by Jonathan Latham, PhD and Allison Wilson, PhD via Independent Science News (emphasis ours)
The Case Is Building That COVID-19 Had a Lab Origin
If the public has learned a lesson from
the COVID-19 pandemic it is that science does not generate certainty. Do
homemade face masks work? What is the death rate of COVID-19? How
accurate are the tests? How many people have no symptoms? And so on.
Practically the lone undisputed assertion made so far is that all the
nearest known genetic relatives of its cause, the Sars-CoV-2 virus, are
found in horseshoe bats (
Zhou et al., 2020). Therefore, the likely viral reservoir was a bat.
However, most of these ancestor-like bat coronaviruses cannot infect humans (
Ge et al., 2013). In consequence, from its beginning,
a
key question hanging over the pandemic has been: How did a bat RNA
virus evolve into a human pathogen that is both virulent and deadly?
The answer almost universally seized upon
is that there was an intermediate species. Some animal, perhaps a snake,
perhaps a palm civet, perhaps a pangolin, served as a temporary host.
This bridging animal would probably have had an ACE2 cellular receptor
(the molecule which allows cellular entry of the virus) intermediate in
protein sequence (or at least structure) between the bat and the human
one (
Wan et al., 2020).
In the press and in the scientific
literature, scenarios by which this natural zoonotic transfer might have
occurred have been endlessly mulled. Most were fuelled by early
findings that many of the earliest COVID-19 cases seem to have occurred
in and around Wuhan’s Huanan live animal market. [The latest data are
that 14 of the 41 earliest cases, including the first, had no connection
to the animal market (
Huang et al. 2020)].
Since the two previous coronavirus
near-pandemics of SARS (2002-3) and MERS (2012) both probably came from
bats and both are thought (but not proven) to have transitioned to
humans via intermediate animals (civets and dromedaries respectively), a
natural zoonotic pathway is a reasonable first assumption (
Andersen et al., 2020).
The idea, as it applied to the original
(2002) SARS outbreak, is that the original bat virus infected a civet.
The virus then evolved briefly in this animal species, but not enough to
cause a civet pandemic, and then was picked up by a human before it
died out in civets. In this first human (patient zero) the virus
survived, perhaps only barely, but was passed on, marking the first case
of human to human transmission. As it was successively passed on in its
first few human hosts the virus rapidly evolved, adapting to better
infect its new hosts. After a few such tentative transmissions the
pandemic proper began.
Perhaps this scenario is approximately how the current COVID-19 pandemic began.
But one other troubling
possibility must be dispensed with. It follows from the fact that the
epicentre city, Wuhan (pop. 11 million), happens to be the global
epicentre of bat coronavirus research (e.g. Hu et al., 2017).
Unfortunately, in the US at least, the
question of the pandemic’s origin has become a political football;
either an opportunity for Sinophobia or a partisan “
blame game“.
But
the potential of a catastrophic lab release is not a game and systemic problems of competence and opacity are certainly not limited to China (
Lipsitch, 2018). The US Department of Homeland Security (DHS) is currently constructing a new and expanded national
Bio and Agro-defense facility in Manhattan, Kansas.
DHS has estimated that the 50-year risk (defined as having an economic
impact of $9-50 billion) of a release from its lab at 70%.
A subsequent committee report (
NAP, 2012) continued:
“the committee was instructed to judge
the adequacy and validity of the uSSRA [updated Site-Specific Risk
Assessment]. The committee has identified serious concerns about (1) the
misapplication of methods used to assess risk, (2) the failure to make
clear whether and how the evidence used to support risk assessment
assumptions had been thoroughly reviewed and adequately evaluated, (3)
the limited breadth of literature cited and the misinterpretation of
some of the significant supporting literature, (4) the failure to
explain the criteria used to select assumptions when supporting
literature is conflicting, (5) the failure to consider important risk
pathways, and (6) the inadequate treatment of uncertainty. Those
deficiencies are not equally problematic, but they occur with sufficient
frequency to raise doubts about the adequacy and validity of the risk
results presented. In most instances (e.g., operational activities at
the NBAF), the identified problems lead to an underestimation of risk;
in other instances (e.g., catastrophic natural hazards), the risks may
be overestimated. As a result, the committee concludes that the uSSRA is
technically inadequate in critical respects and is an insufficient
basis on which to judge the risks associated with the proposed NBAF in
Manhattan, Kansas.”
China, meanwhile, having opened its first in Wuhan in 2018, is planning to roll out a national network of BSL-4 labs (
Zhiming, 2019).
