupted lives around the world for more than a year. The death toll will soon reach three million people.[Note: this article is dated May 5, 2021!] Yet the origins of the pandemic remain uncertain: the political agendas of governments and scientists have erected smokescreens that the mainstream press helplessly wants to stay far away from.

In what follows, I will examine the available scientific facts, which contain many clues as to what happened, and provide readers with the evidence to make their own judgments. I will then try to assess the complex issue of guilt, which begins with, but extends far beyond the government of China.

By the end of this article, you may have learned a lot about the molecular biology of viruses. I will try to keep this process as painless as possible. But science cannot be avoided, because for the time being, and probably for a long time, it provides the only sure thread through the maze.

The virus that caused the pandemic is officially known as SARS-CoV-2, but it can be referred to as SARS2 for short. As many people know, there are two main theories about its origins. One is that it naturally jumped from wildlife to humans. The other is that the virus was studied in a laboratory, from which it escaped. That makes a lot of difference when it comes to preventing a second such incident.

I will describe the two theories, explain why each is plausible, and then ask which one gives the better explanation of the available facts. It is important to note that so far there have beenthere is no direct evidencefor both theories. Each depends on a range of reasonable suspicions, but so far there is a lack of evidence. So I only have clues, not conclusions, to offer. But those clues point in a certain direction. And after distracting that direction, I'm going to delineate some of the wires in this tangled strand of disaster.

A story of two theories.After the pandemic first broke out in December 2019, the Chinese authorities reported that many cases had occurred on the 'Wet Market' – a place where wild animals are sold for meat – in Wuhan. This reminded experts of the SARS1 epidemic of 2002, in which a bat virus had first spread to civets, an animal sold in those markets, and from civets to humans. A similar bat virus caused a second epidemic in 2012, known as MERS. This time, camels were the intermediate host.

The decoding of the genome of the SARS-2 virus showed that it belonged to a viral family known as beta-coronaviruses, which also includes the SARS1 and MERS viruses. That relationship supported the idea that it was also a natural virus that had managed to jump from bats, via another animal host, to humans. The connection to the Wet Market, the main point of similarity with the SARS1 and MERS epidemics, was quickly broken: Chinese researchers found previous cases in Wuhan where the link with the Wet Market Lacked.But that didn't seem to matter; More evidence in support of natural emergence was expected in the near term.

However, Wuhan is home to the Wuhan Institute of Virology, a leading world center for coronavirus research. Thus, the possibility that the SARS2 virus had escaped from the laboratory could not be ruled out. There were therefore two plausible scenarios of origin on the table.

From the beginning, the perceptions of the public and the media were shaped in favor of the natural emergence scenario by strong statements made by two scientific groups. Initially, these statements were not viewed as critically as they should have been.

"We are speaking out collectively to strongly condemn conspiracy theories suggesting that COVID-19 has no natural origin," a group of virologists and others wrote in theLanceton February 19, 2020, when it was really way too early for anyone to be sure what happened. Scientists "overwhelmingly conclude that this coronavirus originates in wildlife," they said, with a rousing call for readers to join Chinese colleagues on the front lines of fighting the disease.

Contrary to what the letter writers claimed, the idea that the virus may have escaped from a lab was an accident, not a conspiracy. It certainly had to be examined, not dismissed out of hand. A characteristic trait of good scientists is that they go to great lengths to distinguish between what they know and what they don't know. According to this criterion, the signatories of the Lancet letter behaved like bad scientists: they assured the public of facts they were not sure were true.

For virologists like Daszak, the stakes were high in assigning blame for the pandemic. For twenty years, they played a dangerous game, usually out of public view.In their laboratories, they routinely created viruses that were more dangerous than those found in nature.They argued that they could do this safely and that by getting ahead of nature, they could predict natural spillovers and thus prevent the transmission of viruses from an animal host to humans. If SARS2 had indeed escaped such a laboratory experiment, a huge backlash could be expected, and the storm of public outrage would hit virologists worldwide, not just in China. "It would shatter the scientific edifice from top to bottom,"SaidAntonio Regalado, editor ofMIT Technology Review, in March 2020.

A second statement that had a huge impact on public opinion was aletter(so an opinion piece, not a scientific article) published in the journal on 17 March 2020Nature Medicine was published. The authors were a group of virologists led by Kristian G. Andersen of the Scripps Research Institute."Our analyses clearly show that SARS-CoV-2 is not a laboratory construct or a purposefully engineered virus," the five virologists stated in the second paragraph of their letter.

Unfortunately, this was another case of bad science, in the sense defined above. It's true that some older methods of cutting and pasting viral genomes retain clear signs of manipulation. But newer methods, called "no-see-um" or "seamless" approaches, don't leave any distinctive traces. Nor other methods of manipulating viruses, such as serial passage, the repeated transmission of viruses from one cell culture to another. If a virus has been manipulated, either by a seamless method or by serial passage, there is no way of knowing that this is the case. Andersen and his colleagues assured their readers of something they couldn't know.

The discussion portion of their letter begins: "Sars-CoV-2 is unlikely to have been created by laboratory manipulation of a related SARS-CoV-like coronavirus." But wait, the leadership didn't say the virusclearwas not manipulated? The authors' degree of certainty seemed to slip a few notches when it came to expounding their reasoning.

The reason for the slip is clear once the technical language has penetrated. The two reasons the authors give for assuming that manipulation is unlikely are by no means convincing.

[Note vv: Later, their mutual Slack communication revealed that they thought very differently about it than what they wrote publicly.]

First, they say that sars2's spike protein binds very well to its target, the human ACE2 receptor, but does so in a different way than would fit best according to physical calculations. Therefore, the virus must have been created by natural selection, not by manipulation.

If this argument seems difficult to understand, it's because it's so far-fetched. The authors' basic assumption, which has not been further explained, is that anyone trying to get a bat virus to bind to human cells can only do so in one way. First, they would calculate the strongest possible fit between the human ACE2 receptor and the spike protein with which the virus attaches to it. They would then design the spike protein accordingly (by selecting the appropriate set of amino acid units that make it up). Since the SARS2 spike protein is not of this calculated best design, the Andersen paper says, it could therefore not have been manipulated.

But this ignores the way virologists actually get spike proteins to bind to chosen targets, which is not by computation, but by spike protein genes from other viruses or by splicing serial passage. With serial passage, every time the offspring of the virus is transferred to new cell cultures or animals, the more successful ones are selected until one emerges that makes a really close bond with human cells. Natural selection has done all the heavy lifting. The Andersen paper's speculation about designing a viral spike protein through computation has no bearing on whether or not the virus is manipulated by either of the other two methods.

The authors' second argument against manipulation is even more artful. While most living things use DNA as their hereditary material, a number of viruses use RNA, the close chemical cousin of DNA. But RNA is difficult to manipulate, so researchers working on coronaviruses, which are based on RNA, will first convert the RNA genome into DNA. They manipulate the DNA version, either by adding or changing genes, and then cause the engineered DNA genome to be converted back into infectious RNA.

Only a certain number of these DNA backbones have been described in the scientific literature. Anyone manipulating the SARS2 virus would "probably" have used one of these known backbones, the Andersen group writes, and since SARS2 is not derived from any of them, it is therefore not manipulated. But the argument is strikingly inconsistent. DNA backbones are fairly easy to create, so it's just possible that SARS2 was engineered with an unpublished DNA backbone.

And that's it. These are the two arguments made by the Andersen group in support of their statement that the SARS2 virus has clearly not been manipulated. And this conclusion, based on nothing but two inconclusive speculations, convinced the world press that SARS2 could not have escaped from a laboratory. A technical critique of Andersen's letter catches upharsher words.

Science is supposedly a self-correcting community of experts who constantly check each other's work. So why didn't other virologists point out that the Andersen group's argument was full of absurdly large holes?Perhaps because in today's universities, speech can be very costly. Careers can be destroyed if they step out of line. Any virologist who questions the community's position runs the risk of having their next grant application rejected by the panel of fellow virologists advising the government grant distribution agency.

