Buliten of Atomic Scientists - Review of Origins of SARS-COV-19 at Wuhan Institute of Virology
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The origin of COVID: Did people or nature open Pandora’s box at Wuhan?
By [68]Nicholas Wade | May 5, 2021
Members of the World Health Organization (WHO) team investigating the
origins of the COVID-19 coronavirus arrive by car at the Wuhan
Institute of Virology on February 3. (Photo by HECTOR RETAMAL/AFP via
Getty Images) Members of the World Health Organization (WHO) team
investigating the origins of the COVID-19 coronavirus arrive by car at
the Wuhan Institute of Virology on February 3. (Photo by HECTOR
RETAMAL/AFP via Getty Images) Members of the World Health Organization
(WHO) team investigating the origins of the COVID-19 coronavirus arrive
by car at the Wuhan Institute of Virology on February 3. (Photo by
HECTOR RETAMAL/AFP via Getty Images)
The COVID-19 pandemic has disrupted lives the world over for more than
a year. Its death toll will soon reach three million people. Yet the
origin of pandemic remains uncertain: The political agendas of
governments and scientists have generated thick clouds of obfuscation,
which the mainstream press seems helpless to dispel.
In what follows I will sort through the available scientific facts,
which hold 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 blame, which starts 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 the science cannot be avoided because for
now, and probably for a long time hence, it offers the only sure thread
through the maze.
The virus that caused the pandemic is known officially as SARS-CoV-2,
but can be called SARS2 for short. As many people know, there are two
main theories about its origin. One is that it jumped naturally from
wildlife to people. The other is that the virus was under study in a
lab, from which it escaped. It matters a great deal which is the case
if we hope to prevent a second such occurrence.
I’ll describe the two theories, explain why each is plausible, and then
ask which provides the better explanation of the available facts. It’s
important to note that so far there is no direct evidence for either
theory. Each depends on a set of reasonable conjectures but so far
lacks proof. So I have only clues, not conclusions, to offer. But those
clues point in a specific direction. And having inferred that
direction, I’m going to delineate some of the strands in this tangled
skein of disaster.
A tale of two theories. After the pandemic first broke out in December
2019, Chinese authorities reported that many cases had occurred in the
wet market — a place selling wild animals for meat — in Wuhan. This
reminded experts of the SARS1 epidemic of 2002, in which a bat virus
had spread first to civets, an animal sold in wet markets, and from
civets to people. A similar bat virus caused a second epidemic, known
as MERS, in 2012. This time the intermediary host animal was camels.
The decoding of the virus’s genome showed it belonged a viral family
known as beta-coronaviruses, to which the SARS1 and MERS viruses also
belong. The relationship supported the idea that, like them, it was a
natural virus that had managed to jump from bats, via another animal
host, to people. The wet market connection, the major point of
similarity with the SARS1 and MERS epidemics, was soon broken: Chinese
researchers found earlier cases in Wuhan with no link to the wet
market. But that seemed not to matter when so much further evidence in
support of natural emergence was expected shortly.
Wuhan, however, is home of the Wuhan Institute of Virology, a leading
world center for research on coronaviruses. So the possibility that the
SARS2 virus had escaped from the lab could not be ruled out. Two
reasonable scenarios of origin were on the table.
From early on, public and media perceptions were shaped in favor of the
natural emergence scenario by strong statements from two scientific
groups. These statements were not at first examined as critically as
they should have been.
“We stand together to strongly condemn conspiracy theories suggesting
that COVID-19 does not have a natural origin,” a group of virologists
and others wrote in the [69]Lancet on February 19, 2020, when it was
really far too soon for anyone to be sure what had happened. Scientists
“overwhelmingly conclude that this coronavirus originated in wildlife,”
they said, with a stirring rallying call for readers to stand with
Chinese colleagues on the frontline of fighting the disease.
Contrary to the letter writers’ assertion, the idea that the virus
might have escaped from a lab invoked accident, not conspiracy. It
surely needed to be explored, not rejected out of hand. A defining mark
of good scientists is that they go to great pains to distinguish
between what they know and what they don’t know. By this criterion, the
signatories of the Lancet letter were behaving as poor scientists: They
were assuring the public of facts they could not know for sure were
true.
It later turned out that the Lancet letter had been [70]organized and
drafted by Peter Daszak, president of the EcoHealth Alliance of New
York. Daszak’s organization funded coronavirus research at the Wuhan
Institute of Virology. If the SARS2 virus had indeed escaped from
research he funded, Daszak would be potentially culpable. This acute
conflict of interest was not declared to the Lancet’s readers. To the
contrary, the letter concluded, “We declare no competing interests.”
Peter Daszak, a member of the World Health Organization (WHO) team
investigating the origins of the COVID-19 coronavirus, talks on his
cellphone at the Hilton Wuhan Optics Valley in Wuhan. (Photo by HECTOR
RETAMAL/AFP via Getty Images) Peter Daszak, a member of the World
Health Organization (WHO) team investigating the origins of the
COVID-19 coronavirus, talks on his cellphone at the Hilton Wuhan Optics
Valley in Wuhan. (Photo by HECTOR RETAMAL/AFP via Getty Images) Peter
Daszak, a member of the World Health Organization (WHO) team
investigating the origins of the COVID-19 coronavirus, talks on his
cellphone at the Hilton Wuhan Optics Valley in Wuhan. (Photo by HECTOR
RETAMAL/AFP via Getty Images)
Virologists like Daszak had much at stake in the assigning of blame for
the pandemic. For 20 years, mostly beneath the public’s attention, they
had been playing a dangerous game. In their laboratories they routinely
created viruses more dangerous than those that exist in nature. They
argued that they could do so safely, and that by getting ahead of
nature they could predict and prevent natural “spillovers,” the
cross-over of viruses from an animal host to people. If SARS2 had
indeed escaped from such a laboratory experiment, a savage blowback
could be expected, and the storm of public indignation would affect
virologists everywhere, not just in China. “It would shatter the
scientific edifice top to bottom,” an MIT Technology Review editor,
Antonio Regalado, [71]said in March 2020.
A second statement that had enormous influence in shaping public
attitudes was a [72]letter (in other words an opinion piece, not a
scientific article) published on 17 March 2020 in the journal Nature
Medicine. Its 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
manipulated virus,” the five virologists declared in the second
paragraph of their letter.
Unfortunately, this was another case of poor science, in the sense
defined above. True, some older methods of cutting and pasting viral
genomes retain tell-tale signs of manipulation. But newer methods,
called “no-see-um” or “seamless” approaches, leave no defining marks.
Nor do other methods for manipulating viruses such as serial passage,
the repeated transfer of viruses from one culture of cells to another.
If a virus has been manipulated, whether with a seamless method or by
serial passage, there is no way of knowing that this is the case.
Andersen and his colleagues were assuring their readers of something
they could not know.
The discussion part of their letter begins, “It is improbable that
SARS-CoV-2 emerged through laboratory manipulation of a related
SARS-CoV-like coronavirus.” But wait, didn’t the lead say the virus had
clearly not been manipulated? The authors’ degree of certainty seemed
to slip several notches when it came to laying out their reasoning.
The reason for the slippage is clear once the technical language has
been penetrated. The two reasons the authors give for supposing
manipulation to be improbable are decidedly inconclusive.
First, they say that the spike protein of SARS2 binds very well to its
target, the human ACE2 receptor, but does so in a different way from
that which physical calculations suggest would be the best fit.
Therefore the virus must have arisen by natural selection, not
manipulation.
If this argument seems hard to grasp, it’s because it’s so strained.
The authors’ basic assumption, not spelt out, is that anyone trying to
make a bat virus bind to human cells could do so in only one way. First
they would calculate the strongest possible fit between the human ACE2
receptor and the spike protein with which the virus latches onto it.
They would then design the spike protein accordingly (by selecting the
right string of amino acid units that compose it). Since the SARS2
spike protein is not of this calculated best design, the Andersen paper
says, therefore it can’t have been manipulated.
But this ignores the way that virologists do in fact get spike proteins
to bind to chosen targets, which is not by calculation but by splicing
in spike protein genes from other viruses or by serial passage. With
serial passage, each time the virus’s progeny are transferred to new
cell cultures or animals, the more successful are selected until one
emerges that makes a really tight bind to human cells. Natural
selection has done all the heavy lifting. The Andersen paper’s
speculation about designing a viral spike protein through calculation
has no bearing on whether or not the virus was manipulated by one of
the other two methods.
The authors’ second argument against manipulation is even more
contrived. Although most living things use DNA as their hereditary
material, a number of viruses use RNA, DNA’s close chemical cousin. But
RNA is difficult to manipulate, so researchers working on
coronaviruses, which are RNA-based, will first convert the RNA genome
to DNA. They manipulate the DNA version, whether by adding or altering
genes, and then arrange for the manipulated 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, therefore it
was not manipulated. But the argument is conspicuously inconclusive.
DNA backbones are quite easy to make, so it’s obviously possible that
SARS2 was manipulated using an unpublished DNA backbone.
And that’s it. These are the two arguments made by the Andersen group
in support of their declaration that the SARS2 virus was clearly not
manipulated. And this conclusion, grounded in nothing but two
inconclusive speculations, convinced the world’s press that SARS2 could
not have escaped from a lab. A technical critique of the Andersen
letter takes it down in [73]harsher 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 for stepping out of line. Any
virologist who challenges the community’s declared view risks having
his next grant application turned down by the panel of fellow
virologists that advises the government grant distribution agency.
The Daszak and Andersen letters were really political, not scientific,
statements, yet were amazingly effective. Articles in the mainstream
press repeatedly stated that a consensus of experts had ruled lab
escape out of the question or extremely unlikely. Their authors relied
for the most part on the Daszak and Andersen letters, failing to
understand the yawning gaps in their arguments. Mainstream newspapers
all have science journalists on their staff, as do the major networks,
and these specialist reporters are supposed to be able to question
scientists and check their assertions. But the Daszak and Andersen
assertions went largely unchallenged.
Doubts about natural emergence. Natural emergence was the media’s
preferred theory until around February 2021 and the visit by a World
Health Organization (WHO) commission to China. The commission’s
composition and access were heavily controlled by the Chinese
authorities. Its members, who included the ubiquitous Daszak, kept
asserting before, during, and after their visit that lab escape was
extremely unlikely. But this was not quite the propaganda victory the
Chinese authorities may have been hoping for. What became clear was
that the Chinese had no evidence to offer the commission in support of
the natural emergence theory.
This was surprising because both the SARS1 and MERS viruses had left
copious traces in the environment. The intermediary host species of
SARS1 was identified [74]within four months of the epidemic’s outbreak,
and the host of MERS within nine months. Yet some 15 months after the
SARS2 pandemic began, and after a presumably intensive search, Chinese
researchers had failed to find either the original bat population, or
the intermediate species to which SARS2 might have jumped, or any
serological evidence that any Chinese population, including that of
Wuhan, had ever been exposed to the virus prior to December 2019.
Natural emergence remained a conjecture which, however plausible to
begin with, had gained not a shred of supporting evidence in over a
year.
And as long as that remains the case, it’s logical to pay serious
attention to the alternative conjecture, that SARS2 escaped from a lab.
Why would anyone want to create a novel virus capable of causing a
pandemic? Ever since virologists gained the tools for manipulating a
virus’s genes, they have argued they could get ahead of a potential
pandemic by exploring how close a given animal virus might be to making
the jump to humans. And that justified lab experiments in enhancing the
ability of dangerous animal viruses to infect people, virologists
asserted.
With this rationale, they have recreated the 1918 flu virus, shown how
the almost extinct polio virus can be synthesized from its published
DNA sequence, and introduced a smallpox gene into a related virus.
These enhancements of viral capabilities are known blandly as
gain-of-function experiments. With coronaviruses, there was particular
interest in the spike proteins, which jut out all around the spherical
surface of the virus and pretty much determine which species of animal
it will target. In 2000 Dutch researchers, for instance, earned the
gratitude of rodents everywhere by [75]genetically engineering the
spike protein of a mouse coronavirus so that it would attack only cats.
The spike proteins on the coronavirus’s surface determine which animal
it can infect. Image credit: CDC.gov
Virologists started studying bat coronaviruses in earnest after these
turned out to be the source of both the SARS1 and MERS epidemics. In
particular, researchers wanted to understand what changes needed to
occur in a bat virus’s spike proteins before it could infect people.
Researchers at the Wuhan Institute of Virology, led by China’s leading
expert on bat viruses, Shi Zheng-li or “Bat Lady,” mounted frequent
expeditions to the bat-infested caves of Yunnan in southern China and
collected around a hundred different bat coronaviruses.
Shi then teamed up with Ralph S. Baric, an eminent coronavirus
researcher at the University of North Carolina. [76]Their work focused
on enhancing the ability of bat viruses to attack humans so as to
“examine the emergence potential (that is, the potential to infect
humans) of circulating bat CoVs [coronaviruses].” In pursuit of this
aim, in November 2015 they created a novel virus by taking the backbone
of the SARS1 virus and replacing its spike protein with one from a bat
virus (known as SHC014-CoV). This manufactured virus was able to infect
the cells of the human airway, at least when tested against a lab
culture of such cells.
The SHC014-CoV/SARS1 virus is known as a chimera because its genome
contains genetic material from two strains of virus. If the SARS2 virus
were to have been cooked up in Shi’s lab, then its direct prototype
would have been the SHC014-CoV/SARS1 chimera, the potential danger of
which concerned many observers and prompted intense discussion.
“If the virus escaped, nobody could predict the trajectory,” [77]said
Simon Wain-Hobson, a virologist at the Pasteur Institute in Paris.