Like many other countries, it is investing significantly in disease
surveillance and collection of viruses from wild animal populations and
in high-risk recombinant virus research with Potential Pandemic
Pathogens (PPPs).
On May 4th, nations and global
philanthropies, meeting in Brussels, committed $7.4 billion to future
pandemic preparedness. But the question hanging over all such
investments is this: the remit of the Wuhan lab at the centre of the
accidental release claims
is pandemic preparedness. If the COVID-19 pandemic began there then we need to
radically rethink
current ideas for pandemic preparation globally. Many researchers
already believe we should, for the sake of both safety and effectiveness
(
Lipsitch and Galvani, 2014;
Weiss et al., 2015;
Lipsitch, 2018). The worst possible outcome would be for those donated billions to accelerate the arrival of the next pandemic.
An accidental lab release is not merely a theoretical possibility. In
1977 a laboratory in Russia (or possibly China), most likely while
developing a flu vaccine, accidentally released the extinct H1N1
influenza virus (
Nakajima et al., 1978).
H1N1 went on to become a global pandemic virus. A large proportion of
the global population became infected. In this case, deaths were few
because the population aged over 20 yrs old had historic immunity to the
virus. This episode is not widely known because only recently has this
conclusion been formally acknowledged in the scientific literature and
the virology community has been reluctant to discuss such incidents (
Zimmer and Burke, 2009;
Wertheim, 2010).
Still, laboratory pathogen escapes leading to human and animal deaths
(e.g. smallpox in Britain; equine encephalitis in South America) are
common enough that they ought to be much better known (summarised in
Furmanski, 2014).
Only rarely have these broken out into actual pandemics on the scale of
H1N1, which, incidentally, broke out again in 2009/2010 as “Swine flu”
causing 3,000 or so deaths on that occasion (
Duggal et al., 2016).
Many scientists have warned that
experiments with PPPs, like the smallpox and Ebola and influenza
viruses, are inherently dangerous and should be subject to strict limits
and oversight (
Lipsitch and Galvani, 2014;
Klotz and Sylvester, 2014).
Even in the limited case of SARS-like coronaviruses, since the quelling
of the original SARS outbreak in 2003, there have been six documented
SARS disease outbreaks originating from research laboratories, including
four in China. These outbreaks caused 13 individual infections and one
death (Furmanski, 2014). In response to such concerns the US
banned certain classes of experiments, called
gain
of
function (GOF) experiments, with PPPs in 2014, but the ban (
actually a funding moratoriumactually a funding moratorium) was lifted in 2017.
For these reasons, and also to ensure the
effectiveness of future pandemic preparedness efforts, it is a matter
of vital international importance to establish whether the laboratory
escape hypothesis has credible evidence to support it. This must be done
regardless of the problem–in the US–of toxic partisan politics and
nationalism.
The COVID-19 Wuhan lab escape thesis
The essence of the lab escape theory is
that Wuhan is the site of the Wuhan Institute of Virology (WIV), China’s
first and only Biosafety Level 4 (BSL-4) facility. (BSL-4 is the
highest pathogen security level). The WIV, which added a BSL-4 lab only
in 2018, has been collecting large numbers of coronaviruses from bat
samples ever since the original SARS outbreak of 2002-2003; including
collecting more in 2016 (
Hu, et al., 2017;
Zhou et al., 2018).
Led by researcher Zheng-Li Shi, WIV
scientists have also published experiments in which live bat
coronaviruses were introduced into human cells (Hu et al., 2017).
Moreover, according to an April 14 article in the Washington Post, US
Embassy staff visited the WIV in 2018 and “
had grave safety concerns”
about biosecurity there. The WIV is just eight miles from the Huanan
live animal market that was initially thought to be the site of origin
of the COVID-19 pandemic.
Thus the lab escape theory is that
researchers from one or both of these labs may have picked up a
Sars-CoV-2-like bat coronavirus on one of their many collecting (aka
‘”virus surveillance”) trips. Or, alternatively, a virus they were
studying, passaging, engineering, or otherwise manipulating, escaped.
Scientific assessments of the lab escape theory
Three (Edward Holmes, Nigel McMillan and
Hassan Vally) dismissed the lab escape suggestion and Vally simply
labeled it, without elaboration, a “conspiracy”.
The fourth virologist interviewed was
Nikolai Petrovsky of Flinders University. Petrovsky first addressed the
question of whether the natural zoonosis pathway was viable. He told the
Media Centre:
“no natural virus matching to COVID-19 has been found in nature despite an intensive search to find its origins.”
