Did Wuhan researchers fail to warn about a bat coronavirus discovered in 2013? Or did they even create SARS-CoV-2?

Fact-checking The Times’ “Seven Years Coronavirus Trail from mine deaths…”: An article entirely based on incorrect and missing information; this is how conspiracy theories emerge.

Introduction

A series of articles in British media starting with a piece in The Times from July 4 (1) accuse Ms. Shi Zhengli and her team from the Wuhan Institute of Virology (WIV) of having failed to inform the world about a new deadly virus. The virus in question is now called RaTG13 and was discovered in an abandoned mine shaft in southwestern China in 2013. The team from the WIV had been alerted about this specific place after six workers, who had been tasked with cleaning the mine shaft, fell ill with symptoms similar to SARS. Three of them died. In 2020, RaTG13 turned out to be the closest relative to SARS-CoV-2 which has been found so far.

Emerging Infectious Diseases Training Event in Meteti, Panama. Source: Wikimedia

In particular, the Times’ article accuses Ms. Shi of having omitted the information about the three deaths when publishing the research results about this virus strain, thereby failing to warn the world about an imminent threat. Many other “inconsistencies” lead the Times to conclude that the WIV or other researchers involved in this research could have played a role in the emergence of SARS-CoV-2, the virus causing COVID-19.

By the same author: The thorny question of the origin of SARS-CoV-2: Who wants to find out, and who does not?

The fact is that Ms. Shi and the international team within which she works have spent more than a decade investigating SARS-related coronaviruses circulating among bats and warning the world in the clearest terms about the potential danger from these viruses. Some of their research has been published in the most influential academic journals and got widespread attention. Other important aspects of their research have been totally ignored in the Times’ article discussed here despite being of utmost importance to prevent future disasters. In particular, humans getting infected by bat viruses seem to be extremely frequent, numbering at least in tens of thousands every year in southern China alone. Most of them do not have any activity related to bats or wildlife except for an ordinary rural lifestyle. Wildlife trade or research activities are absolutely not required for spillover events where a virus jumps from an animal to humans.

We will also see that the specific accusations leveled by this article against the WIV that the lab is possibly responsible for the emergence of SARS-CoV-2 through gain-of-function experiments are absurd. Gain-of-function or other similar experiments are conducted on a regular basis in many labs across the world. Many of these experiments can lead to terrible disasters and should definitely be banned. However, even the most advanced labs are very far from being able to transform RaTG13 into SARS-CoV-2.

Some of the problems with this article might be due to the fact that none of the three journalists who authored the article seem to have any specific competence in science journalism. However, this does not explain everything. Some problematic assertions are direct quotes from academic experts. This article is therefore not simply an example of inadequate media reporting about a topic where the academic community would have provided all the necessary information for the media to do their job properly.

Nobody seems to have noticed any of the serious flaws in the Times’ article. It got almost unanimous praise and became the source of a major number of reports in other media, mainly among the British right-wing tabloids, but also among other British and international media (2) (3) (4) (5) (6) (7) (8) (9) (10). However, a closer examination of the information conveyed in the article, of the structure of its narrative and most importantly of what was omitted reveals that all the main points are actually highly problematic. If The Times claims to stick to accepted standards of responsible journalism, massive corrections are warranted.

Did Ms. Shi Zhengli and the team within which she works warn the world about the potential danger from bat coronaviruses?

One of the main arguments of the whole article is that the discovery of RaTG13 did not give rise to warnings to the world about a new deadly virus strain. Here are some excerpts from the article:

The virus was a huge discovery. It was a “new strain” of a Sars-type coronavirus that, surprisingly, received only a passing mention in an academic paper. The six sick men were not referred to at all.

What happened to the virus in the years between its discovery and the eruption of Covid-19? Why was its existence tucked away in obscure records, and its link to three deaths not mentioned? […]

Researchers in China have been unable to find any news reports of this new Sars-like coronavirus and the three deaths. There appears to have been a media blackout.