Baric and Shi referred to the obvious risks in their paper but argued
they should be weighed against the benefit of foreshadowing future
spillovers. Scientific review panels, they wrote, “may deem similar
studies building chimeric viruses based on circulating strains too
risky to pursue.” Given various restrictions being placed on gain-of
function (GOF) research, matters had arrived in their view at “a
crossroads of GOF research concerns; the potential to prepare for and
mitigate future outbreaks must be weighed against the risk of creating
more dangerous pathogens. In developing policies moving forward, it is
important to consider the value of the data generated by these studies
and whether these types of chimeric virus studies warrant further
investigation versus the inherent risks involved.”
That statement was made in 2015. From the hindsight of 2021, one can
say that the value of gain-of-function studies in preventing the SARS2
epidemic was zero. The risk was catastrophic, if indeed the SARS2 virus
was generated in a gain-of-function experiment.
Inside the Wuhan Institute of Virology. Baric had developed, and taught
Shi, a general method for engineering bat coronaviruses to attack other
species. The specific targets were human cells grown in cultures and
humanized mice. These laboratory mice, a cheap and ethical stand-in for
human subjects, are genetically engineered to carry the human version
of a protein called ACE2 that studs the surface of cells that line the
airways.
Shi returned to her lab at the Wuhan Institute of Virology and resumed
the work she had started on genetically engineering coronaviruses to
attack human cells. How can we be so sure?
A May 20, 2020, photo of the Wuhan Institute of Virology in Wuhan,
where research on bat coronaviruses was conducted. (Photo by Kyodo News
via Getty Images)
Because, by a strange twist in the story, her work was funded by the
National Institute of Allergy and Infectious Diseases (NIAID), a part
of the US National Institutes of Health (NIH). And grant proposals that
funded her work, which are a matter of public record, specify exactly
what she planned to do with the money.
The grants were assigned to the prime contractor, Daszak of the
EcoHealth Alliance, who subcontracted them to Shi. Here are extracts
from the grants for fiscal years 2018 and 2019. (“CoV” stands for
coronavirus and “S protein” refers to the virus’s spike protein.)
“Test predictions of CoV inter-species transmission. Predictive models
of host range (i.e. emergence potential) will be tested experimentally
using reverse genetics, pseudovirus and receptor binding assays, and
virus infection experiments across a range of cell cultures from
different species and [78]humanized mice.”
“We will use S protein sequence data, [79]infectious clone technology,
in vitro and in vivo infection experiments and analysis of receptor
binding to test the hypothesis that % divergence thresholds in S
protein sequences predict spillover potential.”
What this means, in non-technical language, is that Shi set out to
create novel coronaviruses with the highest possible infectivity for
human cells. Her plan was to take genes that coded for spike proteins
possessing a variety of measured affinities for human cells, ranging
from high to low. She would insert these spike genes one by one into
the backbone of a number of viral genomes (“reverse genetics” and
“infectious clone 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 people.
The methodical approach was 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 indeed may have
created the SARS2 virus itself with the right combination of virus
backbone and spike protein.
It cannot yet be stated that Shi did or did not generate SARS2 in her
lab because her records have been sealed, but it seems she was
certainly on the right track to have done so. “It is clear that the
Wuhan Institute of Virology was systematically constructing novel
chimeric coronaviruses and was assessing their ability to infect human
cells and human-ACE2-expressing mice,” says 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 progenitor of SARS-CoV-2.” “Genomic context”
refers to the particular viral backbone used as the testbed for the
spike protein.
The lab escape scenario for the origin of the SARS2 virus, as should by
now be evident, is not mere hand-waving in the direction of the Wuhan
Institute of Virology. It is a detailed proposal, based on the specific
project being funded there by the NIAID.
Even if the grant required the work plan described above, how can we be
sure that the plan was in fact carried out? For that we can rely on the
word of Daszak, who has been much protesting for the last 15 months
that lab escape was a ludicrous [80]conspiracy theory invented by
China-bashers.
On December 9, 2019, before the outbreak of the pandemic became
generally known, Daszak gave an [81]interview in which he talked in
glowing terms of how researchers at the Wuhan Institute of Virology had
been reprogramming the spike protein and generating chimeric
coronaviruses capable of infecting humanized mice.
“And we have now found, 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 of them get into human
cells in the lab, some of them can cause SARS disease in humanized mice
models and are untreatable with therapeutic monoclonals and you can’t
vaccinate against them with a vaccine. So, these are a clear and
present danger….
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“Interviewer: You say these are diverse coronaviruses and you can’t
vaccinate against them, and no anti-virals — so what do we do?
“Daszak: Well I think…coronaviruses — you can manipulate them in the
lab pretty easily. Spike protein drives a lot of what happen with
coronavirus, in zoonotic risk. So you can get the sequence, you can
build the protein, and we work a lot with Ralph Baric at UNC to do
this. Insert into the backbone of another virus and do some work in the
lab. So you can get more predictive when you find a sequence. You’ve
got this diversity. Now the logical progression for vaccines is, if you
are going to develop a vaccine for SARS, people are going to use
pandemic SARS, but let’s insert some of these other things and get a
better vaccine.” The insertions he referred to perhaps included an
element called the furin cleavage site, discussed below, which greatly
increases viral infectivity for human cells.
In disjointed style, Daszak is referring to the fact that once you have
generated a novel coronavirus that can attack human cells, you can take
the spike protein and make it the basis for a vaccine.
One can only imagine Daszak’s reaction when he heard of the outbreak of
the epidemic in Wuhan a few days later. He would have known better than
anyone the Wuhan Institute’s goal of making bat coronaviruses
infectious to humans, as well as the weaknesses in the institute’s
defense against their own researchers becoming infected.
But instead of providing public health authorities with the plentiful
information at his disposal, he immediately launched a public relations
campaign to persuade the world that the epidemic couldn’t possibly have
been caused by one of the institute’s souped-up viruses. “The idea that
this virus escaped from a lab is just pure baloney. It’s simply not
true,” he declared in an April 2020 [82]interview.
The safety arrangements at the Wuhan Institute of Virology. Daszak was
possibly unaware of, or perhaps he knew all too well, the [83]long
history of viruses escaping from even the best run laboratories. The
smallpox virus escaped three times from labs in England in the 1960’s
and 1970’s, causing 80 cases and 3 deaths. Dangerous viruses have
leaked out of labs almost every year since. Coming to more recent
times, the SARS1 virus has proved a true escape artist, leaking from
laboratories in Singapore, Taiwan, and no less than four times from the
Chinese National Institute of Virology in Beijing.
One reason for SARS1 being so hard to handle is that there were no
vaccines available to protect laboratory workers. As Daszak mentioned
in the December 19 interview quoted above, the Wuhan researchers too
had been unable to develop vaccines against the coronaviruses they had
designed to infect human cells. They would have been as defenseless
against the SARS2 virus, if it were generated in their lab, as their
Beijing colleagues were against SARS1.
A second reason for the severe danger of novel coronaviruses has to do
with the required levels of lab safety. There are four degrees of
safety, designated BSL1 to BSL4, with BSL4 being the most restrictive
and designed for deadly pathogens like the Ebola virus.
The Wuhan Institute of Virology had a new BSL4 lab, but its state of
readiness considerably alarmed the State Department inspectors who
visited it from the Beijing embassy in 2018. “The new lab has a serious
shortage of appropriately trained technicians and investigators needed
to safely operate this high-containment laboratory,” the inspectors
wrote in a [84]cable of January 19, 2018.
The real problem, however, was not the unsafe state of the Wuhan BSL4
lab but the fact that virologists worldwide don’t like working in BSL4
conditions. You have to wear a space suit, do operations in closed
cabinets, and accept that everything will take twice as long. So the
rules assigning each kind of virus to a given safety level were laxer
than some might think was prudent.
Before 2020, the rules followed by virologists in China and elsewhere
required that experiments with the SARS1 and MERS viruses be conducted
in BSL3 conditions. But all other bat coronaviruses could be studied in
BSL2, the next level down. BSL2 requires taking fairly minimal safety
precautions, such as wearing lab coats and gloves, not sucking up
liquids in a pipette, and putting up biohazard warning signs. Yet a
gain-of-function experiment conducted in BSL2 might produce an agent
more infectious than either SARS1 or MERS. And if it did, then lab
workers would stand a high chance of infection, especially if
unvaccinated.
Much of Shi’s work on gain-of-function in coronaviruses was performed
at the BSL2 safety level, as is stated in her publications and other
documents. She has said in an[85] interview with Science magazine that
“[t]he coronavirus research in our laboratory is conducted in BSL-2 or
BSL-3 laboratories.”
“It is clear that some or all of this work was being performed using a
biosafety standard — biosafety level 2, the biosafety level of a
standard US dentist’s office — that would pose an unacceptably high
risk of infection of laboratory staff upon contact with a virus having
the transmission properties of SARS-CoV-2,” Ebright says.
“It also is clear,” he adds, “that this work never should have been
funded and never should have been performed.”
This is a view he holds regardless of whether or not the SARS2 virus
ever saw the inside of a lab.
Concern about safety conditions at the Wuhan lab was not, it seems,
misplaced. According to a [86]fact sheet issued by the State Department
on January 21, 2021, “The U.S. government has reason to believe that
several researchers inside the WIV became sick in autumn 2019, before
the first identified case of the outbreak, with symptoms consistent
with both COVID-19 and common seasonal illnesses.”
David Asher, a fellow of the Hudson Institute and former consultant to
the State Department, provided more detail about the incident at a
[87]seminar. Knowledge of the incident came from a mix of public
information and “some high end information collected by our
intelligence community,” he said. Three people working at a BSL3 lab at
the institute fell sick within a week of each other with severe
symptoms that required hospitalization. This was “the first known
cluster that we’re aware of, of victims of what we believe to be
COVID-19.” Influenza could not completely be ruled out but seemed
unlikely in the circumstances, he said.
Comparing the rival scenarios of SARS2 origin. The evidence above adds
up to a serious case that the SARS2 virus could have been created in a
lab, from which it then escaped. But the case, however substantial,
falls short of proof. Proof would consist of evidence from the Wuhan
Institute of Virology, or related labs in Wuhan, that SARS2 or a
predecessor virus was under development there. For lack of access to
such records, another approach is to take certain salient facts about
the SARS2 virus and ask how well each is explained by the two rival
scenarios of origin, those of natural emergence and lab escape. Here
are four tests of the two hypotheses. A couple have some technical
detail, but these are among the most persuasive for those who may care
to follow the argument.
1) The place of origin. Start with geography. The two closest known
relatives of the SARS2 virus were collected from bats living in caves
in Yunnan, a province of 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 spilled over to people naturally.
But this isn’t what happened. The pandemic broke out 1,500 kilometers
away, in Wuhan.
Beta-coronaviruses, the family of bat viruses to which SARS2 belongs,
infect the horseshoe bat Rhinolophus affinis, which ranges across
southern China. The bats’ range is 50 kilometers, so it’s unlikely that
any made it to Wuhan. In any case, the first cases of the COVID-19
pandemic probably occurred in September, when [88]temperatures in Hubei
province are already cold enough to send bats into hibernation.
What if the bat viruses infected some intermediate host first? You
would need a longstanding population of bats in frequent proximity with
an intermediate host, which in turn must often cross paths with people.
All these exchanges of virus must take place somewhere outside Wuhan, a
busy metropolis which so far as is known is not a natural habitat of
Rhinolophus bat colonies. 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 jumped on a train to Wuhan, no fellow passengers fell ill.
It’s a stretch, in other words, to get the pandemic to break out
naturally outside Wuhan and then, without leaving any trace, to make
its first appearance there.
For the lab escape scenario, a Wuhan origin for the virus is a
no-brainer. Wuhan is home to China’s leading center of coronavirus
research where, as noted above, researchers were genetically
engineering bat coronaviruses to attack human cells. They were doing so
under the minimal safety conditions of a BSL2 lab. If a virus with the
unexpected infectiousness of SARS2 had been generated there, its escape
would be no surprise.
2) Natural history and evolution. The initial location of the pandemic
is a small part of a larger problem, that of its natural history.
Viruses don’t just make one time jumps from one species to another. The
coronavirus spike protein, adapted to attack bat cells, needs repeated
jumps to another species, most of which fail, before it gains a lucky
mutation. Mutation — a change in one of its RNA units — causes a
different amino acid unit to be incorporated into its spike protein and
makes the spike protein better able to attack the cells of some other
species.
Through several more such mutation-driven adjustments, the virus adapts
to its new host, say some animal with which bats are in frequent
contact. The whole process then resumes as the virus moves from this
intermediate host to people.
In the case of SARS1, researchers have documented the successive
changes in its spike protein as the virus evolved step by step into a
dangerous pathogen. After it had gotten from bats into civets, there
were six further changes in its spike protein before it became a mild
pathogen in people. After a further 14 changes, the virus was much
better adapted to humans, and with a further four, the [89]epidemic
took off.
But when you look for the fingerprints of a similar transition in
SARS2, a strange surprise awaits. The virus has changed hardly at all,
at least until recently. From its very first appearance, it was well
adapted to human cells. Researchers led by Alina Chan of the Broad
Institute compared SARS2 with late stage SARS1, which by then was well
adapted to human cells, and found that the two viruses were similarly
well adapted. “By the time SARS-CoV-2 was first detected in late 2019,
it was already pre-adapted to human transmission to an extent similar
to late epidemic SARS-CoV,” they [90]wrote.
Even those who think lab origin unlikely agree that SARS2 genomes are
remarkably uniform. Baric writes that “early strains identified in
Wuhan, China, showed limited genetic diversity, which suggests that the
virus may have been introduced from a single source.”
A single source would of course be compatible with lab escape, less so
with the massive variation and selection which is evolution’s hallmark
way of doing business.
The uniform structure of SARS2 genomes gives no hint of any passage
through an intermediate animal host, and no such host has been
identified in nature.
Proponents of natural emergence suggest that SARS2 incubated in a
yet-to-be found human population before gaining its special properties.
Or that it jumped to a host animal outside China.
