Making sense of the world through data
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I agree with those 10 points. Although I would say that the first 9 are just confirmation of facts, some known since the Romans.
The last one to which I now agree comes as a terrible disillusion. If true, then some of the principles on which our Western civilization is based are wrong including the notion of "progress".
One
potential positive from the whole Covid-19 debacle is that we have
learned an incredible amount about the society in which we live. This will be crucial if we manage to stave off a descent into a nightmare future of techno-fascist slavery.
We
will have a new understanding of what our world has become and what we
would like it to be in the decades and centuries to come. And “we” means
we. While the majority have, apparently, learnt nothing at all from
what has happened, they will eventually catch up.
There is no way
that knowledge gained by a wide-awake 15% or 20% of the population will
not end up being shared by almost everyone. Once the truth is out, it
tends to stay out. As H.R. Haldeman so wisely put it, “you can’t put the
toothpaste back in the tube”.
Here are Ten Things We Have Learned During the Covid Coup.
1. Our political system is hopelessly corrupt.
Virtually all politicians are hopelessly corrupt. No political party can be trusted. They all can be, and have been, bought.
2. Democracy is a sham.
It has been a sham for a very long time. There will never be any real democracy when money and power amount to the same thing.
3. The system will stop at nothing to hold on to its power and, if possible, increase its levels of control and exploitation.
It has no scruples. No lie is too outrageous, no hypocrisy too nauseating, no human sacrifice too great.
4. So-called radical movements are usually nothing of the sort.
From
whatever direction they claim to attack the system, they are just
pretending to do so, and serve to channel discontent in directions which
are harmless to the power clique and even useful to its agendas.
5. Any “dissident” voice you have ever heard of through corporate media is probably a fake.
The system does not hand out free publicity to its actual enemies.
6. Most people in our society are cowards.
They
will jettison all the fine values and principles which they have been
loudly boasting about all their lives merely to avoid the slightest
chance of public criticism, inconvenience or even minor financial loss.
7. The mainstream media is nothing but a propaganda machine for the system...
...and
those journalists who work for it have sold their sorry souls, placing
their (often minimal) writing skills entirely at the disposition of
Power.
8. Police are not servants of the public...
...but
servants of a powerful and extremely wealthy minority which seeks to
control and exploit the public for its own narrow and greedy interests.
9. Scientists cannot be trusted.
They
will use the hypnotic power of their white coats and authoritative
status for the benefit of whoever funds their work and lifestyle. He who
pays the piper calls the tune.
Without context, data has no meaning. And so it is for the virus. What you hear in the media day after day is creating a context... but the one, some people want us to believe.
Notice how little food for thought is on display. How doubt is never an option, even from day one when answers are still murky. How diverging views are not offered, even from reputable sources.
We used to make fun of the Pravda and its predictable articles. But from the inside, it felt rather comfortable, for a while...
International Man: It’s been over a year since the COVID lockdowns started, and they have established a terrible precedent.
The International Energy Agency (IEA) has issued what they call a
“dire warning.” They say there will be a 5% increase in carbon emissions
as global economies reopen after the COVID shutdowns this year and that
it will be “anything but sustainable” for the environment. This implies
that the shutdowns have been good for the environment and that
returning to normal is bad.
There has also been a flood of articles in the mainstream media advocating for the use of lockdowns to address so-called climate change.
Do you think that the COVID lockdowns could become climate change lockdowns?
Doug Casey: Without exception, almost everything
they say in the above article is either an overt and intentional lie or
just factually incorrect. Things that are controversial at best are
presented as incontrovertible facts.
Let me first reiterate a few facts about COVID.
It’s hard to be sure because everything about it has become highly
politicized, but COVID itself seems no more serious than the Asian Flu,
Hong Kong Flu, Bird Flu, or Swine Flu that have come and gone in recent
decades and is not even remotely comparable to the Spanish Flu of 1918.
The numbers show that COVID is a risk for people over 70, the obese,
and the sick—but a medical non-problem for everyone else. That’s why the
average age of decedents is 80, even though it appears that everyone
who dies with the virus in their system is reported as a statistic—even
if they die of an auto accident or a heart attack. People with zero
symptoms are, nonetheless, listed as “cases” if they fail the overly
sensitive and very expensive PCR test.