That is to say, the idea of an animal
intermediate is speculation. Indeed, no credible viral or animal host
intermediaries, either in the form of a confirmed animal host or a
plausible virus intermediate, has to-date emerged to explain the natural
zoonotic transfer of Sars-CoV-2 to humans (e.g.
Zhan et al., 2020).
In addition to Petrovsky’s point, there
are two further difficulties with the natural zoonotic transfer thesis
(apart from the weak epidemiological association between early cases and
the Huanan “wet” market).
The first is that researchers from the
Wuhan lab travelled to caves in Yunnan (1,500 Km away) to find horseshoe
bats containing SARS-like coronaviruses. To-date, the closest living
relative of Sars-CoV-2 yet found comes from Yunnan (
Ge et al., 2016). Why would an outbreak of a bat virus therefore occur in Wuhan?
Moreover, China has a population of 1.3
billion. If spillover from the wildlife trade was the explanation, then,
other things being equal, the probability of a pandemic starting in
Wuhan (pop. 11 million) is less than 1%.
“I had never expected this kind of
thing to happen in Wuhan, in central China.” Her studies had shown that
the southern, subtropical provinces of Guangdong, Guangxi and Yunnan
have the greatest risk of coronaviruses jumping to humans from
animals—particularly bats, a known reservoir. If coronaviruses were the
culprit, she remembers thinking, “Could they have come from our lab?”
Wuhan, in short, is a rather unlikely
epicentre for a natural zoonotic transfer. In contrast, to suspect that
Sars-CoV-2 might have come from the WIV is both reasonable and obvious.
Was Sars-CoV-2 created in a lab?
In his statement, Petrovsky goes on to describe the kind of experiment that, in
principle, if done in a lab, would obtain the same result as the
hypothesised natural zoonotic transfer–rapid adaptation of a bat
coronavirus to a human host.
“Take a bat coronavirus that is not
infectious to humans, and force its selection by culturing it with cells
that express human ACE2 receptor, such cells having been created many
years ago to culture SARS coronaviruses and you can force the bat virus
to adapt to infect human cells via mutations in its spike protein, which
would have the effect of increasing the strength of its binding to
human ACE2, and inevitably reducing the strength of its binding to bat
ACE2.
Viruses in prolonged culture will also
develop other random mutations that do not affect its function. The
result of these experiments is a virus that is highly virulent in humans
but is sufficiently different that it no longer resembles the original
bat virus. Because the mutations are acquired randomly by selection
there is no signature of a human gene jockey, but this is clearly a
virus still created by human intervention.”
In other words, Petrovsky believes that current experimental methods could have led to an altered virus that escaped.
Passaging, GOF research, and lab escapes
The experiment mentioned by Petrovsky
represents a class of experiments called passaging. Passaging is the
placing of a live virus into an animal or cell culture to which it is not
adapted and then, before the virus dies out, transferring it to another
animal or cell of the same type. Passaging is often done iteratively.
The theory is that the virus will rapidly evolve (since viruses have
high mutation rates) and become adapted to the new animal or cell type.
Passaging a virus, by allowing it to become adapted to its new
situation, creates a new pathogen.
The most famous such experiment was
conducted in the lab of Dutch researcher Ron Fouchier. Fouchier took an
avian influenza virus (H5N1) that did not infect ferrets (or other
mammals) and serially passaged it in ferrets. The intention of the
experiment was specifically to evolve a PPP. After ten passages the
researchers found that the virus had indeed evolved, to not only infect
ferrets but to transmit to others in neighbouring cages (
Herfst et al., 2012).
They had created an airborne ferret virus, a Potential Pandemic
Pathogen, and a storm in the international scientific community.
The second class of experiments that have frequently been the
recipients of criticism are GOF experiments. In GOF research, a novel virus is deliberately created, either by
in vitro
mutation or by cutting and pasting together two (or more) viruses. The
intention of such reconfigurations is to make viruses more infectious by
adding new functions such as increased infectivity or pathogenicity.
These novel viruses are then experimented on, either in cell cultures or
in whole animals. These are the class of experiments
banned in the US from 2014 to 2017.
Some researchers have even combined GOF and passaging experiments by using recombinant viruses in passaging experiments (e.g.
Sheahan et al., 2008).