[Note vv: it is questionable whether virologists do not accept GoF research and undersecurity as well-kept guild secrecy to secure research. In addition, there are also bio-military interests at play that are not discussed in this entire piece.]

Daszak and Andersen's letters were in fact political, not scientific, statements, but still amazingly effective. Articles in the mainstream press repeatedly stated that a consensus of experts had ruled that escape from the laboratory was out of the question or extremely unlikely. Their authors largely relied on the letters of Daszak and Andersen and did not understand the gaping gaps in their arguments. The mainstream newspapers all employ science journalists, as do the major networks, and these specialized reporters should be able to question scientists and check their claims. But Daszak and Andersen's claims went largely unchallenged.

Doubts about natural origin

Natural origin, zoonosis, was the media's preferred theory until around February 2021 and the visit of a World Health Organization (WHO) committee to China. The composition and access of the committee were strictly controlled by the Chinese authorities. Its members, including the ubiquitous Daszak, continued to argue that escape from the lab was extremely unlikely; before, during and after their visit. But this was not quite the propaganda victory that the Chinese authorities had hoped for. What became clear was that the Chinese had no evidence that the committee would provide support for the zoonosis theory.

The lack of evidence was surprising because both the SARS1 and MERS viruses had left abundant traces in the environment. The intermediate host species SARS1 waswithin four monthsafter the outbreak of the epidemic and the host of MERS within nine months. But some 15 months after the SARS2 pandemic began, and after a presumably intensive search, Chinese researchers had not found the original bat population, or the intermediate species to which SARS2 would have jumped, or any serological evidence that any Chinese population, including that of Wuhan, had ever been exposed to the virus before December 2019. The natural genesis remained a conjecture that, however plausible, had not amassed a shred of supporting evidence in more than a year.

And as long as that remains the case, it makes sense to pay serious attention to the alternative suspicion, that SARS2 escaped from a laboratory.

Why would anyone want to create a new virus that can cause a pandemic? Ever since virologists have been given the tools to manipulate a virus's genes, they have claimed that they can get ahead of a potential pandemic by examining how close a particular animal virus might be to making the jump to humans. And that justified laboratory experiments to increase the ability of dangerous animal viruses to infect humans, virologists claimed.

With this rationale, they recreated the 1918 influenza virus, showed how to synthesize the nearly extinct polio virus from the published DNA sequence, and introduced a smallpox gene into a related virus.

These enhancements of viral capabilities are known as "gain-of-function" experiments. In the case of coronaviruses, there was particular interest in the spike proteins, which protrude around the spherical surface of the virus and virtually determine which species it will target. In 2000, Dutch researchers earned the gratitude of rodents for using the spike protein of a mouse coronavirusmanipulated in such a waythat it would only attack cats.

Virologists began seriously studying bat coronaviruses after they were found to be the source of both the SARS1 and MERS epidemics. In particular, researchers wanted to understand what changes needed to take place in a bat virus's spike proteins before it could infect humans.

Researchers from the Wuhan Institute of Virology, led by China's leading expert on bat viruses, Shi Zheng-li or "Bat Lady," undertook frequent expeditions to the bat-populated caves of Yunnan in southern China and collected about a hundred different bat coronaviruses.

Shi then collaborated with Ralph S. Baric, a leading coronavirus researcher at the University of North Carolina.Their workfocused on increasing the ability of bat viruses to attack humans to "investigate the emergence potential (i.e., the potential to infect humans) of circulating bat CoVs [coronaviruses]". To achieve this goal, they created a new virus in November 2015 by taking the backbone of the SARS1 virus and replacing the spike protein with one from a bat virus (known as SHC014-CoV). This manufactured virus was able to infect the cells of the human respiratory tract, at least when tested against a laboratory culture of such cells.

"If the virus escaped, no one would be able to predict its trajectory,"

SaysSimon Wain-Hobson, a virologist at the Pasteur Institute in Paris.

The SHC014-CoV/SARS1 virus is known as a chimera because its genome contains genetic material from two virus strains. If the SARS2 virus had been created in Shi's lab, then the direct prototype would have been the SHC014-CoV/SARS1 chimaera, the potential danger of which worried many observers and sparked heated debate.

Baric and Shi refer to the clear risks in their article, but argue that these must be weighed against The Advantage of Predicting Future (Zoonosis) Infections. Scientific review committees, they wrote, "may find similar studies of building chimeric viruses from circulating strains too risky to continue." Given the various limitations imposed on GOF (gain-of-function) research, they believe that "concerns about GOF research have reached a crossroads; The potential to prepare for and mitigate future outbreaks must be weighed against the risk of creating more dangerous pathogens. When developing policies for the future, it is important to weigh the value of the data generated by these studies and consider whether these types of studies on chimeric viruses warrant further research versus their inherent risks."

That ruling was made in 2015. In hindsight, in 2021, one can say that the value of gain-of-function studies in preventing the SARS2 epidemic was zero.In fact, the risk was catastrophic, if the SARS2 virus was indeed generated in a gain-of-function experiment.

Inside the Wuhan Institute of Virology

Baric had developed a general method—and explained it to Shi—to develop bat coronaviruses in such a way that they could attack other species. The specific targets were human culture cells and humanized mice. These lab mice, a low-cost and ethically sourced replacement for human subjects, have been genetically engineered to carry the human version of the protein ACE2, which lines the surface of cells lining the airways.

Because, due to a strange twist in the story, her work was funded by the National Institute of Allergy and Infectious Diseases (NIAID), a division of the U.S. National Institutes of Health (NIH). And grant proposals Specify exactly What she was up to to do with the money.

The grants were awarded to the main contractor, Badger bag from the EcoHealth Alliance, which outsourced them to Shi. Below are excerpts from the grants for the financial years 2018 and 2019. ("CoV" stands for coronavirus, and "S protein" refers to the spike protein of the virus.)

"Predictions of CoV transmission between species. Predictive models of host range (i.e., emergence potential) will be experimentally tested using reverse genetics, pseudovirus and receptor binding tests, and virus infection experiments in a range of cell cultures from different species and humanized mice."

"We will use S-protein sequence data,Infectious Cloning Technology, use in vitro and in vivo infection experiments and receptor binding analysis to test the hypothesis that % divergence thresholds in S-protein sequences predict spillover potential."

What this means, in non-technical language, is that Shi was out to create new coronaviruses with the highest possible infectivity to human cells. Her plan was to take genes that coded for spike proteins with a variety of measured affinities for human cells, ranging from high to low. She would insert these spike genes one at a time into the backbone of a number of viral genomes ("reverse genetics" and "infectious cloning technology"), creating a series of chimeric viruses. These chimeric viruses would then be tested for their ability to attack human cell cultures ("in vitro") and humanized mice ("in vivo"). And this information would help predict the likelihood of "spillover," the jump of a coronavirus from bats to humans.

The Methodical Approach is designed to find the best combination of coronavirus backbone and spike protein for infecting human cells. The approach could have generated SARS2-like viruses, and could indeed have created the SARS2 virus itself with the right combination of virus backbone and spike protein.

It can't yet be said whether or not Shi generated SARS2 in her lab because her data is sealed, but it seems that she was at least on the right track. "It is clear that the Wuhan Institute of Virology systematically engineered novel chimeric coronaviruses and assessed their ability to infect human cells and mice with human ACE2 expression," said Richard H. Ebright, a molecular biologist at Rutgers University and leading expert on biosafety.

"It is also clear," Ebright said, "that, depending on the constant genomic contexts chosen for analysis, this work could have produced SARS-CoV-2 or a proximal precursor to SARS-CoV-2." "Genomic context" refers to the specific viral backbone used as a testbed for the spike protein.

The lab-escape scenario for the origin of the SARS2 virus, as should be clear by now, is not just guesswork in the direction of the Wuhan Institute of Virology. It is an elaborate hypothesis, based on the specific project funded by NIAID there.