All these conjectures are possible, but strained. Proponents of a lab
leak have a simpler explanation. SARS2 was adapted to human cells from
the start because it was grown in humanized mice or in lab cultures of
human cells, just as described in Daszak’s grant proposal. Its genome
shows little diversity because the hallmark of lab cultures is
uniformity.
Proponents of laboratory escape joke that of course the SARS2 virus
infected an intermediary host species before spreading to people, and
that they have identified it — a humanized mouse from the Wuhan
Institute of Virology.
3) The furin cleavage site. The furin cleavage site is a minute part of
the virus’s anatomy but one that exerts great influence on its
infectivity. It sits in the middle of the SARS2 spike protein. It also
lies at the heart of the puzzle of where the virus came from.
The spike protein has two sub-units with different roles. The first,
called S1, recognizes the virus’s target, a protein called angiotensin
converting enzyme-2 (or ACE2) which studs the surface of cells lining
the human airways. The second, S2, helps the virus, once anchored to
the cell, to fuse with the cell’s membrane. After the virus’s outer
membrane has coalesced with that of the stricken cell, the viral genome
is injected into the cell, hijacks its protein-making machinery and
forces it to generate new viruses.
But this invasion cannot begin until the S1 and S2 subunits have been
cut apart. And there, right at the S1/S2 junction, is the furin
cleavage site that ensures the spike protein will be cleaved in exactly
the right place.
The virus, a model of economic design, does not carry its own cleaver.
It relies on the cell to do the cleaving for it. Human cells have a
protein cutting tool on their surface known as furin. Furin will cut
any protein chain that carries its signature target cutting site. This
is the sequence of amino acid units proline-arginine-arginine-alanine,
or PRRA in the code that refers to each amino acid by a letter of the
alphabet. PRRA is the amino acid sequence at the core of SARS2’s furin
cleavage site.
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 possesses a furin cleavage site. All the other viruses have
their S2 unit cleaved at a different site and by a different mechanism.
How then did SARS2 acquire 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.
Consider natural origin first. Two ways viruses evolve are by mutation
and by 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 switched for another. Many of these changes harm
the virus but natural selection retains 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 seems a less likely way for SARS2’s furin cleavage site to be
generated, even though it can’t completely be ruled out. The site’s
four amino acid units are all together, and all at just the right place
in the S1/S2 junction. Mutation is a random process triggered by
copying errors (when new viral genomes are being generated) or by
chemical decay of genomic units. So it typically affects single amino
acids at different spots in a protein chain. A string of amino acids
like that of the furin cleavage site is much more likely to be acquired
all together through a quite different process known as recombination.
Recombination is an inadvertent swapping of genomic material that
occurs when two viruses happen to invade the same cell, and their
progeny are assembled with bits and pieces of RNA belonging to the
other. Beta-coronaviruses will only combine with other
beta-coronaviruses but can acquire, by recombination, almost any
genetic element present in the collective genomic pool. What they
cannot acquire is an element the pool does not 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 some as yet unknown beta-coronavirus. But bat SARS-related
beta-coronaviruses evidently don’t need a furin cleavage site to infect
bat cells, so there’s no great likelihood that any in fact possesses
one, and indeed none has been found so far.
The proponents’ next argument is that SARS2 acquired its furin cleavage
site from people. A predecessor of SARS2 could have been circulating in
the human population for months or years until at some point it
acquired a furin cleavage site from human cells. It would then have
been ready to break out as a pandemic.
If this is what happened, there should be traces in hospital
surveillance records of the people infected by the slowly evolving
virus. But none has so far come to light. According to the WHO
[91]report on the origins of the virus, the sentinel hospitals in Hubei
province, home of Wuhan, routinely monitor influenza-like illnesses and
“no evidence to suggest substantial SARSCoV-2 transmission in the
months preceding the outbreak in December was observed.”
So it’s hard to explain how the SARS2 virus picked up its furin
cleavage site naturally, whether by mutation or recombination.
That leaves a gain-of-function experiment. For those who think SARS2
may have escaped from a lab, explaining the furin cleavage site is no
problem at all. “Since 1992 the virology community has known that the
one sure way to make a virus deadlier is to give it a furin cleavage
site at the S1/S2 junction in the laboratory,” [92]writes Steven Quay,
a biotech entrepreneur interested in the origins of SARS2. “At least 11
gain-of-function experiments, adding a furin site to make a virus more
infective, are published in the open literature, including [by] Dr.
Zhengli Shi, head of coronavirus research at the Wuhan Institute of
Virology.”
4) A question of codons. There’s another aspect of the furin cleavage
site that narrows the path for a natural emergence origin even further.
As everyone knows (or may at least recall 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 kinds of DNA
can specify 4 x 4 x 4 or 64 different triplets, or codons as they are
called. Since there are only 20 kinds of amino acid, there are more
than enough codons to go around, allowing some amino acids to be
specified by more than one codon. The amino acid arginine, for
instance, can be designated by any of the six codons CGU, CGC, CGA,
CGG, AGA or AGG, where A, U, G and C stand for the four different kinds
of unit in RNA.
Here’s where it gets interesting. Different organisms have different
codon preferences. Human cells like to designate arginine with the
codons CGT, CGC or CGG. But CGG is coronavirus’s least popular codon
for arginine. Keep that in mind when looking at how the amino acids in
the furin cleavage site are encoded in the SARS2 genome.
Now the functional reason why SARS2 has a furin cleavage site, and its
cousin viruses don’t, can be seen by lining up (in a computer) the
string of nearly 30,000 nucleotides in its genome with those of its
cousin coronaviruses, of which the closest so far known is one called
RaTG13. Compared with RaTG13, SARS2 has a 12-nucleotide insert right at
the S1/S2 junction. The insert is the sequence T-CCT-CGG-CGG-GC. The
CCT codes for proline, the two CGG’s for two arginines, and the GC is
the beginning of a GCA codon that codes for alanine.
There are several curious features about this insert but the oddest is
that of the two side-by-side CGG codons. Only 5 percent of SARS2’s
arginine codons are CGG, and the double codon CGG-CGG has not been
found in any other beta-coronavirus. So how did SARS2 acquire a pair of
arginine codons that are favored by human cells but not by
coronaviruses?
Proponents of natural emergence have an up-hill task to explain all the
features of SARS2’s furin cleavage site. They have to 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 would significantly
expand the virus’s infectivity.
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“Yes, but your wording makes this sound unlikely — viruses are
specialists at unusual events,” is the riposte of David L. Robertson, a
virologist at the University of Glasgow who regards lab escape as a
conspiracy theory. “Recombination is naturally very, very frequent in
these viruses, there are recombination breakpoints in the spike protein
and these codons appear unusual exactly because we’ve not sampled
enough.”
Robertson is correct that evolution is always producing results that
may seem unlikely but in fact are not. Viruses can generate untold
numbers of variants but we see only the one-in-a-billion that natural
selection picks for survival. But this argument could be pushed too
far. For instance, any result of a gain-of-function experiment could be
explained as one that evolution would have arrived at in time. And the
numbers game can be played the other way. For the furin cleavage site
to arise naturally in SARS2, a chain of events has to happen, each of
which is quite unlikely for the reasons given above. A long chain with
several improbable steps is unlikely to ever be completed.
For the lab escape scenario, the double CGG codon is no surprise. The
human-preferred codon is routinely used in labs. So anyone who wanted
to insert a furin cleavage site into the virus’s genome would
synthesize the PRRA-making sequence in the lab and would be likely to
use CGG codons to do so.
A third scenario of origin. There’s a variation on the natural
emergence scenario that’s worth considering. This is the idea that
SARS2 jumped directly from bats to humans, without going through an
intermediate host as SARS1 and MERS did. A leading advocate is the
virologist David Robertson who notes that SARS2 can attack several
other species besides humans. He believes the virus [93]evolved a
generalist capability while still in bats. Because the bats it infects
are widely distributed in southern and central China, the virus had
ample opportunity to jump to people, even though it seems to have done
so on only one known occasion. Robertson’s thesis explains why no one
has so far found a trace of SARS2 in any intermediate host or in human
populations surveilled before December 2019. It would also explain the
puzzling fact that SARS2 has not changed since it first appeared in
humans — it didn’t need to because it could already attack human cells
efficiently.
One problem with this idea, though, is that if SARS2 jumped from bats
to people in a single leap and hasn’t changed much since, it should
still be good at infecting bats. And it seems it isn’t.
“Tested bat species are poorly infected by SARS-CoV-2 and they are
therefore unlikely to be the direct source for human infection,”
[94]write a scientific group skeptical of natural emergence.
Still, Robertson may be onto something. The bat coronaviruses of the
Yunnan caves can infect people directly. In April 2012 six miners
clearing 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 closest 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 Shi [95]reports she collected at the same
time but has not yet published despite their great relevance to the
ancestry of SARS2. But all that is a story for another time. The point
here is that bat viruses can infect people directly, though only in
special conditions.
So who else, besides miners excavating bat guano, comes into
particularly close contact with bat coronaviruses? Well, coronavirus
researchers do. Shi says she and her group collected more than 1,300
bat samples during some eight visits to the Mojiang cave between 2012
and 2015, and there were doubtless many expeditions to other Yunnan
caves.
Imagine the researchers making frequent trips from Wuhan to Yunnan and
back, stirring up bat guano in dark caves and mines, and now you begin
to see a possible missing link between the two places. Researchers
could have gotten infected during their collecting trips, or while
working with the new viruses at the Wuhan Institute of Technology. The
virus that escaped from the lab would have been a natural virus, not
one cooked up by gain of function.
The direct-from-bats thesis is a chimera between the natural emergence
and lab escape scenarios. It’s a possibility that can’t be dismissed.
But against it are the facts that 1) both SARS2 and RaTG13 seem to have
only feeble affinity for bat cells, so one can’t be fully confident
that either ever saw the inside of a bat; and 2) the theory is no
better than the natural emergence scenario at explaining how SARS2
gained its furin cleavage site, or why the furin cleavage site is
determined by human-preferred arginine codons instead of by the
bat-preferred codons.
Where we are so far. Neither the natural emergence nor the lab escape
hypothesis can yet be ruled out. There is still no direct evidence for
either. So no definitive conclusion can be reached.
That said, the available evidence leans more strongly in one direction
than the other. Readers will form their own opinion. But it seems to me
that proponents of lab escape can explain all the available facts about
SARS2 considerably more easily than can those who favor natural
emergence.
It’s documented that researchers at the Wuhan Institute of Virology
were doing gain-of-function experiments designed to make coronaviruses
infect human cells and humanized mice. This is exactly the kind of
experiment from which a SARS2-like virus could have emerged. The
researchers were not vaccinated against the viruses under study, and
they were working in the minimal safety conditions of a BSL2
laboratory. So escape of a virus would not be at all surprising. In all
of China, the pandemic broke out on the doorstep of the Wuhan
institute. The virus was already well adapted to humans, as expected
for a virus grown in humanized mice. It possessed an unusual
enhancement, a furin cleavage site, which is not possessed by any other
known SARS-related beta-coronavirus, and this site included a double
arginine codon also unknown among beta-coronaviruses. What more
evidence could you want, aside from the presently unobtainable lab
records documenting SARS2’s creation?
Proponents of natural emergence have a rather harder story to tell. The
plausibility of their case rests on a single surmise, the expected
parallel between the emergence of SARS2 and that of SARS1 and MERS. But
none of the evidence expected in support of such a parallel history has
yet emerged. No one has found the bat population that was the source of
SARS2, if indeed it ever infected bats. No intermediate host has
presented itself, despite an intensive search by Chinese authorities
that included the testing of 80,000 animals. There is no evidence of
the virus making multiple independent jumps from its intermediate host
to people, as both the SARS1 and MERS viruses did. There is no evidence
from hospital surveillance records of the epidemic gathering strength
in the population as the virus evolved. There is no explanation of why
a natural epidemic should break out in Wuhan and nowhere else. There is
no good explanation of how the virus acquired its furin cleavage site,
which no other SARS-related beta-coronavirus possesses, nor why the
site is composed of human-preferred codons. The natural emergence
theory battles a bristling array of implausibilities.
The records of the Wuhan Institute of Virology certainly hold much
relevant information. But Chinese authorities seem unlikely to release
them given the substantial chance that they incriminate the regime in
the creation of the pandemic. Absent the efforts of some courageous
Chinese whistle-blower, we may already have at hand just about all of
the relevant information we are likely to get for a while.
So it’s worth trying to assess responsibility for the pandemic, at
least in a provisional way, because the paramount goal remains to
prevent another one. Even those who aren’t persuaded that lab escape is
the more likely origin of the SARS2 virus may see reason for concern
about the present state of regulation governing gain-of-function
research. There are two obvious levels of responsibility: the first,
for allowing virologists to perform gain-of-function experiments,
offering minimal gain and vast risk; the second, if indeed SARS2 was
generated in a lab, for allowing the virus to escape and unleash a
world-wide pandemic. Here are the players who seem most likely to
deserve blame.
1. Chinese virologists. First and foremost, Chinese virologists are to
blame for performing gain-of-function experiments in mostly
BSL2-level safety conditions which were far too lax to contain a
virus of unexpected infectiousness like SARS2. If the virus did
indeed escape from their lab, they deserve the world’s censure for
a foreseeable accident that has already caused the deaths of three
million people. True, Shi was trained by French virologists, worked
closely with American virologists and was following international
rules for the containment of coronaviruses. But she could and
should have made her own assessment of the risks she was running.
She and her colleagues bear the responsibility for their actions.
I have been using the Wuhan Institute of Virology as a shorthand for
all virological activities in Wuhan. It’s possible that SARS2 was
generated in some other Wuhan lab, perhaps in an attempt to make a
vaccine that worked against all coronaviruses. But until the role of
other Chinese virologists is clarified, Shi is the public face of
Chinese work on coronaviruses, and provisionally she and her colleagues
will stand first in line for opprobrium.