Such experiments all require recombinant
DNA techniques and animal or cell culture experiments. But the very
simplest hypothesis of how Sars-CoV-2 might have been caused by research
is simply to suppose that a researcher from the WIV or the WCDCP became
infected during a collecting expedition and passed their bat virus on
to their colleagues or family. The natural virus then evolved, in these
early cases, into Sars-CoV-2. For this reason, even collecting trips
have their critics. Epidemiologist
Richard Ebright called them “
the definition of insanity“.
Handling animals and samples exposes collectors to multiple pathogens
and returning to their labs then brings those pathogens back to densely
crowded locations.
Since 2004, shortly after the original
SARS outbreak, researchers from the WIV have been collecting bat
coronaviruses in an intensive search for SARS-like pathogens (
Li et al., 2005). Since the original collecting trip, many more have been conducted (
Ge et al., 2013;
Ge et al., 2016; Hu et al., 2017;
Zhou et al., 2018).
Petrovsky does not mention it but Zheng-Li
Shi’s group at the WIV has already performed experiments very similar
to those he describes, using those collected viruses. In 2013
the Shi lab reported isolating an infectious clone of a bat coronavirus
that they called WIV-1 (Ge et al., 2013). WIV-1 was obtained by
introducing a bat coronavirus into monkey cells, passaging it, and then
testing its infectivity in human (HeLa) cell lines engineered to express
the human ACE2 receptor (Ge et al., 2013).
In 2014, just before the US GOF research
ban went into effect, Zheng-Li Shi of WIV co-authored a paper with the
lab of Ralph Baric in North Carolina that performed GOF research on bat
coronaviruses (
Menachery et al., 2015).
In this particular set of experiments the
researchers combined “the spike of bat coronavirus SHC014 in a
mouse-adapted SARS-CoV backbone” into a single engineered live virus.
The spike was supplied by the Shi lab. They put this bat/human/mouse
virus into cultured human airway cells and also into live mice. The
researchers observed “notable pathogenesis” in the infected mice
(Menachery et al. 2015). The mouse-adapted part of this virus comes from
a 2007 experiment in which the Baric lab created a virus called rMA15
through passaging (
Roberts et al., 2007).
This rMA15 was “highly virulent and lethal” to the mice. According to
this paper, mice succumbed to “overwhelming viral infection”.
In 2017, again with the intent of
identifying bat viruses with ACE2 binding capabilities, the Shi lab at
WIV reported successfully infecting human (HeLa) cell lines engineered
to express the human ACE2 receptor with four different bat
coronaviruses. Two of these were lab-made recombinant (chimaeric) bat
viruses. Both the wild and the recombinant viruses were briefly passaged
in monkey cells (Hu et al., 2017).
Together, what these papers show
is that: 1) The Shi lab collected numerous bat samples with an emphasis
on collecting SARS-like coronavirus strains, 2) they cultured live
viruses and conducted passaging experiments on them, 3) members of
Zheng-Li Shi’s laboratory participated in GOF experiments carried out in
North Carolina on bat coronaviruses, 4) the Shi laboratory produced
recombinant bat coronaviruses and placed these in human cells and monkey
cells. All these experiments were conducted in cells containing human or monkey ACE2 receptors.
The overarching purpose of such
work was to see whether an enhanced pathogen could emerge from the wild
by creating one in the lab. (For a very informative technical summary of WIV research into bat coronaviruses and that of their collaborators we recommend
this post, written by biotech entrepreneur Yuri Deigin).
It also seems that
the Shi lab at WIV intended to do more of such research. In 2013 and again in 2017 Zheng-Li Shi (with the assistance of a non-profit called the
EcoHealth Alliance) obtained a grant from the US National Institutes of Health (NIH). The most recent such grant proposed that:
“
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 humanized mice” (
NIH project #5R01Al110964-04).
It is hard to overemphasize that the
central logic of this grant was to test the pandemic potential of
SARS-related bat coronaviruses by making ones with pandemic potential,
either through genetic engineering or passaging, or both.
Apart from descriptions in their
publications we do not yet know exactly which viruses the WIV was
experimenting with but it is certainly intriguing that numerous
publications since Sars-CoV-2 first appeared have puzzled over the fact
that the SARS-CoV-2 spike protein binds with exceptionally high affinity
to the human ACE2 receptor “at least ten times more tightly” than the
original SARS (
Zhou et al., 2020;
Wrapp et al., 2020;
Wan et al., 2020;
Walls et al., 2020;
Letko et al., 2020).
