The largest newspaper in Norway, VG, recently ran the following top story in its online edition:
Using the headline “- May become the largest scandal of all time”, with the subtitle "Was the world deceived about covid-19?" they have created a story where Sigrid Bratlie, who has a PhD in molecular biology, is the primary source.
Bratlie is also a senior advisor at the think tank Langsikt, which earlier this summer published a paper arguing that the lab-leak hypothesis is the most plausible explanation for the origin of the SARS-CoV-2 virus and the COVID-19 pandemic.
What evidence do we have?
But before we take a closer look at this note, which reviews Bratlie's key arguments for why she now feels 80-90% confident that SARS-CoV-2, the virus that causes COVID-19 disease and the pandemic that really kicked off early in 2020, was laboratory-created, it's important to point out the following:
Since 2020, when it was first discussed whether the virus had a natural origin (zoonotic, i.e. transmitted from animals to humans) or originated from a research laboratory in Wuhan, China, not a single piece of evidence has emerged in favour of the lab-leak hypothesis!
Although new debates have flared up at regular intervals in 2021, 2022, 2023 and now 2024, often kicked off by an opinion piece or newspaper article on the topic, where the proponents of lab-leak declare "victory" in the sense that they believe they have now won the debate, no new evidence has actually emerged. It's all rhetoric and speculation wrapped up in new clothes time and time again. There is zero substance, and only exciting packaging.
On the other hand, the evidence has gradually become stronger and stronger in favour of a natural origin. Several important studies have been published in favour of a zoonotic origin, and an overwhelming majority of virologists and experts in the field believe that this is clearly the most likely.
You wouldn't think so if you only followed the more superficial "vibe"-based debate in podcasts, blogs and newspaper articles!
Conspiratorial and dangerous?
Before we delve into the claims of the think tank Langsikt, it's also worth pointing out how damaging such a VG article is. An article was recently published in the Journal of Virology discussing precisely this:
The authors emphasise that promoting the lab-leak hypothesis in the way that VG and Bratlie are now doing, for example, is detrimental to confidence in the scientific process and leads to dangerous hatred and attacks on scientists. They begin with:
Science is humanity's best insurance against threats from nature, but it is a fragile enterprise that must be nourished and protected. The preponderance of scientific evidence indicates a natural origin for SARS-CoV-2. Yet, the theory that SARS-CoV-2 was engineered in and escaped from a lab dominates media attention, even in the absence of strong evidence. We discuss how the resulting anti-science movement puts the research community, scientific research, and pandemic preparedness at risk.
Spreading unsubstantiated allegations and hypotheses, as well as smearing named scientists and government officials, is not a harmless game. It leads to real harm, conspiracy thinking, and a fear among scientists to speak out. Today, a majority of Americans believe that the virus originated from a leak, and scientists who try to say otherwise are hounded and threatened. We don't want this kind of situation in Norway, so it's very unfortunate that VG is publishing piece so lacking in nuance.
Note that the article in the Journal of Virology has a title that includes "without evidence", because that is the central point here. There is still no evidence for a leak as the origin of the covid pandemic.
This is also why the hypothesis is often characterised as a conspiracy theory. Not because it's a crazy theory that requires a gigantic cover-up on a par with denying the moon landings or global warming. But because the arguments used are predominantly identical to those used to support various conspiracy theories:
- The lab-leak hypothesis is not based on evidence, but on what is known as "anomaly hunting", i.e. the search for "anomalies" or missing pieces of the puzzle that may give rise to doubt. And where there is doubt, exciting explanatory models can be introduced with great appeal to those who find the truth too boring and sobering.
- Another reason why the hypothesis appears conspiratorial is that there is a significant degree of cherry-picking of data, i.e. highlighting claims that speak in favour of lab-leak and ignoring the stronger arguments or data that speak against it. There is an extreme focus on questions about things for which we lack evidence, often because such evidence is impossible to produce, and total denial of some key pieces of evidence that speak very strongly in favour of the virus having a natural origin. We will come back to these in more detail later.
As we will see in this blog post, Bratlie is not a conspiracy theorist. But the way she argues largely overlaps with conspiratorial argumentation.
What do I think?
Personally, I think a leak is much more exciting than natural origin. My personality favours the idea of a lab-leak, because I also love things that are exciting, tangible and "simple". However, a critical review of the evidence leads me to conclude that a natural origin is most likely. Which is kind of a bummer.
It is important to re-emphasise that the lab-leak hypothesis is not in itself a conspiratorial idea, and it is unfortunate that much of the early debate classified supporters of the lab-leak hypothesis as conspiracy theorists. It's also unfortunate that the debate was silenced to some extent, although that "silencing" was considerably less extensive than many would have it.
Personally, I feel that the lab-leak hypothesis has received much more publicity and been debated much more widely and loudly than the "boring" natural origins hypothesis. So I wonder why some people might feel that there has been some censorship or “cancelling” going on.
Yes, Facebook briefly censored posts about the lab-leak hypothesis, which was hardly wise, but understandable in the heat of the pandemic where anti-vaccine rhetoric and other conspiracy theories flooded the discourse with noise. But beyond that, I'd like to hear from a single person who doesn't feel they've been able to discuss the lab-leak hypothesis freely. I don't think that person exists.
Langsikt and Alina Chang
So over to the Langsikt memo. There are many arguments in the paper, and I do not have the opportunity to review absolutely all of them, but I hope that some examples can show that the article is not particularly balanced, fair or convincing.