Even if the grant required the work plan described above, how can we be sure that the plan has actually been implemented? For that, we can rely on the word of Daszak, who from the beginning of 2020 already vehemently protested against the ridiculousconspiracy theoryof an escape from the lab, invented by China-bashers.

On 9 December 2019, before the outbreak of the pandemic became public knowledge, Tie bag ainterviewin which he recounted in radiant terms how researchers at the Wuhan Institute of Virology had reprogrammed the spike protein and generated chimeric coronaviruses capable of infecting humanized mice.

"And we now have, you know, after 6 or 7 years of doing this, over 100 new SARS-related coronaviruses, very close to SARS," Daszak says around minute 28 of the interview. "Some end up in human cells in the lab, others can cause SARS disease in humanized mouse models and are untreatable with therapeutic monoclonal agents and You can't vaccinate against it with a vaccine. So this is a clear and present danger....

"Interviewer: You're saying that these are different coronaviruses and you can't vaccinate against them, and not antivirals – so what do we do?

"Badgerbag: Well, I think... Coronaviruses – you can manipulate them quite easily in the lab. The spike protein determines much of what happens with coronaviruses, in zoonotic risk. So you can get the sequence, you can build the protein, and we're working a lot with Ralph Baric from UNC to do this. We insert it into the backbone of another virus and do some work in the lab. So you can predict more when you find a sequence. You have this diversity. The logical development for vaccines now is that if you're going to develop a vaccine for SARS, people are going to use pandemic SARS [?], but let's add some of these other things to get a better vaccine." The insertions he was referring to may contain an element called the furin cleavage site, discussed below, which significantly increases viral infectivity to human cells.

In incoherent style, Daszak refers to the fact that once you've generated a new coronavirus that can attack human cells, you can take the spike protein as the basis for a vaccine.

You can imagine Daszak's reaction when he heard about the outbreak of the epidemic in Wuhan a few days later. He would know better than anyone the Wuhan Institute's goal of making bat coronaviruses contagious to humans, as well as the weaknesses in the institute's defenses against the contamination of their own researchers.

But instead of providing public health authorities with the abundant information he had, he immediately launched a public relations campaign to convince the world that the epidemic could not possibly have been caused by one of the institute's souped-up viruses. "The idea that this virus escaped from a lab is pure nonsense. It's just not true," he stated in ainterviewin April 2020.

The safety features at the Wuhan Institute of Virology

Daszak may have been unaware of, or perhaps he knew all too well, the Long history of viruses that escaped from even the best-run laboratories. The smallpox virus escaped from laboratories in England three times in the 1960s and 1970s, resulting in 80 cases and 3 deaths. Since then, dangerous viruses have escaped from laboratories almost every year. In more recent times, the SARS1 virus has proven to be a true escape artist. SARS1 has escaped from laboratories in Singapore, Taiwan and no less than four times from the Chinese National Institute of Virology in Beijing.

One of the reasons SARS1 was so difficult to handle was that there were no vaccines available to protect lab workers. As Daszak noted in the Dec. 19 interview quoted above, the Wuhan researchers too had not been able to develop vaccines against the coronaviruses they had designed to infect human cells.Without a vaccine, the researchers would have been as defenseless against a self-generated SARS2 virus as their colleagues in Beijing were against SARS1.

A second reason for the serious danger of novel coronaviruses has to do with the required levels of laboratory safety. There are four safety grades, referred to as BSL1 to BSL4, with BSL4 being the most restrictive and designed for deadly pathogens such as the Ebola virus.

The Wuhan Institute of Virology had a new BSL4 laboratory, but its state of readiness was of great concern to the State Department inspectors who visited it from the Beijing embassy in 2018. "The new lab has a severe shortage of well-trained technicians and researchers needed to keep this high-containment lab operating safely," the inspectors wrote in atelegramof 19 January 2018.

The real problem, however, was not the unsafe state of the Wuhan BSL4 lab, but the fact that virologists worldwide do not like to work in BSL4 conditions. You have to wear a spacesuit, perform surgeries in locked closets, and accept that everything will take twice as long. So the rules that assigned each kind of virus to a certain level of safety were more lax than some might have thought sensible.

Prior to 2020, it was mandatory under the rules of virologists in China and elsewhere to conduct experiments with the SARS1 and MERS virus under BSL3circumstances. But all other bat coronaviruses could be studied in BSL2, the next level down. BSL2 requires taking free Minimum security measures, such as wearing lab coats and gloves, not vacuuming liquids into a pipette, and putting up biohazard warning signs. Still, a gain-of-function experiment conducted in BSL2 could produce an agent more infectious than SARS1 or MERS. And if so, lab workers have a high chance of infection, especially if they are unvaccinated.

A lot of Shi's work on gain-of-function in coronaviruses was carried out at the BSL2 safety level, as stated in its publications and other documents. She has in ainterviewwith the magazineSciencesaid that "the coronavirus research in our laboratory is carried out in BSL-2 or BSL-3 laboratories.“

"It is clear that some or all of this work was carried out using a biosafety standard – biosafety level BSL-2, the biosafety level of a standard U.S. dental office – which would pose an unacceptably high risk of infection to laboratory personnel upon contact with a virus with the transmission properties of SARS-CoV-2," says Ebright.

"It is also clear," he adds, "that this work should never have been funded and should never have been carried out." This is his opinion, regardless of whether the SARS2 virus has ever seen the inside of a laboratory.

Concerns about safety conditions at the Wuhan lab were not misplaced. According to aFactsheetissued by the State Department on January 15, 2021: "The U.S. government has reason to believe that several researchers within the WIV became ill with symptoms consistent with both COVID-19 and common seasonal illnesses in the fall of 2019, before the first identified case of the outbreak."

David Asher, a fellow of the Hudson Institute and former State Department adviser, gave more details about the incident during aseminar. Knowledge of the incident came from a mix of public information and "some high-quality information gathered by our intelligence community," he said. Three people working in a BSL3 lab at the institute became ill within a week of each other with severe symptoms requiring hospitalization. This was "the first known cluster that we are aware of, of victims of what we believe is COVID-19." Influenza could not be completely ruled out, but seemed unlikely in the circumstances, he said.

Comparison of the rival scenarios of SARS2 origin

The evidence above is a serious indication that the SARS2 virus could have been created in a laboratory, from which it then escaped. But the evidence, however substantial, is not enough. Evidence would consist of evidence from the Wuhan Institute of Virology, or related labs in Wuhan, that SARS2 or a precursor to the virus was in development there. In the absence of access to such data, a different approach is needed. To do so, we take some salient facts about the SARS2 virus and see how well they can be explained by the two rival scenarios of origin, that of natural origin and escape from the lab. Here are four tests of those two hypotheses. A few have some technicalities, but these are among the most persuasive for those who want to follow the argumentation.

1) The place of origin.Start with geography. The two closest relatives of the SARS2 virus were collected from bats living in caves in Yunnan, a province in southern China.If the SARS2 virus had first infected people living around the Yunnan Caves, that would strongly support the idea that the virus had naturally passed to humans. But this is not what happened. The pandemic broke out 1500 kilometers away, in Wuhan.

Beta coronaviruses, the family of bat viruses to which SARS2 belongs, infect the horseshoe-nosed batRhinolophus affinis, which is found in southern China. The range of the bats is 50 kilometers, so it is unlikely that they reached Wuhan. In any case, the first cases of the COVID-19 pandemic probably occurred in September, when thetemperatures in Hubei Provincewere already cold enough to send bats into hibernation.

What if the bat viruses first infected an intermediate host?You would need a long-term population of bats that is regularly in the vicinity of an intermediate host, which in turn often has to cross paths with humans. All these virus exchanges must take place somewhere outside Wuhan, a busy metropolis that is not known to be a natural habitat of colonies ofRhinolophus-Bats.The infected person (or animal) carrying this highly transmissible virus must have traveled to Wuhan without infecting anyone else. No one in his or her family got sick. If the person went to Wuhan by train, not one fellow passenger got sick.