This affinity is all the more remarkable
because of the relative lack of fit in modelling studies of the
SARS-CoV-2 spike to other species, including the postulated
intermediates like snakes, civets and pangolins (
Piplani et al., 2020). In this preprint these modellers concluded “This indicates that SARS-CoV-2 is a highly adapted human pathogen”.
Given the research and collection history
of the Shi lab at WIV it is therefore entirely plausible that a bat
SARS-like cornavirus ancestor of Sars-CoV-2 was trained up on the human
ACE2 receptor by passaging it in cells expressing that receptor.
How do viruses escape from high security laboratories?
Pathogen lab escapes take various forms.
According to the US Government Accountability Office, a US defense Department laboratory once “inadvertently sent live
Bacillus anthracis,
the bacterium that causes anthrax, to almost 200 laboratories worldwide
over the course of 12 years. The laboratory believed that the samples
had been inactivated.” In 2007, Britain experienced a foot and mouth
disease outbreak. Its’ origin was a malfunctioning waste disposal system
of a BSL-4 laboratory leaking into a stream from which neighbouring
cows drank. The disposal system had not been properly maintained (
Furmanski, 2014).
In 2004 an outbreak of SARS originating from the National Institute of
Virology (NIV) in Beijing, China, began, again, with the inadequate
inactivation of a viral sample that was then distributed to non-secure
parts of the building (
Weiss et al., 2015).
Writing for the Bulletin of The Atomic Scientists
in February 2019, Lynn Klotz concluded that human error was behind most
laboratory incidents causing exposures to pathogens in US high security
laboratories. While equipment failure was also a factor, of the 749
incidents reported to the US Federal Select Agent Programme between
2009-2015, Klotz concluded that 79% resulted from human error.
But arguably the biggest worry is
incidents that go entirely unreported because escape of the pathogen
goes undetected. It is truly alarming that a significant number of
pathogen escape events were uncovered only because investigators were in
the process of examining a completely different incident (Furmanski,
2014). Such discoveries represent strong evidence that pathogen escapes
are under-reported and that important lessons still need to be learned
(Weiss et al., 2015).
The safety record of the WIV
The final important data point is the
biosafety history of the WIV. The WIV was built in 2015 and became a
commissioned BSL-4 lab in 2018. According to Josh Rogin of the
Washington Post, US embassy officials visited the WIV in 2018. They
subsequently
warned their superiors
in Washington of a “serious shortage of appropriately trained
technicians and investigators needed to safely operate this
high-containment laboratory”.
And
according to VOA News,
a
year before the outbreak, “a security review conducted by a Chinese
national team found the lab did not meet national standards in five
categories.”
Credible reports from within China also
question lab biosafety and its management. In 2019, Yuan Zhiming,
biosecurity specialist at the WIV, cited the “challenges” of biosafety
in China. According to Zhiming: “several high-level BSLs have
insufficient operational funds for routine yet vital processes” and
“Currently, most laboratories lack specialized biosafety managers and
engineers.” He recommends that “We should promptly revise the existing
regulations, guidelines, norms, and standards of biosafety and
biosecurity”. Nevertheless, he also notes that China intends to soon
build “5-7” more BSL-4 laboratories (Zhiming, 2019).
And in February 2020, Scientific American
interviewed Zheng-Li Shi. Accompanying the interview was a photograph of
her releasing a captured bat. In the photo she is wearing a casual pink
unzipped top layer, thin gloves, and no face mask or other protection.
Yet this is the same researcher whose talks give “
chilling” warnings about the dire risks of human contact with bats.
All of which tends to confirm the original State Department assessment. As one anonymous “senior administration official”
told Rogin:
“The idea that it was just a totally
natural occurrence is circumstantial. The evidence it leaked from a lab
is circumstantial. Right now, the ledger on the side of it leaking from
the lab is packed with bullet points and there’s almost nothing on the
other side.”
The leading hypothesis is a lab outbreak
For all these reasons,
a lab escape is by far the leading hypothesis to explain the origins of Sars-CoV-2 and the COVID-19 pandemic.
The sheer proximity of the WIV and WCDCP labs to the outbreak and the
nature of their work represents evidence that can hardly be ignored. The
long international history of lab escapes and the biosafety concerns
from all directions about the labs in Wuhan greatly strengthen the case.
Especially since evidence for the alternative hypothesis, in the form
of a link to wild animal exposure or the wildlife trade, remains
extremely weak, being based primarily on analogy with SARS one (
Bell et al,. 2004;
Andersen et al., 2020).
“There was no viral isolate in the lab.