First, it should be pointed out that many of the arguments in the Langsikt paper coincide with an op-ed in the New York Times by Dr Alina Chang, "Why the Pandemic Probably Started in a Lab, in 5 Key Points", from 3 June 2024. Dr Chang is a molecular biologist and co-author of the book "Viral: The Search for the Origin of Covid-19", which the opinion piece is largely a summary of.
Her five points are well refuted by perhaps the world's foremost vaccine researcher, Dr Paul Offit, in a counter-post he wrote on 24 June on his Substack blog. You should read it:
In addition, the five points are discussed by some virologists in the podcast This Week in Virology, a discussion that can also be viewed here:
Offit's blog post and the podcast episode already refute several of the claims in the Langsikt article, so I recommend reading and watching/listening to these.
The article from the Journal of Virology, mentioned earlier, also discusses much of this, and refers to several scientific references that refute Chang's claims. In an extract from the article we can read:
There is currently no verified scientific evidence to support the lab leak hypothesis. Moreover, the assertions in the Chan article have been challenged by a growing body of scientific data supporting the zoonosis hypothesis (4, 5, 8,10-12). Dr. Chan's five key points are well refuted by the data, as discussed in publicly accessible platforms by Dr. Paul Offit, in the science-based podcast This Week in Virology (TWiV), and in the scientific literature (13, 14). Further, based on the scientific evidence and investigations described in a declassified report, the majority of the US Intelligence community concur with the zoonotic origin of SARS-CoV-2 being more likely. These reports do not identify high confidence evidence for a research-related incident, find no evidence that WIV possessed SARS-CoV-2 or a closely related virus before the end of December 2019, and conclude that it is unlikely that SARS-CoV-2 was engineered (6, 14, 15).
The Langsikt memo
The Langsikt memo discusses the scientific strengths and weaknesses of the zoonosis hypothesis. In the section on the scientific weaknesses, the three key scientific articles that are often cited in favour of the zoonosis theory are discussed. The three articles are:
- The proximal origin of SARS-CoV-2 (Andersen et al, Nature, 2020)
The article argues that it is unlikely that SARS-CoV-2 has arisen through laboratory manipulation of a related SARS-CoV-like coronavirus. Instead, the researchers propose two likely scenarios for the origin of SARS-CoV-2:
1) natural selection in an animal host before transmission to humans, and
2) natural selection in humans after transmission from animals. - The Huanan Seafood Wholesale Market in Wuhan was the early epicentre of the COVID-19 pandemic (Worobey et al, Science, 2022)
The paper shows that the Huanan market in Wuhan was the early epicentre of the COVID-19 pandemic through trade in live wild animals. Some of the evidence they have found is:
- The earliest known COVID-19 cases in December 2019 were geographically centred around Huanan market.
- Live mammals known to be susceptible to SARS-related coronaviruses, such as raccoon dogs, hog badgers, and red foxes, were sold at Huanan market in November 2019.
- SARS-CoV-2 positive environmental samples were spatially associated with areas of the market where live mammals were sold.
- Both SARS-CoV-2 lineage A and B were geographically associated with the Huanan market, suggesting that the market was the epicentre of the pandemic, not just a superspread event. - The molecular epidemiology of multiple zoonotic origins of SARS-CoV-2 (Pekar et al, Science, 2022)
The study shows that SARS-CoV-2 likely had at least two separate zoonotic transmissions to humans in November 2019, resulting in the two main lineages A and B of the virus. It concludes that SARS-CoV-2 was likely introduced into humans multiple times as a result of sustained contact with an animal reservoir and that there was limited cryptic spread prior to December 2019.
Referring to the first article from 2020, Bratlie writes:
One weakness of the article is that there is no experimental data to support the conclusions, but is based on the authors' own professional judgements of the genetic sequence compared to other viral sequences. Such analyses are very sensitive to the underlying assumptions. And the analysis is based on a number of questionable assumptions.
Here she commits one of the common mistakes in the Covid debate. She argues on the basis of weaknesses in the earliest data we had at the very beginning of the pandemic, and ignores the fact that we have gained an enormous amount of knowledge in the four years since then.
The criticism could have been relevant if most experts agreed with her. But as we've seen, most virologists seem to support these assessments made in Nature, even four years later. The fact that Bratlie herself disagrees is not so relevant as most experts in the field do not seem to support her views.
Unfiltered Perception is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.
But the biggest problem is that she engages in what is known as "JAQing off", where JAQ stands for Just Asking Questions, which is the primary rhetorical tool used by conspiracy theorists. As previously mentioned, it's "anomaly hunting", while at the same time she fails to mention all the arguments that speak against the scepticism she herself has towards the arguments in Nature.
For example, there is widespread agreement that SARS-CoV-2 has approximately 1,200 base pairs (nucleotide differences) that differ from the closest virus in the laboratory, RaTG13, which was found in a horseshoe bat (Rhinolophus affinis). RaTG13 has 96.1% nucleotide similarity to SARS-CoV-2. If the virus is genetically modified, it makes no sense whatsoever to randomly change 1,200 base pairs scattered around the virus where you will have no control over the effects of this. Genetic modification of viruses usually involves targeted changes to specific genes or regions, in this case most likely in the spike protein, not random changes scattered throughout the genome.
This alone points heavily in the direction that the virus cannot be "man-made", because it is not consistent with what we would have seen in practice if it were.
Furin Cleavage Site
Bratlie also points to perhaps the most important difference between SARS-CoV-2 and other coronaviruses found in nature, namely the presence of a so-called Furin Cleavage Site. She writes:
The biggest weakness of the paper, however, is that it fails to provide a good explanation for the most mysterious feature of SARS2: a genetic element called a Furin Cleavage Site (FCS) that allows the virus to enter cells (infect) much more efficiently than without the element. There is not a single known natural SARS coronavirus (among thousands) that has such an FCS.