In other words, it is a daunting task to allow the pandemic to break out naturally outside of Wuhan and then, without leaving any trace, make its first appearance there.

For a lab escape scenario, Wuhan is the first, obvious candidate. Wuhan is home to China's leading center for coronavirus research, where, as mentioned above, researchers genetically engineered bat coronaviruses to attack human cells. They did this under the minimum safety conditions of a BSL2 lab. If a virus with the unexpected infectiousness of SARS2 had emerged there, it would not be a surprise that it would escape.

2)Natural History and Evolution.The original location of the pandemic is a small part of a larger problem, that of natural history. Viruses don't just jump from one species to another. The coronavirus spike protein, modified to attack bat cells, needs repeated jumps to another species, most of which fail, before it gets a happy mutation. Mutation – a change in one of its RNA units – causes another amino acid unit to be incorporated into its spike protein and makes the spike protein better able to attack the cells of another species.

Through even more such mutation-driven adaptations, the virus adapts to its new host, for example an animal with which bats often come into contact. The whole process is then resumed as the virus moves from this intermediate host to humans.

In the case of SARS1, researchers have documented the sequential changes in the spike protein as the virus evolved step by step into a dangerous pathogen. After it changed from bats to civets, there were six more changes to the spike protein before it became a mild pathogen in humans. After a further 14 changes, the virus was much better adapted to humans, and with a further four, the virusEpidemic a flight.

But if you start looking for the fingerprints of a similar transition in SARS2, you're in for a strange surprise.The virus has hardly changed until recently.From the very beginning, it was well adapted to human cells. Researchers led by Alina Chan of the Broad Institute compared SARS2 to late-stage SARS1, which by then was well adapted to human cells, and found that the two viruses were equally well adapted."By the time SARS-CoV-2 was first detected in late 2019, it had already been pre-adapted to human transmission to a degree similar to the late epidemic SARS-CoV",Wrotethey.

Even those who think its origin in the lab is unlikely agree that SARS2 genomes are remarkably uniform. Baric writes that "early strains identified in Wuhan, China showed limited genetic diversity, suggesting that the virus may have been introduced from a single source."

A single source would, of course, be compatible with laboratory escape, but less so with the massive variation and selection that characterizes the way evolution operates.

The uniform structure of SARS2 genomes does not provide any indication of a passage through an intermediate animal host, and no such host has been identified in nature.

Proponents of natural emergence suggest that SARS2 was incubated in a yet-to-be-found human population before it acquired its special traits. Or that it has jumped to a host animal outside of China.

All these conjectures are possible, but very far-fetched. Proponents of a lab leak have a simpler explanation. SARS2 was adapted to human cells from the outset because it was grown in humanized mice or in laboratory cultures of human cells, as described in Daszak's grant proposal.The genome shows little diversity because the hallmark of laboratory cultures is uniformity.

Lab escape proponents joke that the SARS2 virus, of course, infected an intermediate host species before spreading to humans, and that they identified it — a humanized mouse from the Wuhan Institute of Virology.

3)The furin cleavage site.The furin cleavage site is a minuscule part of the virus's anatomy, but one that exerts a major impact on its infectivity. It sits in the middle of the SARS2 spike protein. It's also at the heart of the puzzle of where the virus came from.

The spike protein has two subunits with different roles. The first, called S1, recognizes the target of the virus, a protein called angiotensin-converting enzyme-2 (or ACE2) that covers the surface of cells lining the human respiratory tract. The second, S2, helps the virus, once anchored to the cell, fuse with the cell membrane. After the virus's outer membrane fuses with that of the affected cell, the viral genome is injected into the cell, hijacking its protein-making machinery and forcing it to generate new viruses.

But this invasion can't begin until the S1 and S2 sub-units are taken apart. And right there, right at the S1/S2 junction, is the furin cleavage site that causes the spike protein to cleave in just the right place.

The virus, a textbook example of economic design, does not have its own cleaver. It depends on the cell to split. Human cells have a protein cutting tool on their surface known as furin. Furin will cut through any protein chain that carries its distinctive target cut site. This is the sequence of amino acid units proline-arginine-arginine-alanine, or PRRA in the code that refers to each amino acid with a letter of the alphabet. PRRA is the amino acid sequence at the nucleus of the furin cleavage site of SARS2.

Viruses have all kinds of clever tricks, so why does the furin cleavage site stand out? Because of all known SARS-related beta-coronaviruses, only SARS2 has a furin cleavage site. In all other viruses, their S2 unit is split in a different place and by a different mechanism.

So how did SARS2 get its furin cleavage site? Either the site evolved naturally, or it was inserted by researchers at the S1/S2 junction in a gain-of-function experiment.

First, consider its natural origin. Two ways in which viruses evolve are through mutation and through recombination. Mutation is the process of random change in DNA (or RNA for coronaviruses) that usually results in one amino acid in a protein chain being swapped for another. Many of these changes are detrimental to the virus, but natural selection preserves the few that do something useful. Mutation is the process by which the SARS1 spike protein gradually switched its preferred target cells from those of bats to civets and then to humans.

Mutation appears to be a less likely way to generate the furin cleavage site of SARS2, although it cannot be completely ruled out. The four amino acid units of the site are all together, and all in exactly the right place in the S1/S2 junction. Mutation is a random process triggered by copying errors (when new viral genomes are generated) or by chemical decay of genomic units. Thus, it typically affects some amino acids at different places in a protein chain. It is much more likely that a series of amino acids such as those from the furin cleavage site are all obtained together through a completely different process known as recombination.

Recombination is an unintentional swapping of genomic material that occurs when two viruses enter the same cell and their offspring are joined together with bits and pieces of RNA belonging to the other. Beta coronaviruses will only combine with other beta coronaviruses, but can acquire through recombination almost any genetic element present in the collective genomic pool. What they can't acquire is an element that the pool doesn't possess. And no known SARS-related beta-coronavirus, the class to which SARS2 belongs, possesses a furin cleavage site.

Proponents of natural emergence say SARS2 could have picked up the site from an as-yet-unknown beta-coronavirus. But vSARS-related beta-coronaviruses apparently don't need a furin cleavage site to infect bat cells, so it's not very likely that anyone has one, and so far none has even been found.

The proponents' next argument is that SARS2 obtained its furin cleavage site from humans. A precursor to SARS2 could circulate in the human population for months or years until, at some point, it gained a furin cleavage site of human cells. It would then have been ready to break out as a pandemic.

If this has happened, there should be traces in the hospital surveillance records of the people infected with the slow-developing virus. But so far, none have come to light. According to the WHOreport on the origin of the virushospitals in Hubei province, home to Wuhan, routinely monitor influenza-like illnesses and "no evidence of substantial transmission of SARSCoV-2 was found in the months leading up to the December outbreak."

Thus, it is difficult to explain how the SARS2 virus picked up its furin cleavage site naturally, either by mutation or recombination.

That leaves a gain-of-function experiment. For those who think SARS2 escaped from a lab, explaining the furin cleavage site is not a problem at all. "Since 1992, the virological community has known that the only way to make a virus more lethal is to give it a furin cleavage site at the S1/S2 junction in the laboratory," Writes Steven Quay, a biotech entrepreneur interested in the origins of SARS2. "At least 11 gain-of-function experiments, in which a furin site is added to make a virus more infectious, have been published in the open literature, including by Dr. Zhengli Shi, head of coronavirus research at the Wuhan Institute of Virology."

4)It's a matter of codons.There is another aspect of the furin cleavage site that narrows the path for a natural origin even further.

As everyone knows (or at least remembers from high school), the genetic code uses three units of DNA to specify each amino acid unit of a protein chain. When read in groups of 3, the 4 different types of DNA units can specify 4 x 4 x 4 or 64 different triplets, or codons as they are called. Since there are only 20 types of amino acids, there are more than enough codons to go around, allowing some amino acids to be specified by more than one codon. For example, the amino acid arginine can be denoted by one of the six codons CGU, CGC, CGA, CGG, AGA, or AGG, where A, U, G, and C represent the four different types of units in RNA.