The first thing to clarify is that most of the research at the WIV was done within extensive international cooperation. Peter Daszak, a researcher who often works with Ms. Shi, is also president of EcoHealth Alliance. This NGO funds research in global health, conservation and international development (11); for this purpose, it got funds among others from the US health authorities, including for projects investigating coronaviruses circulating in bats (12). Ralph S. Baric from the University of North Carolina has also done several research projects with Ms. Shi or using the viruses she and her team collected. This international team has warned the world repeatedly about the danger emanating from SARS-related coronaviruses circulating among bats in the most pressing terms. On Nov. 9 2015, Ms. Shi was among the coauthors of an article (13) in Nature with the title “A SARS-like cluster of circulating bat coronaviruses shows potential for human emergence.” It is difficult to warn in clearer terms of a possible epidemic. When it was published, this paper got widespread attention in the media and social media (14). Many other papers by these authors over a range of several years doubled down on this warning. The two last papers by Ms. Shi and her lab date back to the end of 2018 (15) and the beginning of 2019 (16).

So why were these warnings not heeded? Why did we not use the time since this discovery to prepare cures and vaccines? This question is not difficult to answer, but obviously beyond the competence of journalists and academic experts who are now so obsessed with COVID-19 that they are unable to see anything else.

In 2012, the MERS virus emerged for the first time in the Middle East. Like SARS and SARS-CoV-2, it is a coronavirus, more precisely a β-coronavirus, but within this group, MERS is part of the lineage C called merbecoviruses, whereas SARS and SARS-CoV-2 are part of the lineage B called sarbecoviruses or SARS-like viruses. MERS is thought to have originated in bats, with similar viruses being found all over the globe, from Asia to Latin America (17). In the Middle East, one of these viruses is thought to have jumped over into dromedaries. From this new intermediary host, there are frequent spillover events to humans, with some further human-to-human transmission, mainly within hospitals. So far, all outbreaks among humans fizzled out, but from 2012 to January 2020, WHO recorded 2519 confirmed cases and 866 deaths, i.e. a case fatality rate of over 30% (18). Reproduction number R was found to be consistently above 0.85, i.e. close to levels which can trigger a pandemic (19). The last 17 cases were recorded in January 2020, overlapping with the COVID-19 epidemic, but got virtually no media attention.

In Asia and beyond, the 2015 outbreak in South Korea caused heightened concern. One South Korean businessman caught the virus in the Middle East and returned to his home country without knowing that he was infected. After being admitted to hospital, more than 180 people got infected through various transmission chains, mostly within hospitals. 38 of them died. The outbreak is estimated to have cost South Korea an equivalent of around 8 billion US dollars (20). The fact that one single infected person despite not having engaged in any risky behavior could have such an impact showed clearly that MERS was not just a Middle Eastern problem.

Genetic sequencing of the South Korean virus strain did not show any specific ability to spread faster among humans than the strains common in the Middle East. Apparently, only more favorable conditions in South Korea, simply bad luck or a mix of both allowed one case to cause a massive outbreak which could only be brought under control by quarantining roughly 17,000 people. Experts were very well aware of the fact that each single spillover could lead in the infected humans to a better adapted virus strain with a potential to cause a worldwide pandemic (21) (22).

The actual threat and the even greater potential future threat from MERS were well understood. The countries mainly affected, mainly oil-rich Middle Eastern countries, had all the necessary resources. The WHO had warned about MERS and called for the urgent development of cures and vaccines (23). The results of these efforts can be seen in an article in The Lancet from April 2020 (24). It describes phase 1 human trial of one vaccine candidate in detail and mentions that “several MERS vaccine candidates are currently being tested in phase 1 and 2 clinical trials.”

It is totally absurd to claim that a publication about a new virus strain discovered among bats in 2013 which might (!) have caused three deaths (see below) would have led to more efficient preparations for a possible coronavirus outbreak.

Why was the information about the death of three workers not published?