At this point, it may be worth reminding readers that coronaviruses as a class of viruses are nothing new. It is a common type of virus that can cause colds and other respiratory infections. It has also previously caused more serious illnesses such as SARS (discovered in 2002 and caused by the SARS-CoV coronavirus) and MERS (discovered in 2012 and caused by the MERS-CoV coronavirus). SARS-CoV is now often referred to as SARS1, as opposed to SARS-CoV-2, which is often abbreviated to SARS2, and which gave us COVID-19.
What Bratlie again fails to mention is that if you were to genetically modify a coronavirus to get an FCS, it is remarkable that the virus has 1,200 other base pairs that deviate from the nearest natural virus in the laboratory, but no such deviations in FCS. It seems extremely unlikely that random mutations would occur in the virus anywhere other than the FCS.
She continues:
As we describe below, this genetic element raised suspicions among the authors of the article that the virus could have been genetically modified by researchers. Yet that possibility is not even discussed in the article. Nor is there any explanation of how it could have arisen naturally.
No, they gave no explanation in 2020. But since then, many articles have been published explaining just that.
We know that such Furin Cleavage Sites have occurred many times in other natural coronaviruses through various mechanisms that are well known. In an article from 2021, "Furin cleavage sites naturally occur in coronaviruses", they write:
The spike protein is a focused target of COVID-19, a pandemic caused by SARS-CoV-2. A 12-nt insertion at S1/S2 in the spike coding sequence yields a furin cleavage site, which raised controversial views on origin of the virus. Here we analysed the phylogenetic relationships of coronavirus spike proteins and mapped furin recognition motif on the tree. Furin cleavage sites occurred independently for multiple times in the evolution of the coronavirus family, supporting the natural occurring hypothesis of SARS-CoV-2.
Several other scientific papers also conclude that the existence of FCS in coronaviruses appears to be a natural, evolutionary process, e.g. this one: The Emergence of the Spike Furin Cleavage Site in SARS-CoV-2.
Another important point that Bratlie mysteriously fails to mention is that if such an FCS was "inoculated" into the virus in a laboratory, and the virus was grown there, then the FCS would have gradually evolved out of the virus because it gives the virus no advantage when it does not replicate in humans. However, FCS was already found in the viruses in the earliest cases of infection in humans. This contradicts the hypothesis that the FCS in SARS2 was artificially created.
In addition, a laboratory-created variant of the coronavirus would have been manipulated to infect, for example, mice very easily, as it would be in such laboratory animals that the effects of the virus could be studied. But the earliest samples of SARS-CoV-2 that we have show no signs of having been adapted specifically for laboratory mice. This also contradicts the hypothesis that the virus was created or manipulated in a laboratory.
Bratlie also oversimplifies the meaning of FCS. It has recently been discovered that the presence of FCS in the virus spikes is not in itself enough to make the virus more infectious in humans. It's more complicated than that, and we didn't have this knowledge pre-2020. Ergo, it is highly unlikely that anyone could have genetically modified or engineered a virus with these properties without knowing what was needed.
These and several other counter-arguments against laboratory-created viruses are summarised in the article "A Critical Analysis of the Evidence for the SARS-CoV-2 Origin Hypotheses".
Was the Huanan market the epicentre?
Regarding the weaknesses in the second scientific article Bratlie highlights, she writes, among other things:
One problem with article two, which finds that most cases of infection come from the Huanan market, is that we cannot trust the data on registered cases of infection. To be registered as infected early in the pandemic, the person had to have a link to the Huanan market. In addition, the Chinese authorities focused their surveillance on the market. It is therefore likely that cases of infection that were not linked to the market were overlooked, as the World Health Organization has pointed out.
This point is also discussed in the podcast episode/video from TWIV at the top of the blog post. But what Bratlie doesn't say is that there have been many different analyses of this, all of which point out that the first cases of infection were linked to the wet market in Wuhan. For example, the cases of infection where the person demonstrably visited the market are from people living in different locations relative to the market itself. On the other hand, the cases of infection in people who did not visit the market are only in people who live geographically close to the market.
This is a strong signal that the infection originated in the wet market and spread from there.
In addition, there is no similar pattern if the Wuhan Institute of Virology is placed at the centre. There are no cases of infection that can be linked to the laboratory, which is odd if the virus first emerged there.
Or do such cases exist? Bratlie continues:
If you try to find out where an outbreak started and you select many more cases of infection from one of the locations, the result will be as skewed as the selection method. The researchers' statistical analysis was also recently disputed by statisticians. They argued that the premises for the analyses were wrong, and that an improved analysis of the geographical spread of the cases showed that it was just as likely, based on the data, that the cases were linked to the Wuhan Institute of Virology as to the market.
Here she refers to a study by Stoyan and Chiu from January 2024. However, she does not mention that this has again been disputed in the article "Confirmation of the centrality of the Huanan market among early COVID-19 cases Reply to Stoyan and Chiu (2024)" where they write:
The centrality of Wuhan's Huanan market in maps of December 2019 COVID-19 case residential locations, established by Worobey et al. (2022a), has recently been challenged by Stoyan and Chiu (2024, SC2024). SC2024 proposed a statistical test based on the premise that the measure of central tendency (hereafter, "centre") of a sample of case locations must coincide with the exact point from which local transmission began. Here we show that this premise is erroneous. SC2024 put forward two alternative centres (centroid and mode) to the centre-point which was used by Worobey et al. for some analyses, and proposed a bootstrapping method, based on their premise, to test whether a particular location is consistent with it being the point source of transmission.