Here's where it gets interesting. Different organisms have different codon preferences. Human cells like to denote arginine with the codons CBT, CGC or CGG. But CGG is the least popular coronavirus codon for arginine. Keep that in mind when you look at how the amino acids in the furin cleavage site are encoded in the SARS2 genome.

The functional reason why SARS2 has a furin cleavage site and its cousin viruses do not can be seen by aligning (in a computer) the array of nearly 30,000 nucleotides in its genome with those of its cousin coronaviruses, the closest known to date being one called RaTG13. Compared to RaTG13, SARS2 has an insert of 12 nucleotides right at the S1/S2 junction. The insert is the sequence T-CCT-CGG-CGG-GC. The CCT encodes proline, the two CGGs encode two arginines, and the GC is the beginning of a GCA codon encoding alanine.

There are several curious features of this insert, but the strangest is that of the two adjacent CGG codons. Only 5 percent of SARS2's arginine codons are CGG, and the CGG-CGG double codon has not been found in any other beta-coronavirus. So how did SARS2 get a few arginine codons preferred by human cells, but not by coronaviruses?

Proponents of natural emergence have an uphill task to explain all the features of SARS2's furin cleavage site. They must postulate a recombination event at a site on the virus's genome where recombinations are rare, and the insertion of a 12-nucleotide sequence with a double arginine codon unknown in the beta-coronavirus repertoire, at the only site in the genome that significantly increases the infectivity of the virus.

"Yes, but your phrasing makes this sound unlikely – viruses are specialists in unusual events," is the response of David L. Robertson, a virologist at the University of Glasgow, who considers escape from the lab to be a conspiracy theory. "Recombination is naturally very, very common in these viruses, there are recombination breakpoints in the spike protein, and these codons seem unusual, precisely because we haven't sampled enough."

Robertson is right that evolution always produces results that may seem improbable, but in fact are not. Viruses can generate an untold number of variants, but we only see the one in a billion that natural selection chooses to survive. But this argument could go too far. For example, any result of a gain-of-function experiment could be explained as a result that evolution would have achieved in time. And the numbers game can also be played the other way around. In order for the furin cleavage site to arise naturally in SARS2, a series of events must occur, each of which is quite unlikely for the reasons listed above. It is unlikely that a long chain with several improbable steps will ever be completed.

For the lab escape scenario, the double CGG codon is no surprise. The human-preferred codon is routinely used in laboratories.So anyone who wanted to insert a furin cleavage site into the genome of the virus would synthesize the PRRA-making sequence in the lab and would likely use CGG codons to do so. "When I first saw the furin cleavage site in the viral sequence, with its arginine codons, I told my wife that this was the smoking gun was for the origin of the virus," said David Baltimore, an eminent virologist and former president of CalTech."These features pose a powerful challenge to the idea of a natural origin for SARS2," he said. [1]

[1]A third scenario of origin.There is a variation of the natural rise scenario that is worth considering. This is the idea that SARS2 jumped directly from bats to humans, without passing through an intermediate host like SARS1 and MERS did. A leading advocate is the virologist David Robertson who notes that SARS2 can attack several species other than humans. He believes that the virusdeveloped a generalist ability while it was still in bats. Because the bats it infects are widespread in southern and central China, the virus had ample opportunity to jump to humans, although it appears to have done so only on one known occasion. Robertson's dissertation explains why no one has so far found a trace of SARS2 in an intermediate host or in human populations surveilled before December 2019. It would also explain the puzzling fact that SARS2 hasn't changed since it first appeared in humans – it didn't think it was necessary because it could already attack human cells efficiently.

One problem with this idea, however, is that if SARS2 jumped from bat to humans in one jump and hasn't changed much since then, it should still be good at infecting bats. And it looks like it isn't.

"Tested bat species are poorly infected by SARS-CoV-2 and therefore are unlikely to be the direct source for human infection,"writes a scientific group thatis skeptical of natural emergence.

Still, Robertson may be on to something. The bat coronaviruses of the Yunnan Caves can infect humans directly. In April 2012, six miners cleaning up bat guano from the Mojiang mine contracted severe pneumonia with COVID-19-like symptoms, and three eventually died. A virus isolated from the Mojiang mine, called RaTG13, is still the most well-known relative of SARS2. Much mystery surrounds the origin, reporting, and strangely low affinity of RaTG13 for bat cells, as well as the nature of 8 similar viruses that Shireports thatze tegelijkertijd verzamelde maar nog niet heeft gepubliceerd, ondanks hun grote relevantie voor de voorouders van SARS2. Maar dat is allemaal een verhaal voor een andere keer. Het punt hier is dat vleermuisvirussen mensen rechtstreeks kunnen infecteren, zij het alleen in speciale omstandigheden.

So wie anders, behalve mijnwerkers die vleermuisguano opgraven, komt in bijzonder nauw contact met vleermuiscoronavirussen? Welnu, coronavirusonderzoekers wel.Shi zegt dat zij en haar groep meer dan 1.300 vleermuismonsters hebben verzameld tijdens zo’n acht bezoeken aan de Mojiang-grot tussen 2012 en 2015, en er waren ongetwijfeld veel expedities naar andere Yunnan-grotten.

Stel je voor dat de onderzoekers regelmatig reizen van Wuhan naar Yunnan en terug, terwijl ze vleermuis-guano verzamelen in donkere grotten en mijnen, en je begint een mogelijke ontbrekende schakel tussen de twee plaatsen te zien. Onderzoekers kunnen besmet zijn geraakt tijdens hun verzamelreizen, of tijdens het werken met de nieuwe virussen bij het Wuhan Institute of Virology. Het virus dat uit het lab ontsnapte, zou een natuurlijk virus zijn geweest, niet een virus dat is ontstaan ​​door functiewinst.

De direct-van-vleermuizen-these is een hersenschim tussen de scenario’s voor natuurlijke opkomst en laboratoriumontsnapping. Het is een mogelijkheid die niet kan worden afgewezen. Maar daartegenover staan ​​de feiten dat 1) zowel SARS2 als RaTG13 slechts een zwakke affiniteit lijken te hebben met vleermuiscellen, dus men kan er niet volledig zeker van zijn dat een van beide ooit de binnenkant van een vleermuis heeft gezien; en 2) de theorie is niet beter dan het natuurlijke opkomstscenario om uit te leggen hoe SARS2 zijn furine-splitsingsplaats heeft gekregen, of waarom de furine-splitsingsplaats wordt bepaald door argininecodons die de voorkeur hebben bij de mens in plaats van door de codons die de voorkeur hebben voor vleermuizen.

Waar we tot nu toe zijn

Noch de natuurlijke opkomst, noch de laboratoriumontsnappingshypothese kunnen nog worden uitgesloten. Voor beide is op 5 mei 2021 nog geen direct bewijs. Er kan dus op dit moment geen definitieve conclusie worden getrokken.

Dat gezegd hebbende, leunt het beschikbare bewijs sterker in de ene richting dan in de andere. Lezers zullen hun eigen mening vormen. Maar het lijkt mij dat voorstanders van laboratoriumontsnapping alle beschikbare feiten over SARS2 aanzienlijk gemakkelijker kunnen verklaren dan degenen die voorstander zijn van natuurlijke opkomst.

Het is gedocumenteerd dat onderzoekers van het Wuhan Institute of Virology bezig waren met gain-of-function-experimenten die waren ontworpen om coronavirussen menselijke cellen en gehumaniseerde muizen te laten infecteren. Dit is precies het soort experiment waaruit een SARS2-achtig virus zou kunnen zijn voortgekomen. De onderzoekers waren niet gevaccineerd tegen de onderzochte virussen en werkten in de minimale veiligheidsomstandigheden van een BSL2-laboratorium. Ontsnappen van een virus zou dus helemaal niet verwonderlijk zijn. In heel China brak de pandemie uit op de stoep van het Wuhan-instituut. Het virus was al goed aangepast aan de mens, zoals verwacht voor een virus dat wordt gekweekt in gehumaniseerde muizen. Het bezat een ongebruikelijke verbetering, een furine-splitsingsplaats, die niet wordt bezeten door enig ander bekend SARS-gerelateerd bèta-coronavirus, en deze plaats bevatte een dubbel arginine-codon dat ook onbekend is bij bèta-coronavirussen.