2. Chinese authorities. China’s central authorities did not generate
SARS2, but they sure did their utmost to conceal the nature of the
tragedy and China’s responsibility for it. They suppressed all records
at the Wuhan Institute of Virology and closed down its virus databases.
They released a trickle of information, much of which may have been
outright false or designed to misdirect and mislead. They did their
best to manipulate the WHO’s inquiry into the virus’s origins, and led
the commission’s members on a fruitless run-around. So far they have
proved far more interested in deflecting blame than in taking the steps
necessary to prevent a second pandemic.
3. The worldwide community of virologists. Virologists around the world
are a loose-knit professional community. They write articles in the
same journals. They attend the same conferences. They have common
interests in seeking funds from governments and in not being
overburdened with safety regulations.
Virologists knew better than anyone the dangers of gain-of-function
research. But the power to create new viruses, and the research funding
obtainable by doing so, was too tempting. They pushed ahead with
gain-of-function experiments. They lobbied against the moratorium
imposed on Federal funding for gain-of-function research in 2014, and
it was raised in 2017.
The benefits of the research in preventing future epidemics have so far
been nil, the risks vast. If research on the SARS1 and MERS viruses
could only be done at the BSL3 safety level, it was surely illogical to
allow any work with novel coronaviruses at the lesser level of BSL2.
Whether or not SARS2 escaped from a lab, virologists around the world
have been playing with fire.
Their behavior has long alarmed other biologists. In 2014 scientists
calling themselves the Cambridge Working Group urged caution on
creating new viruses. In prescient words, they specified the risk of
creating a SARS2-like virus. “Accident risks with newly created
‘potential pandemic pathogens’ raise grave new concerns,” they
[96]wrote. “Laboratory creation of highly transmissible, novel strains
of dangerous viruses, especially but not limited to influenza, poses
substantially increased risks. An accidental infection in such a
setting could trigger outbreaks that would be difficult or impossible
to control.”
When molecular biologists discovered a technique for moving genes from
one organism to another, they held a public conference at Asilomar in
1975 to discuss the possible risks. Despite much internal opposition,
they drew up a list of stringent safety measures that could be relaxed
in future — and duly were — when the possible hazards had been better
assessed.
When the CRISPR technique for editing genes was invented, biologists
convened a joint report by the US, UK and Chinese national academies of
science to urge restraint on making heritable changes to the human
genome. Biologists who invented gene drives have also been open about
the dangers of their work and have sought to involve the public.
You might think the SARS2 pandemic would spur virologists to
re-evaluate the benefits of gain-of-function research, even to engage
the public in their deliberations. But no. Many virologists deride lab
escape as a conspiracy theory, and others say nothing. They have
barricaded themselves behind a Chinese wall of silence which so far is
working well to allay, or at least postpone, journalists’ curiosity and
the public’s wrath. Professions that cannot regulate themselves deserve
to get regulated by others, and this would seem to be the future that
virologists are choosing for themselves.
4. The US role in funding the Wuhan Institute of Virology. From June
2014 to May 2019, Daszak’s EcoHealth Alliance had a [97]grant from the
National Institute of Allergy and Infectious Diseases (NIAID), part of
the National Institutes of Health, to do gain-of-function research with
coronaviruses at the Wuhan Institute of Virology. Whether or not SARS2
is the product of that research, it seems a questionable policy to farm
out high-risk research to unsafe foreign labs using minimal safety
precautions. And if the SARS2 virus did indeed escape from the Wuhan
institute, then the NIH will find itself in the terrible position of
having funded a disastrous experiment that led to death of more than 3
million worldwide, including more than half a million of its own
citizens.
The responsibility of the NIAID and NIH is even more acute because for
the first three years of the grant to EcoHealth Alliance, there was a
moratorium on funding gain-of-function research. Why didn’t the two
agencies therefore halt the federal funding, as apparently required to
do so by law? Because someone wrote a loophole into the moratorium.
The moratorium specifically barred funding any gain-of-function
research that increased the pathogenicity of the flu, MERS, or SARS
viruses. But then a [98]footnote on page 2 of the moratorium document
states that “[a]n exception from the research pause may be obtained if
the head of the USG funding agency determines that the research is
urgently necessary to protect the public health or national security.”
This seems to mean that either the director of the NIAID, Anthony
Fauci, or the director of the NIH, Francis Collins, or maybe both,
would have invoked the footnote in order to keep the money flowing to
Shi’s gain-of-function research.
“Unfortunately, the NIAID director and the NIH director exploited this
loophole to issue exemptions to projects subject to the
Pause—preposterously asserting the exempted research was ‘urgently
necessary to protect public health or national security’ — thereby
nullifying the Pause,” Ebright said in an [99]interview with
Independent Science News.
When the moratorium was ended in 2017, it didn’t just vanish but was
replaced by a reporting system, the Potential Pandemic Pathogens
Control and Oversight (P3CO) Framework, which required agencies to
report for review any dangerous gain-of-function work they wished to
fund.
According to Ebright, both Collins and Fauci “have declined to flag and
forward proposals for risk-benefit review, thereby nullifying the P3CO
Framework.”
In his view, the two officials, in dealing with the moratorium and the
ensuing reporting system, “have systematically thwarted efforts by the
White House, the Congress, scientists, and science policy specialists
to regulate GoF [gain-of-function] research of concern.”
Possibly the two officials had to take into account matters not evident
in the public record, such as issues of national security. Perhaps
funding the Wuhan Institute of Virology, which is believed to have ties
with Chinese military virologists, provided a window into Chinese
biowarfare research. But whatever other considerations may have been
involved, the bottom line is that the National Institutes of Health was
supporting gain-of-function research, of a kind that could have
generated the SARS2 virus, in an unsupervised foreign lab that was
doing work in BSL2 biosafety conditions. The prudence of this decision
can be questioned, whether or not SARS2 and the death of 3 million
people were the result of it, which emphasizes the need [100]for some
better system of control.
In conclusion. If the case that SARS2 originated in a lab is so
substantial, why isn’t this more widely known? As may now be obvious,
there are many people who have reason not to talk about it. The list is
led, of course, by the Chinese authorities. But virologists in the
United States and Europe have no great interest in igniting a public
debate about the gain-of-function experiments that their community has
been pursuing for years.
Nor have other scientists stepped forward to raise the issue.
Government research funds are distributed on the advice of committees
of scientific experts drawn from universities. Anyone who rocks the
boat by raising awkward political issues runs the risk that their grant
will not be renewed and their research career will be ended. Maybe good
behavior is rewarded with the many perks that slosh around the
distribution system. And if you thought that Andersen and Daszak might
have blotted their reputation for scientific objectivity after their
partisan attacks on the lab escape scenario, look at the second and
third names on this [101]list of recipients of an $82 million grant
announced by the National Institute of Allergy and Infectious Diseases
in August 2020.
The US government shares a strange common interest with the Chinese
authorities: Neither is keen on drawing attention to the fact that
Shi’s coronavirus work was funded by the US National Institutes of
Health. One can imagine the behind-the-scenes conversation in which the
Chinese government says, “If this research was so dangerous, why did
you fund it, and on our territory too?” To which the US side might
reply, “Looks like it was you who let it escape. But do we really need
to have this discussion in public?”
Fauci is a longtime public servant who served with integrity under
President Trump and has resumed leadership in the Biden Administration
in handling the COVID-19 epidemic. Congress, no doubt understandably,
may have little appetite for hauling him over the coals for the
apparent lapse of judgment in funding gain-of-function research in
Wuhan.
To these serried walls of silence must be added that of the mainstream
media. To my knowledge, no major newspaper or television network has
yet provided readers with an in-depth news story of the lab escape
scenario, such as the one you have just read, although some have run
brief editorials or opinion pieces. One might think that any plausible
origin of a virus that has killed three million people would merit a
serious investigation. Or that the wisdom of continuing
gain-of-function research, regardless of the virus’s origin, would be
worth some probing. Or that the funding of gain-of-function research by
the NIH and NIAID during a moratorium on such research would bear
investigation. What accounts for the media’s apparent lack of
curiosity?
The virologists’ omertà is one reason. Science reporters, unlike
political reporters, have little innate skepticism of their sources’
motives; most see their role largely as purveying the wisdom of
scientists to the unwashed masses. So when their sources won’t help,
these journalists are at a loss.
Another reason, perhaps, is the migration of much of the media toward
the left of the political spectrum. Because President Trump said the
virus had escaped from a Wuhan lab, editors gave the idea little
credence. They joined the virologists in regarding lab escape as a
dismissible conspiracy theory. During the Trump administration, they
had no trouble in rejecting the position of the intelligence services
that lab escape could not be ruled out. But when (((Avril Haines))),
President Biden’s director of national intelligence, said the same
thing, she too was largely ignored. This is not to argue that editors
should have endorsed the lab escape scenario, merely that they should
have explored the possibility fully and fairly.
People round the world who have been pretty much confined to their
homes for the last year might like a better answer than their media are
giving them. Perhaps one will emerge in time. After all, the more
months pass without the natural emergence theory gaining a shred of
supporting evidence, the less plausible it may seem. Perhaps the
international community of virologists will come to be seen as a false
and self-interested guide. The common sense perception that a pandemic
breaking out in Wuhan might have something to do with a Wuhan lab
cooking up novel viruses of maximal danger in unsafe conditions could
eventually displace the ideological insistence that whatever Trump said
can’t be true.
And then let the reckoning begin.
Acknowledgements
The first person to take a serious look at the origins of the SARS2
virus was Yuri Deigin, a biotech entrepreneur in Russia and Canada. In
a long and brilliant [102]essay, he dissected the molecular biology of
the SARS2 virus and raised, without endorsing, the possibility that it
had been manipulated. The essay, published on April 22, 2020, provided
a roadmap for anyone seeking to understand the virus’s origins. Deigin
packed so much information and analysis into his essay that some have
doubted it could be the work of a single individual and suggested some
intelligence agency must have authored it. But the essay is written
with greater lightness and humor than I suspect are ever found in CIA
or KGB reports, and I see no reason to doubt that Deigin is its very
capable sole author.
In Deigin’s wake have followed several other skeptics of the
virologists’ orthodoxy. Nikolai Petrovsky calculated how tightly the
SARS2 virus binds to the ACE2 receptors of various species and found to
his surprise that it seemed [103]optimized for the human receptor,
leading him to infer the virus might have been generated in a
laboratory. Alina Chan published a [104]paper showing that SARS2 from
its first appearance was very well adapted to human cells.
One of the very few establishment scientists to have questioned the
virologists’ absolute rejection of lab escape is Richard Ebright, who
has long warned against the dangers of gain-of-function research.
Another is David A. Relman of Stanford University. “Even though strong
opinions abound, none of these scenarios can be confidently ruled in or
ruled out with currently available facts,” he [105]wrote. Kudos too to
Robert Redfield, former director of the Centers for Disease Control and
Prevention, who [106]told CNN on March 26, 2021 that the “most likely”
cause of the epidemic was “from a laboratory,” because he doubted that
a bat virus could become an extreme human pathogen overnight, without
taking time to evolve, as seemed to be the case with SARS2.
Steven Quay, a physician-researcher, has applied [107]statistical and
bioinformatic tools to ingenious explorations of the virus’s origin,
showing for instance how the hospitals receiving the early patients are
clustered along the Wuhan [108]№2 subway line which connects the
Institute of Virology at one end with the international airport at the
other, the perfect conveyor belt for distributing the virus from lab to
globe.
In June 2020 Milton Leitenberg published an [109]early survey of the
evidence favoring lab escape from gain-of-function research at the
Wuhan Institute of Virology.
Many others have contributed significant pieces of the puzzle. “Truth
is the daughter,” said Francis Bacon, “not of authority but time.” The
efforts of people such as those named above are what makes it so.
As the coronavirus crisis shows, we need science now more than ever.
The Bulletin elevates expert voices above the noise. But as an
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support of readers like you. Help us continue to deliver quality
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[111]Support the Bulletin
Keywords: [112]Anthony Fauci, [113]COVID-19, [114]Kristian G. Andersen,
[115]MERS, [116]Peter Daszak, [117]Ralph S. Baric, [118]SARS,
[119]SARS-CoV-2, [120]Shi Zheng-li, [121]WHO, [122]Wuhan Institute of
Virology, [123]biosafety laboratory, [124]lab escape, [125]pandemic
origin
Topics: [126]Biosecurity
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Robert Schaefer Robert Schaefer
Robert Schaefer
15 hours ago
Dear Mr. Wade, your comment that “no major newspaper or television
network has yet provided readers with an in-depth news story of the lab
escape scenario,” seems untrue given that CBS’s “60 Minutes” ran a
segment on the lab hypothesis. Have you seen the segment, and if so,
what are your opinions?
1
Reply
Dan S Dan S
Dan S
14 hours ago
To my knowledge, no major newspaper or television network has yet
provided readers with an in-depth news story of the lab escape
scenario, such as the one you have just read, although some have run
brief editorials or opinion pieces.
There was this long piece from Nicolson Baker back in January covering
much the same territory, though I don’t know if that counts as major.
[128]https://nymag.com/intelligencer/article/coronavirus-lab-escape-the
ory.html
Usatoday might count as a major newspaper though.
[129]https://www.usatoday.com/in-depth/opinion/2021/03/22/why-covid-lab
-leak-theory-wuhan-shouldnt-dismissed-column/4765985001/
5
Reply
Plebius Plebius
Plebius
12 hours ago
Fantastic to see this piece published here. Would love to hear a
rebuttal from Daszak and the scientific community.
Last edited 12 hours ago by Plebius
9
Reply
ralph ralph
ralph
12 hours ago
Toward the end of the article it said that Trump made a comment
regarding the escape of the virus. I think that Trump was the one who
brought it when he came back from china.