We show that SC2024's concerns about the use of centre-points are inconsequential, and that use of centroids for these data is inadvisable. The mode is an appropriate, even optimal, choice as centre; however, contrary to SC2024's results, we demonstrate that with proper implementation of their methods, the mode falls at the entrance of a parking lot at the market itself, and the 95% confidence region around the mode includes the market. Thus, the market cannot be rejected as central even by SC2024's overly stringent statistical test. Our results directly contradict SC2024's and - together with myriad additional lines of evidence overlooked by SC2024, including crucial epidemiological information - point to the Huanan market as the early epicentre of the COVID-19 pandemic.
Bratlie is very keen to cherry-pick studies and arguments in favour of the lab-leak hypothesis, but consistently fails to include data pointing in the opposite direction.
It is particularly odd that she points to a critique of a statistical analysis used by Worobey et al in their original study, which provided strong evidence that the virus had the wet market as its epicentre, but fails to see this in the context of many other data (serological, physiogenetic, epidemiological) that support this, and now also other documentation that suggests that the criticism she highlights is actually wrong.
In this context, it is worth noting that while Langsikt's paper tries to appear balanced by having a section on the zoonosis hypothesis and one on the lab-leak hypothesis, and then showing the weaknesses and strengths of both, she "forgets" to include the weaknesses of the lab-leak hypothesis. We only find that part in the discussion of the zoonosis hypothesis. Not very balanced after all.
Lines A and B
When we move on to the third scientific article Bratlie points out weaknesses in, she writes:
The third article, which claims to explain the two SARS variants by the fact that there were two cases of infection on the market, also has several weaknesses. It has been revealed that the authors of the original paper excluded data that would have disproved their own hypothesis (gene sequences showing that line B had evolved from line A and not separately), without providing a convincing justification.
The authors of the original Pekar et al study did not "exclude data" in an attempt to hide it and manipulate the results, as Bratlie more than insinuates in her wording. They have provided good justifications for why certain data have been excluded from the analyses.
However, it is true that the authors have been criticised for this by other researchers who believe that this has had an unfortunate impact on the conclusions.
What Bratlie again fails to mention is that these intermediate forms of lines A and B, which critics believe Pekar et al excluded, are very rare. Both lines A and B were detected in samples from the wet market, supporting the theory that this was the origin of the pandemic. And line B was actually detected before A in humans, and B was more prevalent than A early in the pandemic, suggesting that they have evolved in parallel rather than that B has evolved from A.
The two lines are only separated by two specific nucleotide substitutions that have been present from the start, which also argues against B having evolved from A. It is therefore most likely that both came from a common ancestor, A0, rather than B originating from A.
Once again, we see that Bratlie finds a study that says what she wants, but fails to see the big picture and the sum of all the evidence that nevertheless suggests that the pandemic started with two separate transmission events from animals to humans at the wet market in Wuhan.
Coding errors and exaggerations
The tendency to distort the facts in favour of lab-leak is also evident in her writing:
In addition, coding errors have been uncovered in the model they had used in the analysis. When the error was corrected, the probability that the findings corresponded to real patterns in the data fell to a low level. After pressure, this was corrected in an erratum to the Science article.
This is misleading. Admittedly, an error in the code was uncovered, and an erratum was later published here. But it did not change any conclusions in the article. It reduced the probability that the infection had started in at least two separate cases rather than one from 99 per cent to 97 per cent, not from "very likely" to "a low level", as Bratlie describes it.
The change was thus marginal, and as the authors write in their erratum:
The text now represents the corrected Bayes factors and topology frequency (Fig. 2C), which still favours the multiple introduction scenario.
A totally irrelevant criticism put forward by Bratlie, apparently in an attempt to weaken the credibility of one of the central studies in favour of zoonotic origin.
Host animals that do not exist
Bratlie continues with more arguments against the zoonosis theory:
No host animal has been found for SARS2 infection, as one would expect
This is hardly surprising as the Chinese authorities closed the wet market, disinfected the area and slaughtered and burned all the animals there in an attempt to stop potential infection on 1 January 2020. Or perhaps to remove evidence, wise of damage after the SARS1 outbreak that also came from animals in a wet market.
Either way, when the animals from the wet market were not preserved, it is of course difficult to find infection in host animals. Bratlie hopes readers will think that these animals from the wet market have been examined without finding traces of SARS2 in them. But the truth is that there were no host animals to test when this became scientifically relevant. Consequently, the evidence Bratlie is looking for cannot be found either.
Ideally, we would have liked the Chinese authorities to have frozen and preserved some specimens that could later be tested, but this was not done. This makes Bratlie's criticism seem somewhat odd and "tactical" rather than enlightening.
On the other hand, clear traces of SARS-CoV-2 have been found on surfaces and waste residues in the very area of the wet market where the most relevant infectious animals were kept.
Zoonosis unlikely in Wuhan?
Bratlie writes:
Zoonosis was very unlikely in Wuhan
Really? As early as 2014, a virologist visited the wet market in Wuhan and took pictures of some of the cages because he already realised then that this is a perfect place for zoonotic transmission to occur:
What's even weirder - it turns out that one of the co-authors of the study, Eddie Holmes, had been taken to the Huanan market several years before the pandemic and shown raccoon dogs in one of the stalls. He was told, "This is the kind of place that has the ingredients for cross-species transmission of dangerous pathogens."
So he clicks photos of the raccoon dogs. In one photo, the raccoon dogs are in a cage stacked on top of a cage with some birds in it.