We might ask: “What’s behind this insane flu hysteria—which is
radically restructuring the world’s political and economic landscapes?
And why now?” It seems very oddly coincidental with a few other
phenomena.
One is that the world is on the cusp of a fantastically devastating
depression due to the insane creation of currency units all over the
world by central banks. Is the phony COVID hysteria—and, yes, I believe
it’s 80% phony—being used as an excuse for the coming collapse, a way to
recuse those responsible for the insane economic policies causing the
depression? In other words, is the COVID hysteria an artificially
constructed force majeure used to distract from the real cause of the Greater Depression?
Another phenomenon is that the COVID hysteria has proved an excellent
way to scare the hell out of the public everywhere. Terrified people
demand “strong” leaders and strict controls. It’s a godsend for the kind
of people who go into government, anxious for any excuse to
self-aggrandize and take more power. “Never let a serious crisis go to
waste” has been an operating principle of powermongers since Day One.
And war is the most serious kind of crisis. Don’t forget what Randolf
Bourne said in 1914: “War is the health of the State.” But a real war
with a real enemy is always risky and may not always be feasible. So
powermongers create phony wars. In order to fight a war—any kind of
war—you need a State to organize and legitimize it.
The first major phony war in living memory was Lyndon Johnson’s war
on poverty—the poor lost. Then came Richard Nixon’s war on drugs. Then,
Baby Bush declared war on terror. They’re all still ongoing, but it
seems time for a two-front war. A war on global warming combined with a
war on COVID will be ultra-effective for breeding fear in Boobus americanus.
They say global warming can destroy the planet and COVID can kill
everyone. A sure-fire combination. They’re certain to get widespread
support from the usual suspects.
As a bonus, there’s a very high correlation between those who support
the COVID hysteria and those supporting the climate change agenda. And
both of them claim to have a new ally, “the science,” to sell the wars
to scared chimpanzees. Not just in the US, but everywhere in the world.
These two new wars will bring out the worst in everyone, everywhere.
Once you wash away their social veneer, the patina of civilization,
you find that humans are tribal. Put them in groups and they revert to
the lowest common denominator—they act like our anthropoid ancestors and
relatives. Get people excited, hooting and panting like chimps, and
they’re anxious to wage war on one thing after another. Imagine them as
the anthropoids contesting the watering hole in “2001: A Space Odyssey.” Conflict gives them a sense of solidarity and gives their lives meaning.
That’s especially true of humans with collectivist views, which is to
say, Leftists and busybodies. In today’s world, they include the
“woke,” social justice warriors, progressives, BLM supporters, Antifa,
and, of course, socialists, communists, Marxists, and all their fellow
travelers. They’re all Puritans motivated to control other humans. The
Left has always been that way, although it occasionally disguises itself
as pro-freedom to seduce the naive.
For instance, during the ’60s, the Left was pro-drugs. But that’s not
because they were for personal freedom or because they believed you
have the right to do what you want with your own body. They were
pro-drugs because widespread and irresponsible drug use can destroy
civilization.
Even when the Left seems to have good intentions, it’s not the case.
For instance, the Left was against the Vietnam War. It wasn’t because
they were anti-war, but because the war was against their fellow
communists. It was clever, in both cases showing up the Republicans as
dim-witted, unethical, and hypocritical.
Today the Left, in its various incarnations, is all for the COVID
lockdowns. Those will mutate into climate change lockdowns. Both will
act to compromise human freedom—even more than previous phony wars. It’s
ironic that the word “lockdown” used to be used mainly in prisons—it’s
rather indicative of where the world in general and the US, in
particular, are headed.
International Man: What are the chances climate lockdowns will work if and when governments try them?
Doug Casey: Climate change lockdowns will work. Why
shouldn’t they? COVID lockdowns worked wonderfully. They’ll work even
better because they’re not just about saving a few old, sick people but
the planet itself. People have been brainwashed into being green
eco-warriors for decades. The kids especially treat climate change and
Greenism as a new religion and take it much more seriously than what’s
left of Christianity. Yahweh is being replaced by Gaia.