-37
Reply
[130]Nicholas Wade
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The origin of COVID: Did people or nature open Pandora’s box at Wuhan?
By [68]Nicholas Wade | May 5, 2021
Members of the World Health Organization (WHO) team investigating the
origins of the COVID-19 coronavirus arrive by car at the Wuhan
Institute of Virology on February 3. (Photo by HECTOR RETAMAL/AFP via
Getty Images) Members of the World Health Organization (WHO) team
investigating the origins of the COVID-19 coronavirus arrive by car at
the Wuhan Institute of Virology on February 3. (Photo by HECTOR
RETAMAL/AFP via Getty Images) Members of the World Health Organization
(WHO) team investigating the origins of the COVID-19 coronavirus arrive
by car at the Wuhan Institute of Virology on February 3. (Photo by
HECTOR RETAMAL/AFP via Getty Images)
The COVID-19 pandemic has disrupted lives the world over for more than
a year. Its death toll will soon reach three million people. Yet the
origin of pandemic remains uncertain: The political agendas of
governments and scientists have generated thick clouds of obfuscation,
which the mainstream press seems helpless to dispel.
In what follows I will sort through the available scientific facts,
which hold 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 blame, which starts 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 the science cannot be avoided because for
now, and probably for a long time hence, it offers the only sure thread
through the maze.
The virus that caused the pandemic is known officially as SARS-CoV-2,
but can be called SARS2 for short. As many people know, there are two
main theories about its origin. One is that it jumped naturally from
wildlife to people. The other is that the virus was under study in a
lab, from which it escaped. It matters a great deal which is the case
if we hope to prevent a second such occurrence.
I’ll describe the two theories, explain why each is plausible, and then
ask which provides the better explanation of the available facts. It’s
important to note that so far there is no direct evidence for either
theory. Each depends on a set of reasonable conjectures but so far
lacks proof. So I have only clues, not conclusions, to offer. But those
clues point in a specific direction. And having inferred that
direction, I’m going to delineate some of the strands in this tangled
skein of disaster.
A tale of two theories. After the pandemic first broke out in December
2019, Chinese authorities reported that many cases had occurred in the
wet market — a place selling wild animals for meat — in Wuhan. This
reminded experts of the SARS1 epidemic of 2002, in which a bat virus
had spread first to civets, an animal sold in wet markets, and from
civets to people. A similar bat virus caused a second epidemic, known
as MERS, in 2012. This time the intermediary host animal was camels.
The decoding of the virus’s genome showed it belonged a viral family
known as beta-coronaviruses, to which the SARS1 and MERS viruses also
belong. The relationship supported the idea that, like them, it was a
natural virus that had managed to jump from bats, via another animal
host, to people. The wet market connection, the major point of
similarity with the SARS1 and MERS epidemics, was soon broken: Chinese
researchers found earlier cases in Wuhan with no link to the wet
market. But that seemed not to matter when so much further evidence in
support of natural emergence was expected shortly.
Wuhan, however, is home of the Wuhan Institute of Virology, a leading
world center for research on coronaviruses. So the possibility that the
SARS2 virus had escaped from the lab could not be ruled out. Two
reasonable scenarios of origin were on the table.
From early on, public and media perceptions were shaped in favor of the
natural emergence scenario by strong statements from two scientific
groups. These statements were not at first examined as critically as
they should have been.
“We stand together to strongly condemn conspiracy theories suggesting
that COVID-19 does not have a natural origin,” a group of virologists
and others wrote in the [69]Lancet on February 19, 2020, when it was
really far too soon for anyone to be sure what had happened. Scientists
“overwhelmingly conclude that this coronavirus originated in wildlife,”
they said, with a stirring rallying call for readers to stand with
Chinese colleagues on the frontline of fighting the disease.
Contrary to the letter writers’ assertion, the idea that the virus
might have escaped from a lab invoked accident, not conspiracy. It
surely needed to be explored, not rejected out of hand. A defining mark
of good scientists is that they go to great pains to distinguish
between what they know and what they don’t know. By this criterion, the
signatories of the Lancet letter were behaving as poor scientists: They
were assuring the public of facts they could not know for sure were
true.
It later turned out that the Lancet letter had been [70]organized and
drafted by Peter Daszak, president of the EcoHealth Alliance of New
York. Daszak’s organization funded coronavirus research at the Wuhan
Institute of Virology. If the SARS2 virus had indeed escaped from
research he funded, Daszak would be potentially culpable. This acute
conflict of interest was not declared to the Lancet’s readers. To the
contrary, the letter concluded, “We declare no competing interests.”
Peter Daszak, a member of the World Health Organization (WHO) team
investigating the origins of the COVID-19 coronavirus, talks on his
cellphone at the Hilton Wuhan Optics Valley in Wuhan. (Photo by HECTOR
RETAMAL/AFP via Getty Images) Peter Daszak, a member of the World
Health Organization (WHO) team investigating the origins of the
COVID-19 coronavirus, talks on his cellphone at the Hilton Wuhan Optics
Valley in Wuhan. (Photo by HECTOR RETAMAL/AFP via Getty Images) Peter
Daszak, a member of the World Health Organization (WHO) team
investigating the origins of the COVID-19 coronavirus, talks on his
cellphone at the Hilton Wuhan Optics Valley in Wuhan. (Photo by HECTOR
RETAMAL/AFP via Getty Images)
Virologists like Daszak had much at stake in the assigning of blame for
the pandemic. For 20 years, mostly beneath the public’s attention, they
had been playing a dangerous game. In their laboratories they routinely
created viruses more dangerous than those that exist in nature. They
argued that they could do so safely, and that by getting ahead of
nature they could predict and prevent natural “spillovers,” the
cross-over of viruses from an animal host to people. If SARS2 had
indeed escaped from such a laboratory experiment, a savage blowback
could be expected, and the storm of public indignation would affect
virologists everywhere, not just in China. “It would shatter the
scientific edifice top to bottom,” an MIT Technology Review editor,
Antonio Regalado, [71]said in March 2020.
A second statement that had enormous influence in shaping public
attitudes was a [72]letter (in other words an opinion piece, not a
scientific article) published on 17 March 2020 in the journal Nature
Medicine. Its 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
manipulated virus,” the five virologists declared in the second
paragraph of their letter.
Unfortunately, this was another case of poor science, in the sense
defined above. True, some older methods of cutting and pasting viral
genomes retain tell-tale signs of manipulation. But newer methods,
called “no-see-um” or “seamless” approaches, leave no defining marks.
Nor do other methods for manipulating viruses such as serial passage,
the repeated transfer of viruses from one culture of cells to another.
If a virus has been manipulated, whether with a seamless method or by
serial passage, there is no way of knowing that this is the case.
Andersen and his colleagues were assuring their readers of something
they could not know.
The discussion part of their letter begins, “It is improbable that
SARS-CoV-2 emerged through laboratory manipulation of a related
SARS-CoV-like coronavirus.” But wait, didn’t the lead say the virus had
clearly not been manipulated? The authors’ degree of certainty seemed
to slip several notches when it came to laying out their reasoning.
The reason for the slippage is clear once the technical language has
been penetrated. The two reasons the authors give for supposing
manipulation to be improbable are decidedly inconclusive.
First, they say that the spike protein of SARS2 binds very well to its
target, the human ACE2 receptor, but does so in a different way from
that which physical calculations suggest would be the best fit.
Therefore the virus must have arisen by natural selection, not
manipulation.
If this argument seems hard to grasp, it’s because it’s so strained.
The authors’ basic assumption, not spelt out, is that anyone trying to
make a bat virus bind to human cells could do so in only one way. First
they would calculate the strongest possible fit between the human ACE2
receptor and the spike protein with which the virus latches onto it.
They would then design the spike protein accordingly (by selecting the
right string of amino acid units that compose it). Since the SARS2
spike protein is not of this calculated best design, the Andersen paper
says, therefore it can’t have been manipulated.
But this ignores the way that virologists do in fact get spike proteins
to bind to chosen targets, which is not by calculation but by splicing
in spike protein genes from other viruses or by serial passage. With
serial passage, each time the virus’s progeny are transferred to new
cell cultures or animals, the more successful are selected until one
emerges that makes a really tight bind to human cells. Natural
selection has done all the heavy lifting. The Andersen paper’s
speculation about designing a viral spike protein through calculation
has no bearing on whether or not the virus was manipulated by one of
the other two methods.
The authors’ second argument against manipulation is even more
contrived. Although most living things use DNA as their hereditary
material, a number of viruses use RNA, DNA’s close chemical cousin. But
RNA is difficult to manipulate, so researchers working on
coronaviruses, which are RNA-based, will first convert the RNA genome
to DNA. They manipulate the DNA version, whether by adding or altering
genes, and then arrange for the manipulated 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, therefore it
was not manipulated. But the argument is conspicuously inconclusive.
DNA backbones are quite easy to make, so it’s obviously possible that
SARS2 was manipulated using an unpublished DNA backbone.
And that’s it. These are the two arguments made by the Andersen group
in support of their declaration that the SARS2 virus was clearly not
manipulated. And this conclusion, grounded in nothing but two
inconclusive speculations, convinced the world’s press that SARS2 could
not have escaped from a lab. A technical critique of the Andersen
letter takes it down in [73]harsher 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 for stepping out of line. Any
virologist who challenges the community’s declared view risks having
his next grant application turned down by the panel of fellow
virologists that advises the government grant distribution agency.
The Daszak and Andersen letters were really political, not scientific,
statements, yet were amazingly effective. Articles in the mainstream
press repeatedly stated that a consensus of experts had ruled lab
escape out of the question or extremely unlikely. Their authors relied
for the most part on the Daszak and Andersen letters, failing to
understand the yawning gaps in their arguments. Mainstream newspapers
all have science journalists on their staff, as do the major networks,
and these specialist reporters are supposed to be able to question
scientists and check their assertions. But the Daszak and Andersen
assertions went largely unchallenged.
Doubts about natural emergence. Natural emergence was the media’s
preferred theory until around February 2021 and the visit by a World
Health Organization (WHO) commission to China. The commission’s
composition and access were heavily controlled by the Chinese
authorities. Its members, who included the ubiquitous Daszak, kept
asserting before, during, and after their visit that lab escape was
extremely unlikely. But this was not quite the propaganda victory the
Chinese authorities may have been hoping for. What became clear was
that the Chinese had no evidence to offer the commission in support of
the natural emergence theory.
This was surprising because both the SARS1 and MERS viruses had left
copious traces in the environment. The intermediary host species of
SARS1 was identified [74]within four months of the epidemic’s outbreak,
and the host of MERS within nine months. Yet some 15 months after the
SARS2 pandemic began, and after a presumably intensive search, Chinese
researchers had failed to find either the original bat population, or
the intermediate species to which SARS2 might have jumped, or any
serological evidence that any Chinese population, including that of
Wuhan, had ever been exposed to the virus prior to December 2019.
Natural emergence remained a conjecture which, however plausible to
begin with, had gained not a shred of supporting evidence in over a
year.
And as long as that remains the case, it’s logical to pay serious
attention to the alternative conjecture, that SARS2 escaped from a lab.
Why would anyone want to create a novel virus capable of causing a
pandemic? Ever since virologists gained the tools for manipulating a
virus’s genes, they have argued they could get ahead of a potential
pandemic by exploring how close a given animal virus might be to making
the jump to humans. And that justified lab experiments in enhancing the
ability of dangerous animal viruses to infect people, virologists
asserted.
With this rationale, they have recreated the 1918 flu virus, shown how
the almost extinct polio virus can be synthesized from its published
DNA sequence, and introduced a smallpox gene into a related virus.
These enhancements of viral capabilities are known blandly as
gain-of-function experiments. With coronaviruses, there was particular
interest in the spike proteins, which jut out all around the spherical
surface of the virus and pretty much determine which species of animal
it will target. In 2000 Dutch researchers, for instance, earned the
gratitude of rodents everywhere by [75]genetically engineering the
spike protein of a mouse coronavirus so that it would attack only cats.
The spike proteins on the coronavirus’s surface determine which animal
it can infect. Image credit: CDC.gov
Virologists started studying bat coronaviruses in earnest after these
turned out to be the source of both the SARS1 and MERS epidemics. In
particular, researchers wanted to understand what changes needed to
occur in a bat virus’s spike proteins before it could infect people.
Researchers at the Wuhan Institute of Virology, led by China’s leading
expert on bat viruses, Shi Zheng-li or “Bat Lady,” mounted frequent
expeditions to the bat-infested caves of Yunnan in southern China and
collected around a hundred different bat coronaviruses.
Shi then teamed up with Ralph S. Baric, an eminent coronavirus
researcher at the University of North Carolina. [76]Their work focused
on enhancing the ability of bat viruses to attack humans so as to
“examine the emergence potential (that is, the potential to infect
humans) of circulating bat CoVs [coronaviruses].” In pursuit of this
aim, in November 2015 they created a novel virus by taking the backbone
of the SARS1 virus and replacing its spike protein with one from a bat
virus (known as SHC014-CoV). This manufactured virus was able to infect
the cells of the human airway, at least when tested against a lab
culture of such cells.
The SHC014-CoV/SARS1 virus is known as a chimera because its genome
contains genetic material from two strains of virus. If the SARS2 virus
were to have been cooked up in Shi’s lab, then its direct prototype
would have been the SHC014-CoV/SARS1 chimera, the potential danger of
which concerned many observers and prompted intense discussion.
“If the virus escaped, nobody could predict the trajectory,” [77]said
Simon Wain-Hobson, a virologist at the Pasteur Institute in Paris.