And at the end of our sleuth work, we checked the GPS coordinates on his camera, and we find that he took the photo at the same stall, where five samples tested positive for SARS-CoV-2.
Molecular clock
She goes on to write:
The evolutionary clock of the virus suggests that the infection occurred before the Huanan outbreak
The first cases linked to the Huanan wetland in Wuhan were detected in mid-December 2019, but the virus may have existed in humans before this, perhaps as early as October.
Simulations show that in around 70 per cent of cases in a densely populated megacity like Wuhan, animal-to-human transmission would die out within a few days without becoming an epidemic. In more rural areas, the infection dies out quickly in almost 100% of cases.
So it's possible that humans were repeatedly exposed to the virus before it finally "took hold" and was able to infect enough others to finally become an epidemic, and later a pandemic.
But this point from Bratlie says little about whether SARS-CoV-2 originally came from a laboratory or from animals, and speaks more in favour of repeated infection via the wet market than a single event in a laboratory.
Infected researchers at the laboratory?
Bratlie then goes on to discuss the arguments in favour of a laboratory leak. She first writes about "Suspected infection at the Wuhan Institute of Virology". Here she writes:
The outbreak at Huanan market started in December 2019. But there have been stories of infections as early as September 2019 (although it has been difficult to identify infections from the early phase of the outbreak). The US State Department says it has reason to believe that three researchers at the Wuhan Institute of Virology were infected in November 2019.
Infected with what? Bratlie wants you to believe that they were infected with SARS-CoV-2, but if you read Bratlie's source from the US State Department, it says (my emphasis):
The U.S. government has reason to believe that several researchers inside the WIV became ill in autumn 2019, before the first identified case of the outbreak, with symptoms consistent with both COVID-19 and common seasonal illnesses.
As autumn is the peak season for respiratory illnesses such as influenza, this is about as expected. It would perhaps be even stranger if none of the researchers there fell ill during the autumn.
What Bratlie (of course) also fails to mention is that a declassified memo from the US Secret Service points out that some of the symptoms these researchers had were not consistent with COVID-19:
Several WIV researchers were ill in Fall 2019 with symptoms; some of their symptoms were consistent with but not diagnostic of COVID-19. The IC continues to assess that this information neither supports nor refutes either hypothesis of the pandemic's origins because the researchers' symptoms could have been caused by a number of diseases and some of the symptoms were not consistent with COVID-19.
Furthermore, one can read:
We have no indications that any of these researchers were hospitalised because of the symptoms consistent with COVID-19. One researcher may have been hospitalised in this timeframe for treatment of a non-respiratory medical condition.
China's National Security Commission investigated the WIV in early 2020 and took blood samples from WIV researchers. According to the World Health Organization's March 2021 public report, WIV officials including Shi Zhengli-who leads the WIV laboratory group that conducts coronavirus research-stated lab employee samples all tested negative for SARS-CoV-2 antibodies.
In other words: There is absolutely no evidence that these researchers actually had COVID-19 in November 2019. But why won't Bratlie be open about this? Why is she cherry-picking data to support an already favoured conclusion?
Is SARS2 characterised by manipulation?
She then moves on to her next point: "SARS2 has characteristics that suggest manipulation" and makes three points:
The virus immediately spread very quickly, far faster than other viruses, right after it was transmitted from animals to humans.
Yes, SARS2 spread faster than both SARS1 and MERS did, with a higher basic reproductive rate (R0). But that's partly because SARS2 was less dangerous, produced many asymptomatic and mild cases, and thus had the ability to spread quickly because infected people did not immediately become seriously ill and immobile.
This in itself is not an argument in favour of the virus being manipulated.
Her next point:
There was no rapid initial period of genetic adaptation (mutations) when the outbreak started, as would be expected of a virus that has just crossed over into a new species. This may indicate that the virus had previously "practised" infecting humans.
Earlier in his memo, Bratlie referred to sources that say that most such infection events will die out and not turn into an epidemic. So yes, it seems likely that humans may have been infected many times from animals before it eventually became an epidemic.
This is thus an argument against genetic manipulation, because if the origin of the pandemic was infection in a laboratory, it would most likely only have happened once. Whereas in a wet market it is more likely that infection could have occurred several times, hence the point of the two lines A and B in at least two different transmissions from animals to humans - pointing in the direction of zoonotic origin.
The claim is also not correct, as the virus does not appear to be specially adapted to humans, but I will come back to that later.
Her third point:
It has (as previously described) a genetic element, a Furin Cleavage Site (FCS) in the so-called spike protein, which helps the virus enter cells in mammals and increases infectivity. Such an FCS could theoretically arise through natural evolution, but has not been observed in any other SARS coronaviruses
Yet. The origin of the swine flu pandemic took around 7 years to be found, and we have yet to find the natural origin of MERS (2013) or the Ebola virus (EBOV), so it is still entirely possible that bats with a very close relative to SARS2 will be found in the future.
Remember that "Absence of evidence is not evidence of absence."
And as previously mentioned, several scientific articles have been published that point out that natural evolution is a likely reason why SARS2 has a Furin Cleavage Site. In addition, I would remind you that knowledge that we only gained after 2020 shows that an FCS is not enough to make SARS2 so infectious, so it is difficult to imagine that the virus was genetically manipulated if it required knowledge that was not available before the outbreak of the pandemic.
American intelligence
The next item on the list of arguments in favour of lab-leak from Bratlie is that "Leading national experts consider it more likely that the virus has been manipulated".
She writes
When [Lawrence Livermore National Laboratory] analysed SARS2 using this methodology, they came to the conclusion that it is more likely that the virus had been manipulated in a lab than that it was natural.