Voorstanders van natuurlijke opkomst hebben een wat moeilijker verhaal te vertellen. De aannemelijkheid van hun zaak berust op één enkele veronderstelling, de verwachte parallel tussen de opkomst van SARS2 en die van SARS1 en MERS. Maar geen van het verwachte bewijs ter ondersteuning van een dergelijke parallelle geschiedenis is tot nu toe naar voren gekomen.Niemand heeft de vleermuispopulatie gevonden die de bron was van SARS2, als het inderdaad ooit vleermuizen heeft besmet.Er heeft zich geen tussengastheer gemeld, ondanks een intensieve zoektocht door de Chinese autoriteiten, waaronder het testen van 80.000 dieren. Er is geen bewijs dat het virus meerdere onafhankelijke sprongen maakt van zijn tussengastheer naar mensen, zoals zowel het SARS1- als het MERS-virus deden. Er is geen bewijs uit de bewakingsgegevens van ziekenhuizen dat de epidemie aan kracht won onder de bevolking naarmate het virus zich ontwikkelde.Er is geen verklaring waarom er een natuurlijke epidemie zou moeten uitbreken in Wuhan en nergens anders.Er is geen goede verklaring voor hoe het virus zijn furine-splitsingsplaats heeft verkregen, die geen ander SARS-gerelateerd bèta-coronavirus bezit, noch waarom de plaats is samengesteld uit door mensen geprefereerde codons.De theorie van natuurlijke opkomst bestrijdt een reeks onaannemelijkheden.

De archieven van het Wuhan Institute of Virology bevatten zeker veel relevante informatie. Maar het lijkt onwaarschijnlijk dat de Chinese autoriteiten die zullen vrijgeven, gezien de aanzienlijke kans dat ze het regime beschuldigen bij het ontstaan ​​van de pandemie. Zonder de inspanningen van een moedige Chinese klokkenluider, hebben we misschien al een tijdje zo ongeveer alle relevante informatie die we waarschijnlijk zullen krijgen.

Het is dus de moeite waard om te proberen de verantwoordelijkheid voor de pandemie te beoordelen, althans op een voorlopige manier, omdat het belangrijkste doel blijft om een ​​nieuwe pandemie te voorkomen. Zelfs degenen die er niet van overtuigd zijn dat ontsnapping uit het laboratorium de meest waarschijnlijke oorsprong van het SARS2-virus is, kunnen reden tot bezorgdheid zien over de huidige staat van regulering van gain-of-function-onderzoek. Er zijn twee voor de hand liggende niveaus van verantwoordelijkheid: de eerste, om virologen in staat te stellen om gain-of-function-experimenten uit te voeren, met minimale winst en een groot risico; de tweede, als SARS2 inderdaad in een laboratorium is gegenereerd, om het virus te laten ontsnappen en een wereldwijde pandemie te ontketenen. Dit zijn de spelers die het meest waarschijnlijk de schuld zouden krijgen.

1. Chinese virologen.Eerst en vooral zijn Chinese virologen verantwoordelijk voor het uitvoeren van gain-of-function-experimenten in veiligheidsomstandigheden op BSL2-niveau die veel te laks waren om een ​​virus met onverwachte besmettelijkheid zoals SARS2 te bevatten. Als het virus inderdaad uit hun laboratorium is ontsnapt, verdienen ze ’s werelds afkeuring voor een voorzienbaar ongeval dat al de dood van drie miljoen mensen heeft veroorzaakt. Toegegeven, Shi werd opgeleid door Franse virologen, werkte nauw samen met Amerikaanse virologen en volgde de internationale regels voor de inperking van coronavirussen. Maar ze had zelf kunnen en moeten inschatten welke risico’s ze liep. Zij en haar collega’s dragen de verantwoordelijkheid voor hun handelen.

Ik heb het Wuhan Institute of Virology gebruikt als afkorting voor alle virologische activiteiten in Wuhan. Het is mogelijk dat SARS2 werd gegenereerd in een ander laboratorium in Wuhan, misschien in een poging om een ​​vaccin te maken dat werkte tegen alle coronavirussen. Maar totdat de rol van andere Chinese virologen is opgehelderd, is Shi het publieke gezicht van het Chinese werk aan coronavirussen, en voorlopig zullen zij en haar collega’s als eerste in de rij staan ​​voor smaad.

2. Chinese autoriteiten.De centrale autoriteiten van China hebben geen SARS2 gegenereerd, maar ze hebben zeker hun best gedaan om de aard van de tragedie en de verantwoordelijkheid van China ervoor te verbergen.Ze onderdrukten alle records bij het Wuhan Institute of Virology en sloten de virusdatabases.Ze gaven een straaltje informatie vrij, waarvan een groot deel ronduit vals was of bedoeld was om te misleiden. Ze deden hun best om het onderzoek van de WHO naar de oorsprong van het virus te manipuleren en leidden de leden van de commissie op een vruchteloze rondwandeling.Tot nu toe zijn ze veel meer geïnteresseerd in het afwenden van de schuld dan in het nemen van de nodige stappen om een ​​tweede pandemie te voorkomen.

3. De wereldwijde gemeenschap van virologen.Virologen over de hele wereld vormen een losse professionele gemeenschap. Ze schrijven artikelen in dezelfde tijdschriften. Ze wonen dezelfde conferenties bij. Ze hebben gemeenschappelijk belang bij het zoeken naar fondsen van overheden en om niet te worden overspoeld met veiligheidsvoorschriften.

Virologen kenden als geen ander de gevaren van gain-of-function-onderzoek. Maar de macht om nieuwe virussen te creëren, en de onderzoeksfinanciering die daarmee kon worden verkregen, was te verleidelijk. Ze gingen door met gain-of-function-experimenten.Ze lobbyden tegen het moratorium dat in 2014 werd opgelegd op federale financiering voor gain-of-function-onderzoek, en het werd verhoogd in 2017.

De voordelen van het onderzoek bij het voorkomen van toekomstige epidemieën zijn tot dusver nihil, de risico’s enorm.Als onderzoek naar de SARS1- en MERS-virussen alleen zou kunnen worden gedaan op het BSL3-veiligheidsniveau, zou het zeker onlogisch zijn om enig werk met nieuwe coronavirussen op het lagere niveau van BSL2 toe te staan. Of SARS2 nu wel of niet uit een laboratorium is ontsnapt, virologen over de hele wereld spelen met vuur.

Hun gedrag heeft andere biologen lange tijd gealarmeerd. In 2014 drongen wetenschappers, die zichzelf de Cambridge Working Group noemden, aan op voorzichtigheid bij het maken van nieuwe virussen. In vooruitziende woorden, specificeerden ze het risico van het creëren van een SARS2-achtig virus. “Ongevallenrisico’s met nieuw gecreëerde ‘potentiële pandemische pathogenen’ roepen ernstige nieuwe zorgen op”,Wroteze . “Het in laboratoria creëren van zeer overdraagbare, nieuwe stammen van gevaarlijke virussen, met name maar niet beperkt tot influenza, brengt aanzienlijk verhoogde risico’s met zich mee. Een accidentele infectie in een dergelijke omgeving zou uitbraken kunnen veroorzaken die moeilijk of onmogelijk te beheersen zijn.”

Toen moleculair biologen een techniek ontdekten om genen van het ene organisme naar het andere te verplaatsen, hielden ze in 1975 een openbare conferentie in Asilomar om de mogelijke risico’s te bespreken. Ondanks veel interne tegenstand, stelden ze een lijst op van strenge veiligheidsmaatregelen die in de toekomst zouden kunnen worden versoepeld – en naar behoren waren – wanneer de mogelijke gevaren beter waren ingeschat.