Baric and Shi referred to the obvious risks in their paper but argued
they should be weighed against the benefit of foreshadowing future
spillovers. Scientific review panels, they wrote, “may deem similar
studies building chimeric viruses based on circulating strains too
risky to pursue.” Given various restrictions being placed on gain-of
function (GOF) research, matters had arrived in their view at “a
crossroads of GOF research concerns; the potential to prepare for and
mitigate future outbreaks must be weighed against the risk of creating
more dangerous pathogens. In developing policies moving forward, it is
important to consider the value of the data generated by these studies
and whether these types of chimeric virus studies warrant further
investigation versus the inherent risks involved.”
That statement was made in 2015. From the hindsight of 2021, one can
say that the value of gain-of-function studies in preventing the SARS2
epidemic was zero. The risk was catastrophic, if indeed the SARS2 virus
was generated in a gain-of-function experiment.
Inside the Wuhan Institute of Virology. Baric had developed, and taught
Shi, a general method for engineering bat coronaviruses to attack other
species. The specific targets were human cells grown in cultures and
humanized mice. These laboratory mice, a cheap and ethical stand-in for
human subjects, are genetically engineered to carry the human version
of a protein called ACE2 that studs the surface of cells that line the
airways.
Shi returned to her lab at the Wuhan Institute of Virology and resumed
the work she had started on genetically engineering coronaviruses to
attack human cells. How can we be so sure?
A May 20, 2020, photo of the Wuhan Institute of Virology in Wuhan,
where research on bat coronaviruses was conducted. (Photo by Kyodo News
via Getty Images)
Because, by a strange twist in the story, her work was funded by the
National Institute of Allergy and Infectious Diseases (NIAID), a part
of the US National Institutes of Health (NIH). And grant proposals that
funded her work, which are a matter of public record, specify exactly
what she planned to do with the money.
The grants were assigned to the prime contractor, Daszak of the
EcoHealth Alliance, who subcontracted them to Shi. Here are extracts
from the grants for fiscal years 2018 and 2019. (“CoV” stands for
coronavirus and “S protein” refers to the virus’s spike protein.)
“Test predictions of CoV inter-species transmission. Predictive models
of host range (i.e. emergence potential) will be tested experimentally
using reverse genetics, pseudovirus and receptor binding assays, and
virus infection experiments across a range of cell cultures from
different species and [78]humanized mice.”
“We will use S protein sequence data, [79]infectious clone technology,
in vitro and in vivo infection experiments and analysis of receptor
binding to test the hypothesis that % divergence thresholds in S
protein sequences predict spillover potential.”
What this means, in non-technical language, is that Shi set out to
create novel coronaviruses with the highest possible infectivity for
human cells. Her plan was to take genes that coded for spike proteins
possessing a variety of measured affinities for human cells, ranging
from high to low. She would insert these spike genes one by one into
the backbone of a number of viral genomes (“reverse genetics” and
“infectious clone 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 people.
The methodical approach was 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 indeed may have
created the SARS2 virus itself with the right combination of virus
backbone and spike protein.
It cannot yet be stated that Shi did or did not generate SARS2 in her
lab because her records have been sealed, but it seems she was
certainly on the right track to have done so. “It is clear that the
Wuhan Institute of Virology was systematically constructing novel
chimeric coronaviruses and was assessing their ability to infect human
cells and human-ACE2-expressing mice,” says 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 progenitor of SARS-CoV-2.” “Genomic context”
refers to the particular viral backbone used as the testbed for the
spike protein.
The lab escape scenario for the origin of the SARS2 virus, as should by
now be evident, is not mere hand-waving in the direction of the Wuhan
Institute of Virology. It is a detailed proposal, based on the specific
project being funded there by the NIAID.
Even if the grant required the work plan described above, how can we be
sure that the plan was in fact carried out? For that we can rely on the
word of Daszak, who has been much protesting for the last 15 months
that lab escape was a ludicrous [80]conspiracy theory invented by
China-bashers.
On December 9, 2019, before the outbreak of the pandemic became
generally known, Daszak gave an [81]interview in which he talked in
glowing terms of how researchers at the Wuhan Institute of Virology had
been reprogramming the spike protein and generating chimeric
coronaviruses capable of infecting humanized mice.
“And we have now found, 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 of them get into human
cells in the lab, some of them can cause SARS disease in humanized mice
models and are untreatable with therapeutic monoclonals and you can’t
vaccinate against them with a vaccine. So, these are a clear and
present danger….
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“Interviewer: You say these are diverse coronaviruses and you can’t
vaccinate against them, and no anti-virals — so what do we do?
“Daszak: Well I think…coronaviruses — you can manipulate them in the
lab pretty easily. Spike protein drives a lot of what happen with
coronavirus, in zoonotic risk. So you can get the sequence, you can
build the protein, and we work a lot with Ralph Baric at UNC to do
this. Insert into the backbone of another virus and do some work in the
lab. So you can get more predictive when you find a sequence. You’ve
got this diversity. Now the logical progression for vaccines is, if you
are going to develop a vaccine for SARS, people are going to use
pandemic SARS, but let’s insert some of these other things and get a
better vaccine.” The insertions he referred to perhaps included an
element called the furin cleavage site, discussed below, which greatly
increases viral infectivity for human cells.
In disjointed style, Daszak is referring to the fact that once you have
generated a novel coronavirus that can attack human cells, you can take
the spike protein and make it the basis for a vaccine.
One can only imagine Daszak’s reaction when he heard of the outbreak of
the epidemic in Wuhan a few days later. He would have known better than
anyone the Wuhan Institute’s goal of making bat coronaviruses
infectious to humans, as well as the weaknesses in the institute’s
defense against their own researchers becoming infected.
But instead of providing public health authorities with the plentiful
information at his disposal, he immediately launched a public relations
campaign to persuade the world that the epidemic couldn’t possibly have
been caused by one of the institute’s souped-up viruses. “The idea that
this virus escaped from a lab is just pure baloney. It’s simply not
true,” he declared in an April 2020 [82]interview.
The safety arrangements at the Wuhan Institute of Virology. Daszak was
possibly unaware of, or perhaps he knew all too well, the [83]long
history of viruses escaping from even the best run laboratories. The
smallpox virus escaped three times from labs in England in the 1960’s
and 1970’s, causing 80 cases and 3 deaths. Dangerous viruses have
leaked out of labs almost every year since. Coming to more recent
times, the SARS1 virus has proved a true escape artist, leaking from
laboratories in Singapore, Taiwan, and no less than four times from the
Chinese National Institute of Virology in Beijing.
One reason for SARS1 being so hard to handle is that there were no
vaccines available to protect laboratory workers. As Daszak mentioned
in the December 19 interview quoted above, the Wuhan researchers too
had been unable to develop vaccines against the coronaviruses they had
designed to infect human cells. They would have been as defenseless
against the SARS2 virus, if it were generated in their lab, as their
Beijing colleagues were against SARS1.
A second reason for the severe danger of novel coronaviruses has to do
with the required levels of lab safety. There are four degrees of
safety, designated BSL1 to BSL4, with BSL4 being the most restrictive
and designed for deadly pathogens like the Ebola virus.
The Wuhan Institute of Virology had a new BSL4 lab, but its state of
readiness considerably alarmed the State Department inspectors who
visited it from the Beijing embassy in 2018. “The new lab has a serious
shortage of appropriately trained technicians and investigators needed
to safely operate this high-containment laboratory,” the inspectors
wrote in a [84]cable of January 19, 2018.
The real problem, however, was not the unsafe state of the Wuhan BSL4
lab but the fact that virologists worldwide don’t like working in BSL4
conditions. You have to wear a space suit, do operations in closed
cabinets, and accept that everything will take twice as long. So the
rules assigning each kind of virus to a given safety level were laxer
than some might think was prudent.
Before 2020, the rules followed by virologists in China and elsewhere
required that experiments with the SARS1 and MERS viruses be conducted
in BSL3 conditions. But all other bat coronaviruses could be studied in
BSL2, the next level down. BSL2 requires taking fairly minimal safety
precautions, such as wearing lab coats and gloves, not sucking up
liquids in a pipette, and putting up biohazard warning signs. Yet a
gain-of-function experiment conducted in BSL2 might produce an agent
more infectious than either SARS1 or MERS. And if it did, then lab
workers would stand a high chance of infection, especially if
unvaccinated.
Much of Shi’s work on gain-of-function in coronaviruses was performed
at the BSL2 safety level, as is stated in her publications and other
documents. She has said in an[85] interview with Science magazine that
“[t]he coronavirus research in our laboratory is conducted in BSL-2 or
BSL-3 laboratories.”
“It is clear that some or all of this work was being performed using a
biosafety standard — biosafety level 2, the biosafety level of a
standard US dentist’s office — that would pose an unacceptably high
risk of infection of laboratory staff upon contact with a virus having
the transmission properties of SARS-CoV-2,” Ebright says.
“It also is clear,” he adds, “that this work never should have been
funded and never should have been performed.”
This is a view he holds regardless of whether or not the SARS2 virus
ever saw the inside of a lab.
Concern about safety conditions at the Wuhan lab was not, it seems,
misplaced. According to a [86]fact sheet issued by the State Department
on January 21, 2021, “The U.S. government has reason to believe that
several researchers inside the WIV became sick in autumn 2019, before
the first identified case of the outbreak, with symptoms consistent
with both COVID-19 and common seasonal illnesses.”
David Asher, a fellow of the Hudson Institute and former consultant to
the State Department, provided more detail about the incident at a
[87]seminar. Knowledge of the incident came from a mix of public
information and “some high end information collected by our
intelligence community,” he said. Three people working at a BSL3 lab at
the institute fell sick within a week of each other with severe
symptoms that required hospitalization. This was “the first known
cluster that we’re aware of, of victims of what we believe to be
COVID-19.” Influenza could not completely be ruled out but seemed
unlikely in the circumstances, he said.
Comparing the rival scenarios of SARS2 origin. The evidence above adds
up to a serious case that the SARS2 virus could have been created in a
lab, from which it then escaped. But the case, however substantial,
falls short of proof. Proof would consist of evidence from the Wuhan
Institute of Virology, or related labs in Wuhan, that SARS2 or a
predecessor virus was under development there. For lack of access to
such records, another approach is to take certain salient facts about
the SARS2 virus and ask how well each is explained by the two rival
scenarios of origin, those of natural emergence and lab escape. Here
are four tests of the two hypotheses. A couple have some technical
detail, but these are among the most persuasive for those who may care
to follow the argument.
1) The place of origin. Start with geography. The two closest known
relatives of the SARS2 virus were collected from bats living in caves
in Yunnan, a province of 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 spilled over to people naturally.
But this isn’t what happened. The pandemic broke out 1,500 kilometers
away, in Wuhan.
Beta-coronaviruses, the family of bat viruses to which SARS2 belongs,
infect the horseshoe bat Rhinolophus affinis, which ranges across
southern China. The bats’ range is 50 kilometers, so it’s unlikely that
any made it to Wuhan. In any case, the first cases of the COVID-19
pandemic probably occurred in September, when [88]temperatures in Hubei
province are already cold enough to send bats into hibernation.
What if the bat viruses infected some intermediate host first? You
would need a longstanding population of bats in frequent proximity with
an intermediate host, which in turn must often cross paths with people.
All these exchanges of virus must take place somewhere outside Wuhan, a
busy metropolis which so far as is known is not a natural habitat of
Rhinolophus bat colonies. 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 jumped on a train to Wuhan, no fellow passengers fell ill.
It’s a stretch, in other words, to get the pandemic to break out
naturally outside Wuhan and then, without leaving any trace, to make
its first appearance there.
For the lab escape scenario, a Wuhan origin for the virus is a
no-brainer. Wuhan is home to China’s leading center of coronavirus
research where, as noted above, researchers were genetically
engineering bat coronaviruses to attack human cells. They were doing so
under the minimal safety conditions of a BSL2 lab. If a virus with the
unexpected infectiousness of SARS2 had been generated there, its escape
would be no surprise.
2) Natural history and evolution. The initial location of the pandemic
is a small part of a larger problem, that of its natural history.
Viruses don’t just make one time jumps from one species to another. The
coronavirus spike protein, adapted to attack bat cells, needs repeated
jumps to another species, most of which fail, before it gains a lucky
mutation. Mutation — a change in one of its RNA units — causes a
different amino acid unit to be incorporated into its spike protein and
makes the spike protein better able to attack the cells of some other
species.
Through several more such mutation-driven adjustments, the virus adapts
to its new host, say some animal with which bats are in frequent
contact. The whole process then resumes as the virus moves from this
intermediate host to people.
In the case of SARS1, researchers have documented the successive
changes in its spike protein as the virus evolved step by step into a
dangerous pathogen. After it had gotten from bats into civets, there
were six further changes in its spike protein before it became a mild
pathogen in people. After a further 14 changes, the virus was much
better adapted to humans, and with a further four, the [89]epidemic
took off.
But when you look for the fingerprints of a similar transition in
SARS2, a strange surprise awaits. The virus has changed hardly at all,
at least until recently. From its very first appearance, it was well
adapted to human cells. Researchers led by Alina Chan of the Broad
Institute compared SARS2 with late stage SARS1, which by then was well
adapted to human cells, and found that the two viruses were similarly
well adapted. “By the time SARS-CoV-2 was first detected in late 2019,
it was already pre-adapted to human transmission to an extent similar
to late epidemic SARS-CoV,” they [90]wrote.
Even those who think lab origin unlikely agree that SARS2 genomes are
remarkably uniform. Baric writes that “early strains identified in
Wuhan, China, showed limited genetic diversity, which suggests that the
virus may have been introduced from a single source.”
A single source would of course be compatible with lab escape, less so
with the massive variation and selection which is evolution’s hallmark
way of doing business.
The uniform structure of SARS2 genomes gives no hint of any passage
through an intermediate animal host, and no such host has been
identified in nature.
Proponents of natural emergence suggest that SARS2 incubated in a
yet-to-be found human population before gaining its special properties.
Or that it jumped to a host animal outside China.