Here she refers to the fact that the US Department of Energy concluded with a "low degree of confidence" that the virus most likely came from a lab leak. The same goes for the FBI.
A low degree of confidence is explained as follows:
A low confidence assessment generally means that the information obtained is not reliable enough or is too fragmented to make a more definitive analytic judgement or that there is not enough information available to draw a more robust conclusion.
Not very robust, in other words. And again we see an example of cherry-picking, because Bratlie could also have mentioned that four other US intelligence agencies have come to the opposite conclusion, and three have not concluded in any direction.
(She does mention this later in the memo, but not as part of the arguments in favour of genetic manipulation being likely).
The report from Lawrence Livermore National Laboratory is not as robust as Bratlie makes it out to be:
Multiple sources cautioned CNN that the document doesn't offer any "smoking gun" that proves one theory over the other. The report largely comes to the same conclusion that the intelligence community has disclosed publicly in recent weeks, according to multiple people familiar with it - namely, that the "zoonotic" theory of the virus' origins and the lab leak theory are both plausible. But it does offer some circumstantial evidence supporting the lab leak theory, validating what was then considered a fringe notion.
Put another way: A majority of US intelligence agencies have concluded that lab-leak is the least likely explanation for the origin of the COVID-19 pandemic. Yet Bratlie chooses to emphasise only the one that best suits her argument.
The DEFUSE project
She then goes on to write about "Extreme coincidence with planned research".
Here she describes how "the international research collaboration EcoHealth Alliance, led by the aforementioned researcher Peter Daszak" was to conduct research on coronavirus, and applied for funding for a project called DEFUSE. This project was to "genetically modify existing SARS coronaviruses from bats: they would insert a Furin Cleavage Site (FCS) into the spike gene". They would also "assemble the genetic sequence of the virus from six synthetic pieces, a bit like biological building blocks".
And:
They would then allow the viruses to multiply in cell cultures and so-called humanised mice (mice to which the human version of the ACE2 receptor that SARS coronaviruses use to enter cells has been added), allowing the viruses to adapt to the new "host".
As previously mentioned, genetic analyses show that SARS-CoV-2 does not show any signs of being adapted to mice. Ergo, this argues against the virus originating from research done at WIV or as part of the DEFUSE project. Bratlie does not mention this.
Unfiltered Perception is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.
She goes on to write that "SARS2 has exactly the characteristics that the DEFUSE project was supposed to introduce into a coronavirus":
- An FCS at exactly the location in the spike gene that the application had outlined.
- SARS2 has exactly the same pattern of "splices" in the genetic sequence that was described in the DEFUSE application.
- SARS2 has a number of other genetic properties that suggest that it was already adapted to bind the human variant of the ACE2 receptor (which is SARS2's "gateway" into the cells) from the start of the outbreak.
But again, Bratlie fails to mention that these points have been met with considerable criticism from other researchers. One example is a reanalysis of the study preprint Bratlie relies on, which states:
The analysis clearly shows that the endonuclease fingerprint does not indicate a synthetic origin of SARS-CoV-2 and engineering a SARS-CoV-2 virus in the laboratory is extremely challenging both scientifically and financially. On the contrary, current scientific evidence does support the animal origin of SARS-CoV-2.
He also points out that natural viruses have already been found in bats that are even more similar to SARS-2 than previously known. And:
Although no furin cleavage site (FCS) was discovered in those genomes, the sequence recombination analysis did show a mosaic genome of SARS-CoV-2 from multiple donors (Temmam et al., 2022). Further analysis by Robert F. Garry showed that the SARS-CoV-2 FCS is not a product of bioengineering (Garry, 2022b).
[...]
With the increasing discovery of new betacoronaviruses, there may be multiple SARS-CoV linages (SARS-CoV-x) harbouring an S1/S2 FCS insertion in the genome.
Most recently, Wang et al. discovered a high frequency of mammalian-associated viral co-infections and identified 12 viruses that are shared among different bat species by meta-transcriptomic analysis of 149 individual bat samples in Yunnan, China (Wang et al., 2022). The authors also found two coronaviruses closely related to SARS-CoV-2 (92%-93% genetic identities), with only five amino acid differences in the receptor-binding domain of one genome compared to the Wuhan-Hu-1 strain. These findings indicate that viral co-infections and spillover are common in bats, which explains the high recombinant events in coronavirus and points to the origin of SARS-CoV-2 from recombinational exchanges among multiple related genomes (Li et al., 2020; Pollett et al., 2021; Temmam et al., 2022; Turakhia et al., 2022).
More arguments against genetic manipulation
Robert F Garry has also written an article, "The evidence remains clear: SARS-CoV-2 emerged via the wildlife trade", in PNAS, in which he explains why a zoonotic origin of SARS2 is most likely. Here are some of his points:
Many proponents of the lab-leak hypothesis argue that it's too much of a coincidence that there would be a laboratory researching the coronavirus at the very place where the pandemic started. But they don't know, or don't say, that most Chinese cities have one or more coronavirus research laboratories. These labs were established by the Chinese government after the outbreak of SARS in 2002-2004, which led to around 8,000 illnesses and nearly 800 deaths. The laboratory in Wuhan is there precisely because it is one of many areas where an outbreak could be expected.
Many supporters of the lab-leak hypothesis, including Bratlie herself, argue that the bats that are the closest relatives of SARS-CoV-2 are located in southern China and Laos, which are around 1200-1500 kilometres away. The virus could never have travelled all the way from there to Wuhan without infecting others along the way, they claim. But we saw the same thing with the Ebola outbreak in Congo in 2013-2016, which is around 2500 kilometres away from the nearest known site of previous Ebola transmission in West Africa. In addition, the same was seen with SARS1, which also created localised outbreaks in various Chinese cities at similar distances from the origin of the virus. So this is not unique to SARS2.