Toen de CRISPR-techniek voor het bewerken van genen werd uitgevonden, brachten biologen een gezamenlijk rapport uit van de Amerikaanse, Britse en Chinese nationale academies van wetenschap om aan te dringen op terughoudendheid bij het aanbrengen van erfelijke veranderingen in het menselijk genoom. Biologen die gene drives hebben uitgevonden, zijn ook open geweest over de gevaren van hun werk en hebben geprobeerd het publiek erbij te betrekken.

Je zou kunnen denken dat de SARS2-pandemie virologen zou aansporen om de voordelen van gain-of-function-onderzoek opnieuw te evalueren, zelfs om het publiek bij hun overwegingen te betrekken. Maar nee. Veel virologen spotten met laboratoriumontsnapping als een complottheorie, en anderen zeggen niets.Ze hebben zich gebarricadeerd achter een Chinese muur van stilte die tot nu toe goed werkt om de nieuwsgierigheid van journalisten en de woede van het publiek te temperen, of in ieder geval uit te stellen. Beroepen die zichzelf niet kunnen reguleren, verdienen het om door anderen gereguleerd te worden, en dit lijkt de toekomst te zijn die virologen voor zichzelf kiezen.

4. De rol van de VS bij de financiering van het Wuhan Institute of Virology.[2] Van juni 2014 tot mei 2019 ontving de EcoHealth Alliance van Daszak eensubsidievan het National Institute of Allergy and Infectious Diseases (NIAID), onderdeel van de National Institutes of Health, om functiewinstonderzoek te doen met coronavirussen in Wuhan Instituut voor Virologie. Of SARS2 nu wel of niet het product is van dat onderzoek, het lijkt een twijfelachtig beleid om risicovol onderzoek uit te besteden aan buitenlandse laboratoria met minimale veiligheidsmaatregelen.En als het SARS2-virus inderdaad is ontsnapt uit het Wuhan-instituut, dan zal de NIH zich in de verschrikkelijke positie bevinden dat ze een rampzalig experiment heeft gefinancierd dat heeft geleid tot de dood van meer dan 3 miljoen wereldwijd, waaronder meer dan een half miljoen van zijn eigen burgers.

De verantwoordelijkheid van het NIAID en de NIH is nog acuter omdat er gedurende de eerste drie jaar van de subsidie ​​aan EcoHealth Alliance een moratorium was op de financiering van Gain-of-Function onderzoek. Toen het moratorium in 2017 afliep, verdween het niet alleen, maar werd het vervangen door een rapportagesysteem, het Potential Pandemic Pathogens Control and Oversight (P3CO) Framework, dat agentschappen verplichtte om elk gevaarlijk GoF-werk dat ze wilden financieren, te rapporteren voor beoordeling.

Het moratorium, officieel een ‘pauze’ genoemd, blokkeerde specifiek de financiering van elk gain-of-function-onderzoek dat de pathogeniciteit van het griep-, MERS- of SARS-virus verhoogde. Hetdefinieerde functiewinstheel eenvoudig en ruim als “onderzoek dat het vermogen van een pathogeen om ziekte te veroorzaken verbetert.”

Maar dan staat in eenvoetnootop p.2 van het moratoriumdocument dat “een uitzondering op de onderzoekspauze kan worden verkregen als het hoofd van de USG-financieringsinstantie bepaalt dat het onderzoek dringend noodzakelijk is om de volksgezondheid of de nationale veiligheid te beschermen. .”

Dit leek te betekenen dat ofwel de directeur van de NIAID, Anthony Fauci, ofwel de directeur van de NIH, Francis Collins, of misschien beide, de vrijstelling zouden hebben ingeroepen om het geld naar Shi’s gain-of-function-onderzoek te laten stromen en het federale rapportagesysteem niet op de hoogte te stellen van haar onderzoek.

“Helaas maakten de NIAID-directeur en de NIH-directeur gebruik van deze maas in de wet om vrijstellingen te verlenen voor projecten die onder de Pauze vallen – belachelijk bewerend dat het vrijgestelde onderzoek ‘dringend noodzakelijk was om de volksgezondheid of de nationale veiligheid te beschermen’ – waardoor de Pauze teniet werd gedaan,” Dr. Richard Ebright zei in eeninterviewmet Independent Science News.

Maar het is niet zo duidelijk dat de NIH het nodig vond om eventuele mazen in de wet in te voeren. Fauci vertelde een hoorzitting van de Senaat op 11 mei dat “de NIH en NIAID categorisch geen gain-of-function-onderzoek hebben gefinancierd dat moet worden uitgevoerd in het Wuhan Institute of Virology.”

Dit was een verrassende uitspraak gezien al het bewijsmateriaal over Shi’s experimenten met het versterken van coronavirussen en de taal van het moratoriumstatuut dat gain-of-function definieert als “elk onderzoek dat het vermogen van een pathogeen om ziekte te veroorzaken verbetert.”

De verklaring kan een definitiekwestie zijn. Daszak’s EcoHealth Alliance is bijvoorbeeld van mening dat de term gain-of-function alleen van toepassing is op verbeteringen van virussen die mensen infecteren, niet op dierlijke virussen. “Dus functiewinstonderzoek verwijst specifiek naar de manipulatie van menselijke virussen om ofwel gemakkelijker overdraagbaar te zijn, een ergere infectie te veroorzaken of gemakkelijker te verspreiden”, vertelde een functionaris van de Alliantie aan The Dispatch Fact Check.

Als de NIH de opvatting van de EcoHealth Alliance deelt dat “functiewinst” alleen van toepassing is op menselijke virussen, zou dat verklaren waarom Fauci de Senaat kon verzekeren dat het nooit dergelijk onderzoek aan het Wuhan Institute of Virology had gefinancierd.Maar de juridische basis van een dergelijke definitie is onduidelijk en verschilt van die van de moratoriumtaal die vermoedelijk van toepassing was.

Afgezien van de definities, komt het erop neer dat de National Institutes of Health onderzoek ondersteunden van een soort dat het SARS2-virus had kunnen genereren, in een onbewaakt buitenlands laboratorium dat werk deed in BSL2-bioveiligheids­omstandigheden.

Finally

Als de kwestie of SARS2 in een laboratorium is ontstaan ​​zo substantieel is, waarom is die dan niet breder bekend? Zoals nu duidelijk mag zijn, zijn er veel mensen die reden hebben om er niet over te praten. De lijst wordt uiteraard geleid door de Chinese autoriteiten. Maar virologen in de Verenigde Staten en Europa hebben geen groot belang bij het aanwakkeren van een publiek debat over de gain-of-function-experimenten waar hun gemeenschap al jaren mee bezig is.

Evenmin zijn andere wetenschappers naar voren gestapt om de kwestie aan de orde te stellen. Onderzoeksgelden van de overheid worden verdeeld op advies van commissies van wetenschappelijke experts van universiteiten. Wie het roer omgooit door lastige politieke kwesties aan de orde te stellen, loopt het risico dat zijn beurs niet wordt verlengd en zijn onderzoekscarrière wordt beëindigd. Misschien wordt goed gedrag beloond met de vele voordelen die rond het distributiesysteem klotsen.En als je dacht dat Andersen en Daszak hun reputatie van wetenschappelijke objectiviteit zouden hebben aangetast na hun partijdige aanvallen op het ontsnappingsscenario van het lab, kijk dan eens naar de tweede en derde namen op dezelijst van ontvangersvan een subsidie ​​van $ 82 miljoen, aangekondigd door het National Institute of Allergy en Infectieziekten in augustus 2020.

De Amerikaanse regering deelt een vreemd gemeenschappelijk belang met de Chinese autoriteiten: geen van beiden wil de aandacht vestigen op het feit dat Shi’s coronaviruswerk werd gefinancierd door de Amerikaanse National Institutes of Health.Je kunt je het gesprek achter de schermen voorstellen waarin de Chinese regering zegt: “Als dit onderzoek zo gevaarlijk was, waarom heb je het dan gefinancierd, en ook op ons grondgebied?” Waarop de Amerikaanse kant zou kunnen antwoorden: “Het lijkt erop dat jij het was die het liet ontsnappen. Maar moeten we deze discussie echt in het openbaar voeren?”