All these conjectures are possible, but strained. Proponents of a lab
leak have a simpler explanation. SARS2 was adapted to human cells from
the start because it was grown in humanized mice or in lab cultures of
human cells, just as described in Daszak’s grant proposal. Its genome
shows little diversity because the hallmark of lab cultures is
uniformity.
Proponents of laboratory escape joke that of course the SARS2 virus
infected an intermediary host species before spreading to people, and
that they have identified it — a humanized mouse from the Wuhan
Institute of Virology.
3) The furin cleavage site. The furin cleavage site is a minute part of
the virus’s anatomy but one that exerts great influence on its
infectivity. It sits in the middle of the SARS2 spike protein. It also
lies at the heart of the puzzle of where the virus came from.
The spike protein has two sub-units with different roles. The first,
called S1, recognizes the virus’s target, a protein called angiotensin
converting enzyme-2 (or ACE2) which studs the surface of cells lining
the human airways. The second, S2, helps the virus, once anchored to
the cell, to fuse with the cell’s membrane. After the virus’s outer
membrane has coalesced with that of the stricken cell, the viral genome
is injected into the cell, hijacks its protein-making machinery and
forces it to generate new viruses.
But this invasion cannot begin until the S1 and S2 subunits have been
cut apart. And there, right at the S1/S2 junction, is the furin
cleavage site that ensures the spike protein will be cleaved in exactly
the right place.
The virus, a model of economic design, does not carry its own cleaver.
It relies on the cell to do the cleaving for it. Human cells have a
protein cutting tool on their surface known as furin. Furin will cut
any protein chain that carries its signature target cutting site. This
is the sequence of amino acid units proline-arginine-arginine-alanine,
or PRRA in the code that refers to each amino acid by a letter of the
alphabet. PRRA is the amino acid sequence at the core of SARS2’s furin
cleavage site.
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 possesses a furin cleavage site. All the other viruses have
their S2 unit cleaved at a different site and by a different mechanism.
How then did SARS2 acquire 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.
Consider natural origin first. Two ways viruses evolve are by mutation
and by 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 switched for another. Many of these changes harm
the virus but natural selection retains 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 seems a less likely way for SARS2’s furin cleavage site to be
generated, even though it can’t completely be ruled out. The site’s
four amino acid units are all together, and all at just the right place
in the S1/S2 junction. Mutation is a random process triggered by
copying errors (when new viral genomes are being generated) or by
chemical decay of genomic units. So it typically affects single amino
acids at different spots in a protein chain. A string of amino acids
like that of the furin cleavage site is much more likely to be acquired
all together through a quite different process known as recombination.
Recombination is an inadvertent swapping of genomic material that
occurs when two viruses happen to invade the same cell, and their
progeny are assembled with bits and pieces of RNA belonging to the
other. Beta-coronaviruses will only combine with other
beta-coronaviruses but can acquire, by recombination, almost any
genetic element present in the collective genomic pool. What they
cannot acquire is an element the pool does not 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 some as yet unknown beta-coronavirus. But bat SARS-related
beta-coronaviruses evidently don’t need a furin cleavage site to infect
bat cells, so there’s no great likelihood that any in fact possesses
one, and indeed none has been found so far.
The proponents’ next argument is that SARS2 acquired its furin cleavage
site from people. A predecessor of SARS2 could have been circulating in
the human population for months or years until at some point it
acquired a furin cleavage site from human cells. It would then have
been ready to break out as a pandemic.
If this is what happened, there should be traces in hospital
surveillance records of the people infected by the slowly evolving
virus. But none has so far come to light. According to the WHO
[91]report on the origins of the virus, the sentinel hospitals in Hubei
province, home of Wuhan, routinely monitor influenza-like illnesses and
“no evidence to suggest substantial SARSCoV-2 transmission in the
months preceding the outbreak in December was observed.”
So it’s hard to explain how the SARS2 virus picked up its furin
cleavage site naturally, whether by mutation or recombination.
That leaves a gain-of-function experiment. For those who think SARS2
may have escaped from a lab, explaining the furin cleavage site is no
problem at all. “Since 1992 the virology community has known that the
one sure way to make a virus deadlier is to give it a furin cleavage
site at the S1/S2 junction in the laboratory,” [92]writes Steven Quay,
a biotech entrepreneur interested in the origins of SARS2. “At least 11
gain-of-function experiments, adding a furin site to make a virus more
infective, are published in the open literature, including [by] Dr.
Zhengli Shi, head of coronavirus research at the Wuhan Institute of
Virology.”
4) A question of codons. There’s another aspect of the furin cleavage
site that narrows the path for a natural emergence origin even further.
As everyone knows (or may at least recall 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 kinds of DNA
can specify 4 x 4 x 4 or 64 different triplets, or codons as they are
called. Since there are only 20 kinds of amino acid, there are more
than enough codons to go around, allowing some amino acids to be
specified by more than one codon. The amino acid arginine, for
instance, can be designated by any of the six codons CGU, CGC, CGA,
CGG, AGA or AGG, where A, U, G and C stand for the four different kinds
of unit in RNA.
Here’s where it gets interesting. Different organisms have different
codon preferences. Human cells like to designate arginine with the
codons CGT, CGC or CGG. But CGG is coronavirus’s least popular codon
for arginine. Keep that in mind when looking at how the amino acids in
the furin cleavage site are encoded in the SARS2 genome.
Now the functional reason why SARS2 has a furin cleavage site, and its
cousin viruses don’t, can be seen by lining up (in a computer) the
string of nearly 30,000 nucleotides in its genome with those of its
cousin coronaviruses, of which the closest so far known is one called
RaTG13. Compared with RaTG13, SARS2 has a 12-nucleotide insert right at
the S1/S2 junction. The insert is the sequence T-CCT-CGG-CGG-GC. The
CCT codes for proline, the two CGG’s for two arginines, and the GC is
the beginning of a GCA codon that codes for alanine.
There are several curious features about this insert but the oddest is
that of the two side-by-side CGG codons. Only 5 percent of SARS2’s
arginine codons are CGG, and the double codon CGG-CGG has not been
found in any other beta-coronavirus. So how did SARS2 acquire a pair of
arginine codons that are favored by human cells but not by
coronaviruses?
Proponents of natural emergence have an up-hill task to explain all the
features of SARS2’s furin cleavage site. They have to 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 would significantly
expand the virus’s infectivity.
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“Yes, but your wording makes this sound unlikely — viruses are
specialists at unusual events,” is the riposte of David L. Robertson, a
virologist at the University of Glasgow who regards lab escape as a
conspiracy theory. “Recombination is naturally very, very frequent in
these viruses, there are recombination breakpoints in the spike protein
and these codons appear unusual exactly because we’ve not sampled
enough.”
Robertson is correct that evolution is always producing results that
may seem unlikely but in fact are not. Viruses can generate untold
numbers of variants but we see only the one-in-a-billion that natural
selection picks for survival. But this argument could be pushed too
far. For instance, any result of a gain-of-function experiment could be
explained as one that evolution would have arrived at in time. And the
numbers game can be played the other way. For the furin cleavage site
to arise naturally in SARS2, a chain of events has to happen, each of
which is quite unlikely for the reasons given above. A long chain with
several improbable steps is unlikely to ever be completed.
For the lab escape scenario, the double CGG codon is no surprise. The
human-preferred codon is routinely used in labs. So anyone who wanted
to insert a furin cleavage site into the virus’s genome would
synthesize the PRRA-making sequence in the lab and would be likely to
use CGG codons to do so.
A third scenario of origin. There’s a variation on the natural
emergence scenario that’s worth considering. This is the idea that
SARS2 jumped directly from bats to humans, without going through an
intermediate host as SARS1 and MERS did. A leading advocate is the
virologist David Robertson who notes that SARS2 can attack several
other species besides humans. He believes the virus [93]evolved a
generalist capability while still in bats. Because the bats it infects
are widely distributed in southern and central China, the virus had
ample opportunity to jump to people, even though it seems to have done
so on only one known occasion. Robertson’s thesis explains why no one
has so far found a trace of SARS2 in any intermediate host or in human
populations surveilled before December 2019. It would also explain the
puzzling fact that SARS2 has not changed since it first appeared in
humans — it didn’t need to because it could already attack human cells
efficiently.
One problem with this idea, though, is that if SARS2 jumped from bats
to people in a single leap and hasn’t changed much since, it should
still be good at infecting bats. And it seems it isn’t.
“Tested bat species are poorly infected by SARS-CoV-2 and they are
therefore unlikely to be the direct source for human infection,”
[94]write a scientific group skeptical of natural emergence.
Still, Robertson may be onto something. The bat coronaviruses of the
Yunnan caves can infect people directly. In April 2012 six miners
clearing 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 closest 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 Shi [95]reports she collected at the same
time but has not yet published despite their great relevance to the
ancestry of SARS2. But all that is a story for another time. The point
here is that bat viruses can infect people directly, though only in
special conditions.
So who else, besides miners excavating bat guano, comes into
particularly close contact with bat coronaviruses? Well, coronavirus
researchers do. Shi says she and her group collected more than 1,300
bat samples during some eight visits to the Mojiang cave between 2012
and 2015, and there were doubtless many expeditions to other Yunnan
caves.
Imagine the researchers making frequent trips from Wuhan to Yunnan and
back, stirring up bat guano in dark caves and mines, and now you begin
to see a possible missing link between the two places. Researchers
could have gotten infected during their collecting trips, or while
working with the new viruses at the Wuhan Institute of Technology. The
virus that escaped from the lab would have been a natural virus, not
one cooked up by gain of function.
The direct-from-bats thesis is a chimera between the natural emergence
and lab escape scenarios. It’s a possibility that can’t be dismissed.
But against it are the facts that 1) both SARS2 and RaTG13 seem to have
only feeble affinity for bat cells, so one can’t be fully confident
that either ever saw the inside of a bat; and 2) the theory is no
better than the natural emergence scenario at explaining how SARS2
gained its furin cleavage site, or why the furin cleavage site is
determined by human-preferred arginine codons instead of by the
bat-preferred codons.
Where we are so far. Neither the natural emergence nor the lab escape
hypothesis can yet be ruled out. There is still no direct evidence for
either. So no definitive conclusion can be reached.
That said, the available evidence leans more strongly in one direction
than the other. Readers will form their own opinion. But it seems to me
that proponents of lab escape can explain all the available facts about
SARS2 considerably more easily than can those who favor natural
emergence.
It’s documented that researchers at the Wuhan Institute of Virology
were doing gain-of-function experiments designed to make coronaviruses
infect human cells and humanized mice. This is exactly the kind of
experiment from which a SARS2-like virus could have emerged. The
researchers were not vaccinated against the viruses under study, and
they were working in the minimal safety conditions of a BSL2
laboratory. So escape of a virus would not be at all surprising. In all
of China, the pandemic broke out on the doorstep of the Wuhan
institute. The virus was already well adapted to humans, as expected
for a virus grown in humanized mice. It possessed an unusual
enhancement, a furin cleavage site, which is not possessed by any other
known SARS-related beta-coronavirus, and this site included a double
arginine codon also unknown among beta-coronaviruses. What more
evidence could you want, aside from the presently unobtainable lab
records documenting SARS2’s creation?
Proponents of natural emergence have a rather harder story to tell. The
plausibility of their case rests on a single surmise, the expected
parallel between the emergence of SARS2 and that of SARS1 and MERS. But
none of the evidence expected in support of such a parallel history has
yet emerged. No one has found the bat population that was the source of
SARS2, if indeed it ever infected bats. No intermediate host has
presented itself, despite an intensive search by Chinese authorities
that included the testing of 80,000 animals. There is no evidence of
the virus making multiple independent jumps from its intermediate host
to people, as both the SARS1 and MERS viruses did. There is no evidence
from hospital surveillance records of the epidemic gathering strength
in the population as the virus evolved. There is no explanation of why
a natural epidemic should break out in Wuhan and nowhere else. There is
no good explanation of how the virus acquired its furin cleavage site,
which no other SARS-related beta-coronavirus possesses, nor why the
site is composed of human-preferred codons. The natural emergence
theory battles a bristling array of implausibilities.
The records of the Wuhan Institute of Virology certainly hold much
relevant information. But Chinese authorities seem unlikely to release
them given the substantial chance that they incriminate the regime in
the creation of the pandemic. Absent the efforts of some courageous
Chinese whistle-blower, we may already have at hand just about all of
the relevant information we are likely to get for a while.
So it’s worth trying to assess responsibility for the pandemic, at
least in a provisional way, because the paramount goal remains to
prevent another one. Even those who aren’t persuaded that lab escape is
the more likely origin of the SARS2 virus may see reason for concern
about the present state of regulation governing gain-of-function
research. There are two obvious levels of responsibility: the first,
for allowing virologists to perform gain-of-function experiments,
offering minimal gain and vast risk; the second, if indeed SARS2 was
generated in a lab, for allowing the virus to escape and unleash a
world-wide pandemic. Here are the players who seem most likely to
deserve blame.
1. Chinese virologists. First and foremost, Chinese virologists are to
blame for performing gain-of-function experiments in mostly
BSL2-level safety conditions which were far too lax to contain a
virus of unexpected infectiousness like SARS2. If the virus did
indeed escape from their lab, they deserve the world’s censure for
a foreseeable accident that has already caused the deaths of three
million people. True, Shi was trained by French virologists, worked
closely with American virologists and was following international
rules for the containment of coronaviruses. But she could and
should have made her own assessment of the risks she was running.
She and her colleagues bear the responsibility for their actions.
I have been using the Wuhan Institute of Virology as a shorthand for
all virological activities in Wuhan. It’s possible that SARS2 was
generated in some other Wuhan lab, perhaps in an attempt to make a
vaccine that worked against all coronaviruses. But until the role of
other Chinese virologists is clarified, Shi is the public face of
Chinese work on coronaviruses, and provisionally she and her colleagues
will stand first in line for opprobrium.