Although the presence of a Furin Cleavage Site in SARS2 makes the virus more infectious, SARS1 is significantly more pathogenic and dangerous without having an FCS. The fact that SARS2 has an FCS is therefore not a decisive factor in making a natural coronavirus dangerous to and infectious in humans.
Analyses of the genetic structure of SARS-CoV-2 have been carried out by several people, including Garry, and have concluded that it is not characterised by genetic manipulation from humans. (However, Bratlie only highlights the one, earliest report that claims to find signs of this, and does not mention all those who have come to a different conclusion).
The argument put forward by Bratlie and others that SARS2 was adapted to humans from the outset, which seems suspicious, does not hold up very well either. SARS2 is adapted to a whole range of mammals, including mink, otters, deer, cats, etc. It has also been shown that SARS2 can survive in some species of deer without humans being infected in the area. In addition, SARS2 has continued to evolve in humans to become even more infectious, which we all remember from the various phases of the pandemic with new variants such as Delta and Omikron, which also indicates that the virus was not "optimised" from the start to be as infectious as possible in humans.
In a discussion on X we can read:
But Garry writes "[...] the short amino acid similarity is quite simply happenstance Several other coronaviruses share five of the eight amino acids (RSVAS) with ENaC (20) (Fig. 2B) It is also certainly not unusual for a FCS to be present at the junction between the S1 and S2 subunits of a betacoronavirus spike protein (21) (Fig. 2C) The two betacoronaviruses that cause common colds, OC43 and HKU1, have a FCS in that location.” So this is not as unique and mysterious as Bratlie wants it to be.
While Bratlie makes it one of her key points that SARS2 has an FCS, Garry points out that this is by no means so special. As I've previously shown, FCSs are often added and removed through random mutations all the time in coronaviruses.
The FCS in SARS2 is a so-called "out-of-frame insertion", i.e. a genetic mutation that shifts the order of the genome. It "doesn't fit in" where it should. This can be expected to happen in a random mutation, but it is very unlikely that it would be done through deliberate genetic manipulation, because then you change the effect of the subsequent genes in an unpredictable way.
Garry also points out "Furthermore, the SARS-CoV-2 FCS contains a previously undescribed feature, O-linked glycans, that a laboratory researcher could not have known to include.", something I have pointed out before, and which Bratlie never mentions.
He also points out that the sum of epidemiological analyses, i.e. how the infection spread from the wet market in Wuhan, phylogenetic analyses, i.e. the evolutionary relationships in the development of the virus, and serological analyses, i.e. traces of SARS-CoV-2 in samples from the specific area in the wet market where live, wild animals were kept in cages, all point to a zoonotic origin.
In other words: None of the arguments Bratlie puts forward as "evidence" that SARS2 is likely to have been genetically engineered hold water when looking at the totality of data, rather than just cherry-picking the few data that support this.
Gain-of-function
As far as the DEFUSE project is concerned, it was denied research funding, so initially there would be no research into genetic modification of coronaviruses, which Bratlie points to as a likely explanation for why SARS2 may have arisen in a laboratory in Wuhan. But Bratlie points out that through various hearings in the U.S. Congress, information has emerged that may indicate that some funds were nevertheless used for this very purpose in the Wuhan laboratory.
The problem is that even if so-called "gain-of-function" research was carried out at the Wuhan Institute of Virology, which scholars still dispute is actually correct, this would not have created SARS-CoV-2 as we know it.
Scientists unanimously told The Intercept that the experiment, which involved infecting genetically engineered mice with "chimeric" hybrid viruses, could not have directly sparked the pandemic. None of the viruses listed in the write-ups of the experiment are related to the virus that causes Covid-19, SARS-CoV-2, closely enough to have evolved into it.
There is also disagreement about whether the research that was done qualifies for the "gain-of-function" classification, and how potentially dangerous it really was
The Intercept consulted 11 scientists who are virologists or work in adjacent fields and hold a range of views on both the ethics of gain-of-function research and the Covid-19 origins search. Seven said that the work appears to meet NIH's criteria for gain-of-function research.
One said that the experiment "absolutely does not meet the bar" for gain-of-function research. "You can't predict that these viruses would be more pathogenic, or even pathogenic at all in people," said Angela Rasmussen, a virologist with the Vaccine and Infectious Disease Organisation at the University of Saskatchewan. "They also did not study transmissibility at all in these experiments," meaning that the scientists did not look at whether the viruses could spread across a population.
However, this is in many ways the most convincing argument that SARS2 came from the Wuhan Institute of Virology (WIV). We know that research into the genetic manipulation of coronavirus from bats was done there. And many scientists believe that this research was too risky and should not have been done. Ergo, it is far from absurd to imagine that such a manipulated virus could have infected a researcher there, and later spread in the population.
But that argument only works if you ignore everything that contradicts it:
- For example, the fact that there appear to have been two different incidents of infection with two different variants of SARS2. It is much more likely that this happened through animal infection, with thousands of people repeatedly coming into contact with carriers of the virus in the wet market, than it happenening two separate times in a laboratory, with two different variants of the virus.
- The pattern of spread is also consistent with the wet market as the epicentre, not WIV.
- Serological tests show that SARS-CoV-2 was present in wild animals in the wet market.
- All other coronavirus epidemics have started with bats as the original source, and then spread via infection to other animals, and then to humans. This scenario has a historical precedent.