One of the main arguments in the Times’ article is that Ms. Shi and her team did not mention the fact that three deaths were allegedly caused by the new virus strain which they found in an abandoned mine shaft. This virus later turned out to be the closest match to SARS-CoV-2. The basic idea behind this argumentation is that if Ms. Shi had mentioned these deaths, it would have pushed experts and governments to prepare for a looming pandemic. The second line of argument is that if they did not mention these deaths, this was probably because they had something to hide. This allegation is clearly formulated both in the title (“Revealed: Seven year coronavirus trail from mine deaths to a Wuhan lab”) and repeatedly in the text itself: “Why was [the] existence [of the RaTG13 virus strain] tucked away in obscure records, and its link to three deaths not mentioned?” It is noteworthy that in July, after the publication of the Times’ article, Ms. Shi sent an answer regarding many open questions to Science Magazine (25) (26). Obviously, the Times’ journalists did not yet have access to this information when writing their article. However, even without it, the argumentation in the Times is more than problematic.

Nothing allows us to link the three deaths to the RaTG13 virus strain with any kind of certitude. Every expert looking at the available evidence in the 2010s would have reached this conclusion. Any attempt to alert the world about the dangers of RaTG13 through a hypothetical link to three deaths would therefore have exposed the authors of such a paper as alarmists unable to do proper scientific research.

Here is the available information, which should also have alerted present-day journalists and experts to the fact that the link between the three deaths and RaTG13 is more than shaky. In the abandoned mine shaft, Ms. Shi and her team identified 152 virus strains. 150 of them were α-coronaviruses, two of them β-coronaviruses. SARS and SARS-CoV-2 are all β-coronaviruses, more precisely part of lineage B among the β-coronaviruses. Viruses in this precise lineage are called “SARS-related viruses” or “sarbecoviruses” in academic literature. In the article where Ms. Shi and her team published the results of their research in this mineshaft, RaTG13 (still called RaBtCov/4991) is classified as a new strain within lineage B, with a 95% amino acid identity with the closest previously known SARS-like virus. The second β-coronavirus called HpBtCoV/3740–2 is classified as “potentially a new lineage E” among β-coronaviruses, with a 89% amino acid identity with the closest previously known SARS-like viruses.

The Times’ article mentions that the sick workers did not test positive to a PCR test for SARS, but they tested positive with an antibody test to SARS-related bat coronaviruses. These antibody tests were developed to help researchers identify bats which had previously been infected with SARS-related bat viruses. This was necessary because finding bats with ongoing infections from these viruses had proven extremely difficult. The antibody tests helped researchers to narrow down the location to maximize their chance of finding what they were looking for, namely β-coronaviruses of lineage B (SARS-related coronaviruses); they were specifically interested in finding the origin of SARS. This illustrates well the fact that the presence of coronaviruses within a bat colony fluctuates over time to a considerable extent.

These antibody tests were therefore not a diagnostic tools; this is also true for the currently available antibody tests for SARS-CoV-2. They are not specific enough to exclude with certitude that the antibodies found are caused by another coronavirus, be it of human or bat origin.

So how do we know that the six workers were infected by “the” new virus RaTG13, and not by the second β-coronavirus of lineage B found there, or another coronavirus? We don’t know. The similarities between the two viruses indicated above are based on a small fragment of the genome around its RdRp gene, not on the whole genome, which had not been sequenced at that time. The RdRp gene plays a role in replication (27), but is not linked to the proteins to which antibodies react. If we consider that the second β-coronavirus found in this cave has got a 89% similarity with the closest known SARS-related virus, and RaTG13 has got a 95% similarity, the probability that the former reacts to the antibody test is not that much smaller than for RaTG13.

RaTG13 was found only during the fourth and last sample collection campaign, one year after the workers were infected by a virus. During this last campaign, the positive test rate was much lower than in the previous campaigns. RaTG13 is therefore not a very common virus. We don’t even know whether RaTG13 or a similar strain was actually present in the cave when the workers cleaned it up. Even though the antibody test was designed to react specifically to SARS-related viruses, since other coronaviruses (e.g. α-coronaviruses) are much more common in this cave, a cross-reaction cannot be excluded. Because of the much higher prevalence of α-coronaviruses, a positive antibody test does not necessarily indicate an infection by a SARS-related virus, despite the fact that this is what the test was designed to detect.