People who can see that the wars on poverty, drugs, and terror were
really just stupid scams are totally on board with new scams, the wars
on the virus and climate change. They’re the same people making the same
phony do-gooder arguments. The popularity of Greta Thunberg is
indicative. She’s become an icon for the people who support this whole
syndrome. It’s disturbing because she’s so pathologically angry. People
don’t care that she’s mildly psychotic, highly indoctrinated, and
irrational. It’s a sign of how degraded society has become that an
autistic and deranged teenager can be an international hero.
I think it’s a natural segue to go from COVID lockdowns to climate
change lockdowns. Although the eco-warriors will eventually see COVID as
a good thing because they actually hate humans and would like to see
Gaia cleansed of them.
As I’ve said many times before, I see both COVID and Global Warming
as vastly overblown manias. Viruses go viral; everybody gets them and
becomes immune. That’s the end of the story unless the virus is
artificial and intended to cull the population. Anything is possible in a
world where technology is advancing exponentially while ethics are
going in reverse. Barring that, COVID will go away. Of course, they may
come up with a COVID 2.0, COVID 3.0, etc., as needed.
As for Global Warming, nobody knows its degree of reality for
sure—it’s all conjecture. But the danger of another ice age is at least
as great as continued global warming. The only thing for certain is that
the public, propagandized by the elite, can’t keep anything in context.
The last ice age only came to an end 12,000 years ago. And the globe
has been warming, more or less, ever since. The public is unaware that
there have been dozens of ice ages, lasting 50 to 100,000 years,
throughout the Pleistocene period. There’s no reason to believe that the
one that ended 12,000 years ago was the last one; we’re currently in an
interglacial. Past ice ages have lasted many millions of years.
International Man: The Guardian recently ran a piece titled “Why Genghis Khan was Good for the Planet.”
The article states:
“His murderous Mongol armies were responsible for the massacre of as
many as 40 million people. Even today, his name remains a byword for
brutality and terror. But boy, was Genghis green.”
It seems to imply that population reduction through mass murder was good for the planet. What are your thoughts on this?
Doug Casey: That’s a great quote from the article.
The abhorrent psychology of its writer borders on the criminal. He
goes on to say, “It’s an intriguing notion, certainly”— meaning that he
actually thinks it might not be a bad idea to wipe out a meaningful
percentage of the population.
I hope he sacrifices himself for the climate, although that’s
unlikely since he likely considers himself one of the elite who should
be preserved because he’s ideologically pure and politically reliable.
These people have Pol Pot’s psychological makeup. In Cambodia during
the ’70s, anybody who wasn’t a manual laborer with callused hands was
liquidated—that’s what they did with roughly a quarter of the
population.
Pol Pot, Stalin, and Mao, as well as Genghis Kahn, are idols for
these people because they all think the same way. They actually hate the
human race. And people are so stupid that they laud their destroyers.
I’ve got news for them: Life is already nasty, brutish, and short
enough. We don’t need political criminals making it worse.
International Man: The COVID hysteria has changed
the way governments react to a real or manufactured global crisis. Now
that this precedent has been established, what do you see happening next?
Doug Casey: It’s shaping up like the 1930s in
Germany, when they led the way with a disastrous form of statism called
National Socialism. It was almost as bad as Communism under Stalin—and
it seems like the Germans might be doing it again. They’ve just passed a law
the “Infection Protection Act” instituting nightly restrictions, school
closures, and stricter regulations for businesses. COVID provides an
excellent cover and excellent justification for the imposition of a
police state. Remember that once these governments pass a law, they
rarely ever repeal them. Those laws have to be financed with new taxes
and enforced by new agencies. The negative effect is cumulative and
compounding.
International Man: While the US and other Western
countries are committing economic and cultural suicide, what do you
think will happen to countries like China, Russia, Brazil, and others?
Will they follow the West or go their own ways?
Doug Casey: It’s hard to say what’s actually
happening in a lot of countries because the quality of news reporting is
so abysmal. But the trend is worldwide.
When it comes to climate change, these countries laugh at Westerners
for their naivete, stupidity, and self-destructive tendencies. They
don’t take it seriously. It’s another reason why the next century
belongs to China.
The same is true of Russia, which, for all of its faults, is
basically an anti-woke country. It’s been said—correctly—that there are
more communists in American universities than there are in all of
Russia.