- Genetic analyses of the SARS-CoV-2 genome support natural evolution, not genetic manipulation. Indeed, in several cases it shows that genetic manipulation could not have been the origin of the virus.
So yes, a lab-leak only seems plausible if you ignore much of the available data - in the same way as in the argumentation for all other conspiracy theories.
Remember that theories about lab-leaks and genetically engineered viruses have appeared in almost all epidemics and pandemics, such as HIV, Ebola, SARS1, MERS, etc. This is not unique to COVID-19, which means that one should be particularly cautious about spreading these types of theories without good evidence.
What is most likely
Bratlie concludes in the memo as follows
We don't yet know which theory is true, although we believe the evidence supports the lab-leak theory more than the zoonosis theory. What we can say with certainty, however, is that the handling of the case has been reprehensible in many ways.
I strongly disagree that the evidence provides more support for the lab-leak theory than the zoonosis theory, and I hope that in this blog post I have shown that one can only conclude as Bratlie does if one is careful to only select the data that fits, and ignore everything that does not fit a lab-leak theory.
We have consistently seen that Bratlie cherry-picks, fails to mention data that contradicts her claims, and repeatedly distorts scientific analyses that support the zoonosis theory rather than genetic manipulation of the virus.
However, I agree that the handling of the case has been reprehensible. Much of the memo is devoted to showing how data has been kept secret, removed and that there has been a lack of transparency in the processes surrounding the question of the origin of the pandemic and the research in Wuhan. But none of that is evidence of anything. And when you look at the purely virological and scientific data pointing towards a zoonotic origin, the more formal and administrative processes become more of a digression.
They are effective in creating a basis for conspiratorial hypotheses, but contain no evidence of lab-leak per se. I can't emphasise that often enough.
It's terribly reminiscent of the debate surrounding UFOs or UAPs. Almost all the "evidence" is about how cases have been handled by the US authorities, and all the suspicion and JAQing off makes many people believe that "no smoke without fire". The problem is that there is still no solid evidence that intelligent life from other planets has visited Earth. But that's easy to forget if you get caught up in all the noise surrounding the more "administrative" aspects of dealing with UAPs.
Bratlie does much the same in the question of the origin of SARS-CoV-2. She is so caught up in all the noise surrounding the hearings on the handling of this issue that she fails to realise that her relatively weak and inadequate "evidence" for genetic manipulation of the virus simply does not hold water. There's no substance there, but that's easy to forget if you get caught up in the excitement of finding out what has been kept secret or how someone high up in the system has lied about something.
It is nevertheless important and good that Bratlie writes in her conclusion:
However, we would like to emphasise that there is nothing to suggest today that it was a deliberate pandemic, i.e. a biological weapon. The aim of the research was to understand pandemics and develop vaccines. The main cause of the disaster, if it was man-made, was poor lab safety.
If, in the future, new data were to show that it was in fact a lab-leak that led to the COVID-19 pandemic, there are still many nuances that are crucial.
A lab-leak does not mean that SARS2 was created as a bioweapon. It could have been an innocent mishap as a consequence of perfectly legitimate research done to improve our understanding of coronaviruses and the ability to create vaccines against them in the future. There may even have been a researcher who was infected with SARS-CoV-2 on a field study in bat areas, who brought this virus back to WIV, becoming "patient zero", without the virus itself being created in the lab.
There are many different scenarios where a lab leak could be the correct explanation, without it saying anything about malicious intent.
Conclusion and consequences
She concludes with
If we are to create good emergency preparedness policies and prevent future pandemics, we need objective knowledge and a transparent and trustworthy political system.
I completely agree with that. But ironically and tragically, Bratlie herself contributes to counteracting such a goal by promoting the lab-leak hypothesis without the necessary evidence.
If we go back to the first article I mentioned, "The harms of promoting the lab leak hypothesis for SARS-CoV-2 origins without evidence", we can read
Despite the absence of evidence for the escape of the virus from a lab, the lab leak hypothesis receives persistent attention in the media, often without acknowledgment of the more solid evidence supporting zoonotic emergence. This discourse has inappropriately led a large portion of the general public to believe that a pandemic virus arose from a Chinese lab. These unfounded assertions are dangerous. As discussed in detail below, they place unfounded blame and responsibility on individual scientists, which drives threats and attacks on virologists. It also stokes the flames of an anti-science, conspiracy-driven agenda, which targets science and scientists even beyond those investigating the origins of SARS-CoV-2. The inevitable outcome is an undermining of the broader missions of science and public health and the misdirecting of resources and effort. The consequence is to leave the world more vulnerable to future pandemics, as well as current infectious disease threats.
Bratlie and the think tank Langsikt devote a lot of space in the memo to casting suspicion and naming and shaming named actors, often based on very unsophisticated considerations of responsibility, knowledge and blame.
She promotes bad science by not presenting the full picture, selectively citing research that suits her cause, and casting suspicion on a Norwegian press that has largely been sensible in relating to scientific consensus, rather than promoting "exciting hypotheses".
I'm all in favour of the lab-leak hypothesis being discussed openly and freely, as long as it's based on good evidence and not just “JAQing off”. But when the debate is based on such a shaky foundation as Langsikt presents, it only leads to scientific mistrust, an unwarranted scepticism towards research and scientists, and provides fertile ground for other conspiracy theories about vaccines, for example.
It's a deadly process that researchers and the press in particular must be incredibly careful to steer clear of. Feel free to engage in the debate, but it must be based on really solid evidence, not on selective data selection, casting of suspicion and gut feelings.