2. Chinese authorities. China’s central authorities did not generate
SARS2, but they sure did their utmost to conceal the nature of the
tragedy and China’s responsibility for it. They suppressed all records
at the Wuhan Institute of Virology and closed down its virus databases.
They released a trickle of information, much of which may have been
outright false or designed to misdirect and mislead. They did their
best to manipulate the WHO’s inquiry into the virus’s origins, and led
the commission’s members on a fruitless run-around. So far they have
proved far more interested in deflecting blame than in taking the steps
necessary to prevent a second pandemic.
3. The worldwide community of virologists. Virologists around the world
are a loose-knit professional community. They write articles in the
same journals. They attend the same conferences. They have common
interests in seeking funds from governments and in not being
overburdened with safety regulations.
Virologists knew better than anyone the dangers of gain-of-function
research. But the power to create new viruses, and the research funding
obtainable by doing so, was too tempting. They pushed ahead with
gain-of-function experiments. They lobbied against the moratorium
imposed on Federal funding for gain-of-function research in 2014, and
it was raised in 2017.
The benefits of the research in preventing future epidemics have so far
been nil, the risks vast. If research on the SARS1 and MERS viruses
could only be done at the BSL3 safety level, it was surely illogical to
allow any work with novel coronaviruses at the lesser level of BSL2.
Whether or not SARS2 escaped from a lab, virologists around the world
have been playing with fire.
Their behavior has long alarmed other biologists. In 2014 scientists
calling themselves the Cambridge Working Group urged caution on
creating new viruses. In prescient words, they specified the risk of
creating a SARS2-like virus. “Accident risks with newly created
‘potential pandemic pathogens’ raise grave new concerns,” they
[96]wrote. “Laboratory creation of highly transmissible, novel strains
of dangerous viruses, especially but not limited to influenza, poses
substantially increased risks. An accidental infection in such a
setting could trigger outbreaks that would be difficult or impossible
to control.”
When molecular biologists discovered a technique for moving genes from
one organism to another, they held a public conference at Asilomar in
1975 to discuss the possible risks. Despite much internal opposition,
they drew up a list of stringent safety measures that could be relaxed
in future — and duly were — when the possible hazards had been better
assessed.
When the CRISPR technique for editing genes was invented, biologists
convened a joint report by the US, UK and Chinese national academies of
science to urge restraint on making heritable changes to the human
genome. Biologists who invented gene drives have also been open about
the dangers of their work and have sought to involve the public.
You might think the SARS2 pandemic would spur virologists to
re-evaluate the benefits of gain-of-function research, even to engage
the public in their deliberations. But no. Many virologists deride lab
escape as a conspiracy theory, and others say nothing. They have
barricaded themselves behind a Chinese wall of silence which so far is
working well to allay, or at least postpone, journalists’ curiosity and
the public’s wrath. Professions that cannot regulate themselves deserve
to get regulated by others, and this would seem to be the future that
virologists are choosing for themselves.
4. The US role in funding the Wuhan Institute of Virology. From June
2014 to May 2019, Daszak’s EcoHealth Alliance had a [97]grant from the
National Institute of Allergy and Infectious Diseases (NIAID), part of
the National Institutes of Health, to do gain-of-function research with
coronaviruses at the Wuhan Institute of Virology. Whether or not SARS2
is the product of that research, it seems a questionable policy to farm
out high-risk research to unsafe foreign labs using minimal safety
precautions. And if the SARS2 virus did indeed escape from the Wuhan
institute, then the NIH will find itself in the terrible position of
having funded a disastrous experiment that led to death of more than 3
million worldwide, including more than half a million of its own
citizens.
The responsibility of the NIAID and NIH is even more acute because for
the first three years of the grant to EcoHealth Alliance, there was a
moratorium on funding gain-of-function research. Why didn’t the two
agencies therefore halt the federal funding, as apparently required to
do so by law? Because someone wrote a loophole into the moratorium.
The moratorium specifically barred funding any gain-of-function
research that increased the pathogenicity of the flu, MERS, or SARS
viruses. But then a [98]footnote on page 2 of the moratorium document
states that “[a]n exception from the research pause may be obtained if
the head of the USG funding agency determines that the research is
urgently necessary to protect the public health or national security.”
This seems to mean that either the director of the NIAID, Anthony
Fauci, or the director of the NIH, Francis Collins, or maybe both,
would have invoked the footnote in order to keep the money flowing to
Shi’s gain-of-function research.
“Unfortunately, the NIAID director and the NIH director exploited this
loophole to issue exemptions to projects subject to the
Pause—preposterously asserting the exempted research was ‘urgently
necessary to protect public health or national security’ — thereby
nullifying the Pause,” Ebright said in an [99]interview with
Independent Science News.
When the moratorium was ended in 2017, it didn’t just vanish but was
replaced by a reporting system, the Potential Pandemic Pathogens
Control and Oversight (P3CO) Framework, which required agencies to
report for review any dangerous gain-of-function work they wished to
fund.
According to Ebright, both Collins and Fauci “have declined to flag and
forward proposals for risk-benefit review, thereby nullifying the P3CO
Framework.”
In his view, the two officials, in dealing with the moratorium and the
ensuing reporting system, “have systematically thwarted efforts by the
White House, the Congress, scientists, and science policy specialists
to regulate GoF [gain-of-function] research of concern.”
Possibly the two officials had to take into account matters not evident
in the public record, such as issues of national security. Perhaps
funding the Wuhan Institute of Virology, which is believed to have ties
with Chinese military virologists, provided a window into Chinese
biowarfare research. But whatever other considerations may have been
involved, the bottom line is that the National Institutes of Health was
supporting gain-of-function research, of a kind that could have
generated the SARS2 virus, in an unsupervised foreign lab that was
doing work in BSL2 biosafety conditions. The prudence of this decision
can be questioned, whether or not SARS2 and the death of 3 million
people were the result of it, which emphasizes the need [100]for some
better system of control.
In conclusion. If the case that SARS2 originated in a lab is so
substantial, why isn’t this more widely known? As may now be obvious,
there are many people who have reason not to talk about it. The list is
led, of course, by the Chinese authorities. But virologists in the
United States and Europe have no great interest in igniting a public
debate about the gain-of-function experiments that their community has
been pursuing for years.
Nor have other scientists stepped forward to raise the issue.
Government research funds are distributed on the advice of committees
of scientific experts drawn from universities. Anyone who rocks the
boat by raising awkward political issues runs the risk that their grant
will not be renewed and their research career will be ended. Maybe good
behavior is rewarded with the many perks that slosh around the
distribution system. And if you thought that Andersen and Daszak might
have blotted their reputation for scientific objectivity after their
partisan attacks on the lab escape scenario, look at the second and
third names on this [101]list of recipients of an $82 million grant
announced by the National Institute of Allergy and Infectious Diseases
in August 2020.
The US government shares a strange common interest with the Chinese
authorities: Neither is keen on drawing attention to the fact that
Shi’s coronavirus work was funded by the US National Institutes of
Health. One can imagine the behind-the-scenes conversation in which the
Chinese government says, “If this research was so dangerous, why did
you fund it, and on our territory too?” To which the US side might
reply, “Looks like it was you who let it escape. But do we really need
to have this discussion in public?”
Fauci is a longtime public servant who served with integrity under
President Trump and has resumed leadership in the Biden Administration
in handling the COVID-19 epidemic. Congress, no doubt understandably,
may have little appetite for hauling him over the coals for the
apparent lapse of judgment in funding gain-of-function research in
Wuhan.
To these serried walls of silence must be added that of the mainstream
media. To my knowledge, no major newspaper or television network has
yet provided readers with an in-depth news story of the lab escape
scenario, such as the one you have just read, although some have run
brief editorials or opinion pieces. One might think that any plausible
origin of a virus that has killed three million people would merit a
serious investigation. Or that the wisdom of continuing
gain-of-function research, regardless of the virus’s origin, would be
worth some probing. Or that the funding of gain-of-function research by
the NIH and NIAID during a moratorium on such research would bear
investigation. What accounts for the media’s apparent lack of
curiosity?
The virologists’ omertà is one reason. Science reporters, unlike
political reporters, have little innate skepticism of their sources’
motives; most see their role largely as purveying the wisdom of
scientists to the unwashed masses. So when their sources won’t help,
these journalists are at a loss.
Another reason, perhaps, is the migration of much of the media toward
the left of the political spectrum. Because President Trump said the
virus had escaped from a Wuhan lab, editors gave the idea little
credence. They joined the virologists in regarding lab escape as a
dismissible conspiracy theory. During the Trump administration, they
had no trouble in rejecting the position of the intelligence services
that lab escape could not be ruled out. But when Avril Haines,
President Biden’s director of national intelligence, said the same
thing, she too was largely ignored. This is not to argue that editors
should have endorsed the lab escape scenario, merely that they should
have explored the possibility fully and fairly.
People round the world who have been pretty much confined to their
homes for the last year might like a better answer than their media are
giving them. Perhaps one will emerge in time. After all, the more
months pass without the natural emergence theory gaining a shred of
supporting evidence, the less plausible it may seem. Perhaps the
international community of virologists will come to be seen as a false
and self-interested guide. The common sense perception that a pandemic
breaking out in Wuhan might have something to do with a Wuhan lab
cooking up novel viruses of maximal danger in unsafe conditions could
eventually displace the ideological insistence that whatever Trump said
can’t be true.
And then let the reckoning begin.
Acknowledgements
The first person to take a serious look at the origins of the SARS2
virus was Yuri Deigin, a biotech entrepreneur in Russia and Canada. In
a long and brilliant [102]essay, he dissected the molecular biology of
the SARS2 virus and raised, without endorsing, the possibility that it
had been manipulated. The essay, published on April 22, 2020, provided
a roadmap for anyone seeking to understand the virus’s origins. Deigin
packed so much information and analysis into his essay that some have
doubted it could be the work of a single individual and suggested some
intelligence agency must have authored it. But the essay is written
with greater lightness and humor than I suspect are ever found in CIA
or KGB reports, and I see no reason to doubt that Deigin is its very
capable sole author.
In Deigin’s wake have followed several other skeptics of the
virologists’ orthodoxy. Nikolai Petrovsky calculated how tightly the
SARS2 virus binds to the ACE2 receptors of various species and found to
his surprise that it seemed [103]optimized for the human receptor,
leading him to infer the virus might have been generated in a
laboratory. Alina Chan published a [104]paper showing that SARS2 from
its first appearance was very well adapted to human cells.
One of the very few establishment scientists to have questioned the
virologists’ absolute rejection of lab escape is Richard Ebright, who
has long warned against the dangers of gain-of-function research.
Another is David A. Relman of Stanford University. “Even though strong
opinions abound, none of these scenarios can be confidently ruled in or
ruled out with currently available facts,” he [105]wrote. Kudos too to
Robert Redfield, former director of the Centers for Disease Control and
Prevention, who [106]told CNN on March 26, 2021 that the “most likely”
cause of the epidemic was “from a laboratory,” because he doubted that
a bat virus could become an extreme human pathogen overnight, without
taking time to evolve, as seemed to be the case with SARS2.
Steven Quay, a physician-researcher, has applied [107]statistical and
bioinformatic tools to ingenious explorations of the virus’s origin,
showing for instance how the hospitals receiving the early patients are
clustered along the Wuhan [108]№2 subway line which connects the
Institute of Virology at one end with the international airport at the
other, the perfect conveyor belt for distributing the virus from lab to
globe.
In June 2020 Milton Leitenberg published an [109]early survey of the
evidence favoring lab escape from gain-of-function research at the
Wuhan Institute of Virology.
Many others have contributed significant pieces of the puzzle. “Truth
is the daughter,” said Francis Bacon, “not of authority but time.” The
efforts of people such as those named above are what makes it so.
As the coronavirus crisis shows, we need science now more than ever.
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Keywords: [112]Anthony Fauci, [113]COVID-19, [114]Kristian G. Andersen,
[115]MERS, [116]Peter Daszak, [117]Ralph S. Baric, [118]SARS,
[119]SARS-CoV-2, [120]Shi Zheng-li, [121]WHO, [122]Wuhan Institute of
Virology, [123]biosafety laboratory, [124]lab escape, [125]pandemic
origin
Topics: [126]Biosecurity
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Robert Schaefer Robert Schaefer
Robert Schaefer
15 hours ago
Dear Mr. Wade, your comment that “no major newspaper or television
network has yet provided readers with an in-depth news story of the lab
escape scenario,” seems untrue given that CBS’s “60 Minutes” ran a
segment on the lab hypothesis. Have you seen the segment, and if so,
what are your opinions?
1
Reply
Dan S Dan S
Dan S
14 hours ago
To my knowledge, no major newspaper or television network has yet
provided readers with an in-depth news story of the lab escape
scenario, such as the one you have just read, although some have run
brief editorials or opinion pieces.
There was this long piece from Nicolson Baker back in January covering
much the same territory, though I don’t know if that counts as major.
[128]https://nymag.com/intelligencer/article/coronavirus-lab-escape-the
ory.html
Usatoday might count as a major newspaper though.
[129]https://www.usatoday.com/in-depth/opinion/2021/03/22/why-covid-lab
-leak-theory-wuhan-shouldnt-dismissed-column/4765985001/
5
Reply
Plebius Plebius
Plebius
12 hours ago
Fantastic to see this piece published here. Would love to hear a
rebuttal from Daszak and the scientific community.
Last edited 12 hours ago by Plebius
9
Reply
ralph ralph
ralph
12 hours ago
Toward the end of the article it said that Trump made a comment
regarding the escape of the virus. I think that Trump was the one who
brought it when he came back from china.
-37
Reply
[130]Nicholas Wade
Nicholas Wade is a science writer, editor, and author who has worked on
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