It is also possible that the six workers were infected by more than one pathogen. They had worked days or even weeks in the mine shaft, cleaning up thick layers of bat and rodent droppings covered with fungus. Not only SARS and SARS-CoV-2, even α-coronaviruses can cause interstitial pneumonia. The same is true for fungus (28). It is all a question of how the human body is exposed to pathogens. More precisely, it is a question of virus load and of which parts are infected. In most cases when people get infected with a respiratory illness, they will get infected in the upper respiratory tract, and if their immune system is not up to the task, the infection can get down to the lungs. If for one reason or another, an otherwise benign respiratory virus can get directly into the lungs in a significant quantity, it can become very dangerous even for healthy persons. The same is true for a mix of various pathogens, in this case potentially several types of α-coronaviruses, one or two types of β-coronaviruses and a whole cocktail of fungus. The fact that Ms. Shi claimed that the three men died from a fungus infection is therefore not a sign of any cover-up. It is perfectly plausible that this is the information she got from one of the attending doctors.

Last but not least, our respiratory system is optimized for filtering pathogens contained in droplets before they reach our lungs. This is by far the most common way of infection. If pathogens are not contained in droplets, but in dust particles, depending on the conditions, they can more easily reach the lungs. We don’t know about the exact conditions in this mineshaft, but working to clean out thick layers of droppings might have produced an important quantity of dust, some of it infected with various pathogens.

All these considerations show that the death of the workers might have been due not so much to the lethality of the pathogen(s) involved, but rather to the conditions under which these pathogens reached the upper respiratory tract or even directly the lungs of the workers. The assertion in the Times’ article that the death of three of them was linked to the RaTG13 virus and not to another one present in the mineshaft and the assertion that RaTG13 is therefore a “deadly new strain” are unwarranted by the available information. It happens on a regular basis that for people who caught a pneumonia under normal everyday conditions, doctors are unable to pin down the exact cause (29). Even larger outbreaks of pneumonia often remain a mystery (30) (31) (32) (33) (34) (35) (36) (37) (38) (39). In other words, the assertion that the three deaths were caused precisely by RaTG13 is irresponsible and simply bad journalism.

That three journalists without any serious training in science might believe that they can nail down the exact cause of the three deaths is problematic, but understandable. But what about the various experts who were quoted in this article? Were they not given all the information available? If this was the case, they should have demanded a correction after reading the full article. The result is an article about a team of researchers who dedicated their lives to doing research and warning about the emergence of coronaviruses in bats which could jump to humans, publishing one article in high profile journals after another. Then come three Times journalists who know little about science and write an article about why these researchers did not mention three deaths which nobody can link for sure to these viruses. This is pathetic, to say the least.

What can researchers presently achieve within gain-of-function experiments?

It is now time to address the second main argument of the Times’ article, namely that SARS-CoV-2, the virus presently causing a pandemic across the world, could have escaped from the Wuhan Institute of Virology (WIV), or that other bat-related research could have contributed to the spillover from bats to humans.

It is obvious that no virus described ever before corresponds exactly to SARS-CoV-2. RaTG13 is different from SARS-CoV-2 by more than 1000 nucleic acids, the building blocks of RNA. The Times alleges that one of the possible origins of SARS-CoV-2 could be so-called “gain-of-function” experiments. These are lab experiments where viruses are somehow enhanced in order to study how new, more dangerous viruses could emerge or how it could be possible to defend against them.

Without stating it assertively, the article makes readers believe that such experiments were not conducted in the US at that time:

This “gain-of-function” work is described in papers released by the WIV between 2015 and 2017, scientists say. Shi’s team combined snippets of different coronaviruses to see if they could be made more transmissible in what they called “virus infectivity experiments”.

It was controversial because it had the potential to turn bat coronaviruses into human pathogens capable of causing a pandemic. In 2014 the US government issued a ban on funding any endeavour to make a virus more contagious.

Shi’s team argued that gain-of-function work increased its understanding of how an ordinary coronavirus might one day transform into a killer such as Sars.

Others disagreed. “The debate is whether in fact you learn more by helping to develop vaccines or even drugs by replicating a more virulent virus than currently exists, versus not doing that,” explained Deenan Pillay, professor of virology at University College London. “And I think the consensus became that the risk was too much.”