Regarding investment advice, I’m much more interested in Chinese and
East Asian stock markets than in Western stock markets. The same is true
of Russian and East European stock markets because they haven’t been
infected by the virus of wokeism. They had a serious bout of it from the
’30s through the ’90s, and it’s given them some immunity. Plus, their
markets aren’t in a bubble, like those in the US especially. The
countries that have hooked their car to the US choo-choo train are going
to go over the cliff with the US.
It’s not as if China and Russia are models of intelligence and probity, but they’re acting far more intelligently than the US.
Editor’s Note: We’ve seen governments institute the strictest
controls on people and businesses in history. It’s been a swift
elimination of individual freedoms.
Based on this article, I do not know if we should halt the vaccine campaign, (the CDC has decided against halting) but at the very least, it should be restricted to the most vulnerable people so that we are certain that the benefits out-weight the risks.
In a public comment to the CDC, molecular biologist and toxicologist
Dr. Janci Chunn Lindsay, Ph.D., called to immediately halt Covid vaccine
production and distribution. Citing fertility, blood-clotting concerns
(coagulopathy), and immune escape, Dr. Lindsay explained to the
committee the scientific evidence showing that the coronavirus vaccines are not safe.
On April 23, 2021, the CDC’s Advisory Committee on Immunization Practices held a meeting in Atlanta, Georgia. The focus of this ACIP meeting was
blood clotting disorders following Covid vaccines. Dr. Janci Chunn
Lindsay spoke to the CDC during the time set aside for public comment.
You can listen to her testimony on YouTube here (for now, anyway. If this link goes viral, YouTube will likely censor it).
Molecular Biologist and Toxicologist Calls to Halt Covid Vaccine
Hi, my name is Dr. Janci Chunn Lindsay. I hold a doctorate in
biochemistry and molecular biology from the University of Texas, and
have over 30 years of scientific experience, primarily in toxicology and
mechanistic biology.
In the mid-1990s, I aided the development of a temporary human
contraceptive vaccine which ended up causing unintended autoimmune
ovarian destruction and sterility in animal test models. Despite efforts
against this and sequence analyses that did not predict this.
I strongly feel that all the gene therapy vaccines must be halted immediately due to safety concerns on several fronts.
Janci Chunn Lindsay: Covid vaccines could induce cross-reactive
antibodies to syncytin, and impair fertility as well as pregnancy
outcomes
First, there is a credible reason to believe that the Covid
vaccines will cross-react with the syncytin and reproductive proteins in
sperm, ova, and placenta, leading to impaired fertility and impaired
reproductive and gestational outcomes.
Respected virologist Dr. Bill Gallaher, Ph.D., made
excellent arguments as to why you would expect cross reaction. Due to
beta sheet conformation similarities between spike proteins and
syncytin-1 and syncytin-2.
I have yet to see a single immunological study which disproves this.
Despite the fact that it would literally take the manufacturers a single
day to do these syncytin studies to ascertain this [once they had serum
from vaccinated individuals]. It’s been over a year since the
assertions were first made that this [the body attacking its own
syncytin proteins due to similarity in spike protein structure] could
occur.
Pregnancy losses reported to VAERS lead to demand to halt Covid vaccine
We have seen 100 pregnancy losses reported in VAERS as of April 9th.
And there have [also] been reports of impaired spermatogenesis and
placental findings from both the natural infection, vaccinated, and
syncytin knockout animal models that have similar placental pathology,
implicating a syncytin-mediated role in these outcomes.
Additionally, we have heard of multiple reports of menses irregularities in those vaccinated. These must be investigated.
We simply cannot put these [vaccines] in our children who are at
.002% risk for Covid mortality, if infected, or any more of the
child-bearing age population without thoroughly investigating this
matter.
[If we do], we could potentially sterilize an entire generation.
Speculation that this will not occur and a few anecdotal reports of
pregnancies within the trial are not sufficient proof that this is not impacting on a population-wide scale.
Covid vaccine causes blood disorders
Secondly, all of the gene therapies [Covid vaccines] are causing coagulopathy. [Coagulopathy when the body’s blood clotting system is impaired.] This is not isolated to one manufacturer. And this is not isolated to one age group.
As we are seeing coagulopathy deaths in healthy young adults with no secondary comorbidities.