Fauci is een oude ambtenaar die integer heeft gediend onder president Trump en heeft het leiderschap in de Biden-regering hervat bij het aanpakken van de COVID-19-epidemie. Het is ongetwijfeld begrijpelijk dat het Congres weinig zin heeft om hem over de kolen te slepen vanwege de schijnbare beoordelingsfout bij het financieren van ‘gain-of-function’-onderzoek in Wuhan.

Aan deze aaneengesloten muren van stilte moet die van de reguliere media worden toegevoegd. Voor zover ik weet, heeft nog geen enkele grote krant of televisiezender de lezers een diepgaand nieuwsverhaal over het lab-ontsnappingsscenario gegeven, zoals het scenario dat je zojuist hebt gelezen, hoewel sommigen korte redactionele artikelen of opiniestukken hebben geplaatst.Je zou kunnen denken dat elke plausibele oorsprong van een virus dat drie miljoen mensen heeft gedood, een serieus onderzoek verdient. Of dat het de moeite waard is om te onderzoeken of de wijsheid van het voortzetten van onderzoek naar functiewinst, ongeacht de oorsprong van het virus, de moeite waard is. Of dat de financiering van gain-of-function-onderzoek door de NIH en NIAID tijdens een moratorium op dergelijke financiering onderzoek zou dragen. Wat verklaart het schijnbare gebrek aan nieuwsgierigheid van de media?

Fromomertà van de virologenis een van de redenen.Wetenschapsverslaggevers hebben, in tegenstelling tot politieke verslaggevers, weinig aangeboren scepsis over de motieven van hun bronnen; de meesten zien hun rol grotendeels als het doorgeven van de wijsheid van wetenschappers aan de ongewassen massa. Dus als hun bronnen niet helpen, zijn deze journalisten ten einde raad.

Een andere reden is misschien de migratie van een groot deel van de media naar de linkerzijde van het politieke spectrum. Omdat president Trump zei dat het virus was ontsnapt uit een laboratorium in Wuhan, hechtten redacteuren weinig geloof aan het idee. Ze sloten zich aan bij de virologen en beschouwden ontsnapping uit het laboratorium als een verwerpelijke samenzweringstheorie. Tijdens de regering-Trump hadden ze geen moeite om het standpunt van de inlichtingendiensten te verwerpen dat ontsnapping uit het lab niet kon worden uitgesloten. Maar toen Avril Haines, directeur van de nationale inlichtingendienst van president Biden, hetzelfde zei, werd ook zij grotendeels genegeerd. Dit wil niet zeggen dat redacteuren het lab-ontsnappingsscenario hadden moeten onderschrijven, alleen dat ze de mogelijkheid volledig en eerlijk hadden moeten onderzoeken.

Mensen over de hele wereld die het afgelopen jaar vrijwel aan hun huis zijn gekluisterd, willen misschien een beter antwoord dan hun media hen geven. Misschien komt er op tijd een tevoorschijn. Immers, hoe meer maanden er verstrijken zonder dat de theorie van natuurlijke opkomst een greintje ondersteunend bewijs verkrijgt, hoe minder aannemelijk het lijkt. Misschien zal de internationale gemeenschap van virologen worden gezien als een valse en egoïstische gids. De gezond verstand perceptie dat een pandemie die uitbreekt in Wuhan iets te maken zou kunnen hebben met een Wuhan-lab dat nieuwe virussen van maximaal gevaar kookt in onveilige omstandigheden, zou uiteindelijk de ideologische aandrang kunnen verdringen dat wat Trump ook zei niet waar kan zijn.

En dan kan de afrekening beginnen.

Opmerkingen:

[1] Dit citaat is na de eerste publicatie aan het artikel toegevoegd.

[2] Sectie herzien 18 mei 2021

Dankbetuigingen

De eerste die serieus naar de oorsprong van het SARS2-virus keek, was Yuri Deigin, een biotech-ondernemer in Rusland en Canada. In een lang en briljantessayontleedde hij de moleculaire biologie van het SARS2-virus en bracht hij, zonder goed te keuren, de mogelijkheid naar voren dat het was gemanipuleerd. Het essay, gepubliceerd op 22 april 2020, bood een routekaart voor iedereen die de oorsprong van het virus wilde begrijpen. Deigin stopte zoveel informatie en analyses in zijn essay dat sommigen betwijfelden of het het werk van één persoon zou kunnen zijn en suggereerden dat een of andere inlichtingendienst het had geschreven. Maar het essay is met meer lichtheid en humor geschreven dan ik vermoed ooit in CIA- of KGB-rapporten te vinden, en ik zie geen reden om te twijfelen dat Deigin de zeer capabele enige auteur is.

In het kielzog van Deigin zijn verschillende andere sceptici van de orthodoxie van de virologen gevolgd. Nikolai Petrovsky berekende hoe nauw het SARS2-virus bindt aan de ACE2-receptoren van verschillende soorten en ontdekte tot zijn verbazing dat hetgeoptimaliseerdleekvoor de menselijke receptor, waardoor hij concludeerde dat het virus mogelijk in een laboratorium is gegenereerd. Alina Chan publiceerde eenpaperwaaruit bleek dat SARS2 vanaf het eerste optreden zeer goed was aangepast aan menselijke cellen.

Een van de weinige gevestigde wetenschappers die de absolute afwijzing van laboratoriumontsnapping door de virologen in twijfel heeft getrokken, is Richard Ebright, die al lang heeft gewaarschuwd voor de gevaren van gain-of-function-onderzoek. Een andere is David A. Relman van de Stanford University. “Hoewel er sterke meningen zijn, kan geen van deze scenario’s met zekerheid worden uitgesloten of uitgesloten met de momenteel beschikbare feiten”,schreefhij . Ook een pluim voor Robert Redfield, voormalig directeur van de Centers for Disease Control and Prevention, dieCNNop 26 maart 2021tolddat de “meest waarschijnlijke” oorzaak van de epidemie “van een laboratorium” kwam, omdat hij betwijfelde of een vleermuisvirus van de ene op de andere dag een extreme menselijke ziekteverwekker worden, zonder de tijd te nemen om te evolueren, zoals het geval leek te zijn met SARS2.

Steven Quay, een arts-onderzoeker, heeftstatistische en bio-informatische hulpmiddelen toegepastop ingenieuze verkenningen van de oorsprong van het virus, waarbij hij bijvoorbeeld laat zien hoe de ziekenhuizen die de vroege patiënten ontvangen, zijn geclusterd langs de Wuhan№2-metrolijndie het Instituut voor Virologie aan het ene uiteinde verbindt met aan de andere kant de internationale luchthaven, de perfecte transportband om het virus van lab naar wereldbol te verspreiden.

In juni 2020 publiceerde Milton Leitenberg eenvroeg overzichtvan het bewijs dat de ontsnapping van laboratoria bevordert uit gain-of-function-onderzoek aan het Wuhan Institute of Virology.

Vele anderen hebben belangrijke stukjes van de puzzel bijgedragen. “De waarheid is de dochter,” zei Francis Bacon, “niet van gezag maar van tijd.” De inspanningen van mensen zoals de hierboven genoemde zijn wat het zo maakt.

Steun het bulletin dat het originele artikel publiceerde

---

Jan Bonte

Bovenstaand artikel is uit 2021 en sindsdien is er nog veel meer informatie vrijgekomen. Alles ondersteunt de grote lijn van het artikel van Wade, van WOB-stukken tot genetische research. De pangolin en de wasbeerhond hebben het niet lang volgehouden. Precies weten hoe het zit? Volg Jan Bonte op X en koop het boek waaraan hij werkt, hij plaatst er net weer een tweet .