Actually, two of the articles which warned most clearly about the potential danger of SARS-related viruses were based on gain-of-function experiments which seem to have been conducted in the US, not in China; one is co-authored by Ms. Shi Zhengli (13), the second thanks her for having provided virus samples (40). One was published in 2015, the second in 2016. Another article from 2008 from the same lab in North Carolina already used the same gain-of-function method (41).

Basically, all three articles use the same method. In order to test whether a bat virus has got the potential to jump to a new host (e.g. humans), they take the gene of its spike protein and dock it to a standard virus body which is compatible with the new host. Practically, the new synthetic virus is not created by putting together RNA pieces from each of the two viruses. The RNA of the new recombined virus is printed from scratch by a specialized company and inserted in the lab doing the experiment into a cell which generates a live virus from it.

This illustrates quite well how gain-of-function experiments are done. Basically, for most virus families, for any virus whose genome sequence is known or designed artificially, its RNA (or DNA) can be printed and inserted into a cell, and the cell will produce live viruses which can then infect humans and cause a global pandemic.

Does this sound scary? It probably does, and for good reasons. You might have heard about smallpox. This highly deadly and contagious virus was eradicated in the 1970s after a worldwide vaccination campaign. It is estimated that it had killed 300 million people in the 20th century alone. For decades, there were discussions whether it was reasonable to keep samples of live smallpox virus in labs. In 1978, one year after the illness was thought to have been eradicated after some last cases in Somalia, a sample escaped in a lab in Great Britain and led directly and indirectly to the death of three people (42). Since the 1980s, this virus is stored officially only in two labs worldwide. Would it not be wiser to destroy these samples? If they escaped accidentally, or worse, if they got into the wrong hands, it could lead to a terrible disaster.

In 2018, the question took another dimension. Three virologists, experts in bioweapons, published an article (43) where they announced that they had synthesized a live horsepox virus. Horsepox cannot infect humans, but is otherwise very similar to smallpox. They had two objectives: clearing the way for developing better vaccines against smallpox, and alerting the world to the danger from synthetic viruses. One expert predicts that by 2040, “it will be possible to synthesize smallpox from home” (44).

This shows two things. Most importantly, we might soon have to face bioterrorist attacks with viruses against which we might or might not have a vaccine or cure. Against most viruses, we have got only vaccines, no cures. Some of these vaccines might have some impact if given after infection took place, but this is not always the case. In addition, it might soon be possible to manipulate viruses in a targeted way to render existing vaccines ineffective. In this case, only the “good old hygiene methods” like face masks, disinfecting hands, physical distancing etc. might allow us to limit the impact.

With regards to the present topic, namely the possible origin of SARS-CoV-2, this shows that modern labs can produce any coronavirus for which they have got the genome sequence. Does this mean that from RaTG13, researchers in the Wuhan Institute of Virology could have created SARS-CoV-2? The Times’ article quotes two experts on this question. Martin Hibberd from the London School of Hygiene & Tropical Medicine does not consider it to be possible. Richard Ebright from Rutgers University is quoted with a radically different view:

Ebright alleges, however, that the type of work required to create Covid-19 from RaTG13 was “identical” to work the laboratory had done in the past. “The very same techniques, the very same experimental strategies using RaTG13 as the starting point, would yield a virus essentially identical to Sars-Cov-2.”

Even though I am not a virologist, I find this assertion extremely problematic, at least misleading and even close to dishonesty. There is a broad literature about gain-of-function experiments. We know therefore pretty well what the most advanced labs in the world are able to achieve. As explained above, as soon as researchers have got a genome sequence, they are able to produce the corresponding live virus. The whole problem is to come up with the genome of a new virus which will actually “work”, i.e. which will be able to replicate in the intended cells. There are mainly three methods applied on a regular basis. One is to produce in a lab what in nature is called a “recombination”, i.e. taking a building block (e.g. a gene or a part of it) from one virus and plug it into the basis provided by another virus. This mechanism is shortly explained in the Times’ article:

Shi’s team combined snippets of different coronaviruses to see if they could be made more transmissible in what they called “virus infectivity experiments”.