There have been 795 reports related to blood clotting disorders as of
April 9th in the VAERS reporting system, 338 of these being due to
thrombocytopenia.
There are forward and backward mechanistic principles for why this is
happening. The natural infection is known to cause coagulopathy due to
the spike protein. All gene therapy vaccines direct the body to make the
spike protein. Zhang et al in [a scientific paper published in the Journal of Hematology & Oncology]
in September 2020 showed that if you infuse spike protein into mice
that have humanized ACE-2 receptors on blood platelets that you also get
disseminated thrombosis.
Spike protein incubated with human blood in vitro also caused blood
clot development which was resistant to fibrinolysis. [Fibrinolysis is
the body’s process of breaking down blood clots]. The spike
protein is causing thrombocytic events, which cannot be resolved through
natural means. And all vaccines must be halted in the hope that they
can be reformulated to guard against this adverse effect.
Third, there is strong evidence for immune escape—
At this point in her oral testimony, Dr. Janci Chunn Lindsay was
interrupted by a man’s voice: “Thank you for your comment, your time has
expired.”
I reached out to Dr. Janci Chunn Lindsay to find out what else she
had wanted to share with ACIP, in addition to her concerns over
fertility and blood-clotting disorders. She sent me back her third
point, which she submitted as written testimony.
Third, there is strong evidence for immune escape,
and that inoculation under pandemic pressure with these leaky vaccines
is driving the creation of more lethal mutants that are both newly
infecting a younger age demographic, and causing more Covid-related
deaths across the population than would have occurred without
intervention. That is, there is evidence that the vaccines are making the pandemic worse.
It is clear that we are seeing a temporal immune depression immediately following the inoculations [see World Meter Global Covid deaths
counts following inoculation dates] and there are immunosuppressive
regions on spike proteins, as well as Syn-2, that could be likely
causing this, through a T-cell mediated mechanism. If we do not stop
this vaccine campaign until these issues can be investigated, we may see
a phenomenon such as we see in chickens with Marek’s disease.
We have enough evidence now to see a clear correlation with increased Covid deaths and the vaccine campaigns. This
is not a coincidence. It is an unfortunate unintended effect of the
vaccines. We simply must not turn a blind eye and pretend this is not
occurring. We must halt all Covid vaccine administration immediately,
before we create a true pandemic that we cannot reign in.
MIT scientist also concerned about blood-clotting, fertility issues
Stephanie Seneff, Ph.D., an expert in protein synthesis, believes
that Dr. Lindsay’s hypothesis is correct. “I absolutely share these
concerns,” Dr. Seneff, who is a senior research scientist at MIT, wrote
to me in a sobering email.
“The potential for blood clotting disorders and the potential for
sterilization are only part of the story. There are other potential
long-term effects of these vaccines as well, such as autoimmune disease
and immune escape, whereby the vaccines administered to
immune-compromised people accelerate the mutation rate of the virus so
as to render both naturally acquired and vaccine-induced antibodies no
longer effective.”
Like Dr. Lindsay, Dr. Seneff believes we need to immediately halt
Covid vaccine campaigns. “This massive clinical trial on the general
population could have devastating and irreversible effects on a huge
number of people,” Seneff explains.
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 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 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.”
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, said in March 2020.
A second statement that had enormous influence in shaping public attitudes was a 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 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 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
genetically engineering the spike protein of a mouse coronavirus so that it would attack only cats.
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. 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,” 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?
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 humanized mice.”
“We will use S protein sequence data, 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 conspiracy theory invented by China-bashers.
On December 9, 2019, before the outbreak of the pandemic became generally known, Daszak gave an 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….
“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 interview.
The safety arrangements at the Wuhan Institute of Virology. Daszak was possibly unaware of, or perhaps he knew all too well, the 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 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 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 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 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 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 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 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 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,” 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.
“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 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,” 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 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.
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 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 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 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 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 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 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 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 optimized for the human receptor, leading him to infer the virus might have been generated in a laboratory. Alina Chan published a 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 wrote. Kudos too to Robert Redfield, former director of the Centers for Disease Control and Prevention, who 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 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 №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 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.
Nicholas
Wade is a science writer, editor, and author who has worked on the
staff of Nature, Science, and, for many years, the New York Times