There was no cultured virus that’s anything related to SARS coronavirus
2. So it’s just not possible.”
Daszak made very similar claims on CNN’s
Sixty Minutes:
“There is zero evidence that this virus came out of a lab in China.”
Instead, Daszak encouraged viewers to blame “hunting and eating
wildlife”.
Daszak’s certainty is highly problematic
on several counts. The closest related known coronaviruses to Sars-CoV-2
are to be found at the WIV so a lot depends on what he means by
“related to”. But it is also dishonest in the sense that Daszak must
know that culturing in the lab is not the only way that WIV researchers
could have caused an outbreak. Third, and this is not Daszak’s fault,
the media are asking the right question to the wrong person.
As alluded to above, Daszak is the named
principal investigator on multiple US grants that went to the Shi lab at WIV. He is also a co-author on numerous papers with Zheng-Li Shi, including the 2013
Nature
paper announcing the isolation of coronavirus WIV-1 through passaging
(Ge et al., 2013). One of his co-authorships is on the collecting paper
in which his WIV colleagues placed the four fully functional bat
coronaviruses into human cells containing the ACE2 receptor (Hu et al.
2017). That is, Daszak and Shi together are collaborators and
co-responsible for most of the published high-risk collecting and
experimentation at the WIV.
If the Shi lab has anything to hide, it is not only the Chinese Government that will be reluctant to see an
impartial investigation proceed.
Much of the work was funded by the US taxpayer, channeled there by
Peter Daszak and the EcoHealth Alliance. Virtually every credible
international organisation that might in principle carry out such an
investigation,
the WHO,
the US CDC,
the FAO,
the US NIH, including
the Gates Foundation,
is either an advisor to, or a partner of, the EcoHealth Alliance. If
the Sars-CoV-2 outbreak originated from the bat coronavirus work at the
WIV then just about every major institution in the global public health
community is implicated.
But to solve many of these questions does
not necessarily require an expensive investigation. It would probably be
enough to inspect the lab notebooks of WIV researchers. All research
scientists keep detailed notes, for intellectual property and other
reasons, but especially in BSL-4 labs. As Yuan Zhiming
told Nature magazine in an article marking the opening of the facility in Wuhan: “We tell them [staff] the most important thing is that they report what they have or haven’t done.”
Meticulous lab records plus staff health
records and incident reports of accidents and near-accidents are all
essential components (
or should be) of BSL work. Their main
purpose
is to enable the tracking of actual incidents. Much speculation could
be ended with the public release of that information. But the WIV has
not provided it.
This is puzzling since the Chinese
government has a very strong incentive to produce those records.
Complete transparency would potentially dispel the gales of blame coming
its way; especially on the question of whether Sars-CoV-2 has an
engineered or passaged origin. If Zheng-Li Shi and Peter Daszak are
correct that nothing similar to Sars-CoV-2 was being studied there, then
those notebooks should definitively exonerate the lab from having
knowingly made an Actual Pandemic Pathogen.
Given the simplicity and utility of this step this lack of transparency suggests that there is something to hide. If so, it must be important. But then the question is: What?
A thorough investigation of the
WIV and its bat coronavirus research is an important first step. But the
true questions are not the specific mishaps and dissemblings of Drs Shi
or Daszak, nor of the WIV, nor even of the Chinese government.
Rather, the bigger question concerns the
current philosophy of pandemic prediction and prevention. Deep enquiries
should be made about the overarching wisdom of plucking and counting
viruses from the wild and then performing dangerous ‘what if’
recombinant research in high tech but fallible biosafety labs. This is a
reductionistic approach, we also note, that has so far failed to
predict pandemics and may never do so.
If this article was useful to you please consider sharing it with your networks.
Jonathan R. Latham PhD is co-founder and Executive Director of
the Bioscience Resource Project and the Editor of Independent Science
News. He holds a PhD in Virology and was a postdoctoral research
associate in the University of Wisconsin Department of Genetics.
Allison K. Wilson, PhD is co-founder and Science Director of the
the Bioscience Resource Project; Editor of the Bioscience Resource
Project website; Assistant Editor of Independent Science News; and a
contributor to the Poison Papers project. She holds a BA in Biology from
Cornell University, a doctorate in Molecular Biology and Genetics from
Indiana University, Bloomington, and was formerly a postdoctoral
research associate at the Fred Hutchinson Cancer Research Center,
Seattle and the John Innes Centre, Norwich, UK.
https://www.zerohedge.com/health/two-doctors-explain-why-covid-19-was-likely-lab-experiment