This method, where the spike from a bat virus or part of it was plugged onto a human virus or inversely, was used in many of the gain-of-function experiments mentioned above, be it in the US or in China (13) (40) (41) (45).

Another method consists in modifying a small number of nucleic acids, sometimes leading to the modification of one single amino acid; this method is mostly used not to enhance the infectivity of a virus, but to see whether certain features of the virus structure have got the suspected function (46). Deleting genes or part of a gene is often used to establish the function of specific genes (47); deletions also happen naturally.

The Times’ article discusses the (to a certain extent controversial) time which RaTG13 would have needed to evolve naturally to become SARS-CoV-2. Virtually all experts consider that this time spam must be estimated in decades, not years, which excludes the possibility that RaTG13 could be the direct ancestor of SARS-CoV-2. The article does not mention the fact that more than one thousand nucleic acids distinguish the two viruses. What is more, these differences are not due to one recombination, i.e. they are not concentrated in one place of the genome. The over 1000 mutations which would be required to change RaTG13 into SARS-CoV-2 are distributed along the whole genome.

From the known sequence of RaTG13, designing the genome of a virus which would be more infectious in humans by finding these over 1000 necessary mutations is orders of magnitude more complex than anything which researchers have been able to achieve so far. Imagining that Chinese scientists, who work with exactly the same tools and publish the same kinds of papers as Western scientists, could possibly achieve this is simply absurd.

Another possibility how a virus can evolve in a lab is to let it evolve naturally in cell cultures. Each time the virus infects cells and is replicated, some mutations might occur, like in a natural host. Such experiments have also been conducted (48). We will see below that such an explanation is not plausible either, for quantitative reasons.

All this does not prove that SARS-CoV-2 could not have been created in a lab. Gain-of-function experiments can obviously result in such terrible disasters. In some cases, their objective is precisely to create new viruses which are more dangerous to humans. If they escape, they can lead to a deadly pandemic. Since alternatives are available, such experiments should be banned. However, claiming that a lab could transform RaTG13 into SARS-CoV-2 with the technology available in 2020 is nonsense. The two viruses were simply too different.

For SARS-CoV-2 to be created in WIV and to escape from there, the lab would have had to set up another program to collect new viruses, without telling anybody, to find new SARS-like viruses without publishing anything about them, and to conduct gain-of-function experiments again without telling anybody. This is technically possible, but totally absurd. The work done in WIV follows the same pattern as the work of all state-of-the-art labs across the world. These labs get funding according to their results, and results are mostly measured through academic publications. Finding SARS-like viruses among bats turned out to be terribly difficult. As soon as the WIV found a few, or even just one or two, they immediately published these results. This was required to get the necessary funding to justify their research. No matter whether we talk about China or Western countries, successful labs get more funding than those which get no results.

As we have seen above, most gain-of-function experiments combine building blocks from different viruses. SARS-CoV-2 is similar in no part of it to previously known viruses. WIV would therefore have had to find two previously unknown viruses, each of them containing another part of SARS-CoV-2, so that WIV only had to combine pieces from them to create a virus which is different from SARS-CoV-2 only in very few nucleic acids. Imagining that WIV had done all this in secret, because they knew in advance that this virus would end up escaping the lab, when all of its funding depended on getting interesting results, is simply absurd. More generally, when you have got a research team which had excellent results and was involved on a large scale in international collaboration with the best teams in the world, and in order to make your case, you have to supposed that all of a sudden, they started to behave in a completely erratic and irrational way, it is time to look for another theory.

The information provided here shows very clearly that the case built in the Times’ article for a possible role of the WIV in the emergence of SARS-CoV-2 is extremely shaky and built on assertions which are outright absurd. But if neither this lab nor the Huanan Market or other forms of wildlife trade played a role, how could this virus emerge in Wuhan, far away from the habitat of the bats which form the reservoir for the presumable precursor(s)? All the information required to understand this is available and was known to the journalists writing the article. However, for whatever reason, they decided not to mention it.

How can a virus jump from bats to humans? And how could it get to Wuhan?

The Times’ article uses a quite simple argument to discard the hypothesis that the virus could have reached Wuhan in a “natural” way, by somebody who was infected by a bat in the south of China and would have traveled to Wuhan:

But how could such an infectious virus avoid causing a single noticeable outbreak during the 1,000-mile journey from Yunnan to the city?

The answer to this question is actually given in an article from Scientific American which the authors of the Times’ article have read and quoted (49):

In October 2015 Shi’s team collected blood samples from more than 200 residents in four of those villages [close to a cave where they had found a multitude of bat viruses]. It found that six people, or nearly 3 percent, carried antibodies against SARS-like coronaviruses from bats — even though none of them had handled wildlife or reported SARS-like or other pneumonialike symptoms. Only one had traveled outside of Yunnan prior to the sampling, and all said they had seen bats flying in their village.

Actually, the results from the roughly 200 people mentioned here are only preliminary results (50). In a larger scale project, published in 2019 (51), more than 1500 people living in three different Chinese provinces had been tested, 9 of them with a positive result to antibodies to SARS-like bat viruses. Even though the ratio (0.6%) is lower than in the preliminary results, it shows that this phenomenon is not limited to one single region in China.

A third project from 2004 in Hong Kong (52) provides similar results from an urban setting. Almost 1000 samples from randomly selected healthy persons had been collected in 2001, more than 18 months before the SARS epidemic, and stored within the framework of a hepatitis B research project. In 2004, they were tested for antibodies to SARS and to SARS-like viruses found in animals. 17 of them (1.8%) tested positive, with a majority having a quantitatively stronger reaction to the test for SARS-like viruses found in animals than to the test for SARS. The control group made of blood samples from SARS patients tested consistently stronger for the SARS test.

How can we interpret these results? There are basically two extreme interpretations. One would be that there have been only a handful of spillover events in China since the beginning of the millennium. The virus which infected the people in Hong Kong in 2001 would therefore probably be the direct ancestor of SARS, circulating among humans for more than a year before becoming more virulent in late 2002. This is the interpretation favored by the authors of the study. The positive results found by Ms. Shi and her team in villagers in 2015–2017 would then be caused by the direct precursor of SARS-CoV-2. If we consider the known outbreaks due to SARS-like viruses before and after the major SARS outbreak, this hypothesis is unlikely. Research in other countries has revealed that spillover events between bats and humans are very far from being rare and that intermediary host animals are not necessary (53).

The other interpretation is that there is a major number of spillover events from bats to humans. Most of them fizzle out after infecting one or just a few people. Some viruses are sufficiently well adapted to humans for them to cause significant outbreaks. For example, it is unlikely that the people infected in Hong Kong with a SARS-like virus were each infected by a bat or other wild animal. On the other hand, the WIV team found more people infected with SARS-like viruses in villages close to major bat caves than in their control group in Wuhan.

The SARS virus might have evolved among bats through the recombination of various bat viruses which were found to contain virtually all the “building blocks” necessary to build the SARS virus. However, the same scenario is less likely for the SARS-CoV-2 virus. An Australian research team claims in a preprint paper (54) that the very first virus sample collected in Wuhan is better adapted to human ACE2 receptors than to the ACE2 receptors of all other possible host or intermediate host animals. They conclude that the SARS-CoV-2 virus must have been bred in a lab, which is ridiculous. They “forget” a second possible explanation, namely that the precursors of SARS-CoV-2 circulated among humans for quite some time before one of them started to perform well enough to cause massive outbreaks. This scenario has been described in detail by a US team of influential experts (55) and labeled the most likely scenario one month and a half before the Australian team put their paper on a preprint server. Other researchers also conclude that some precursors of SARS-CoV-2 have circulated among humans, still in a milder and/or less contagious form, for months or years before December 2019 (56) (57).

We also know (as explained above) that SARS-related coronaviruses have been found through antibody tests to have infected a certain percentage of the population in all research projects of this kind. If instead of the measured percentages of 2.7%, 0.6% and 1.8%, we take a floor value of 0.5% and consider that antibodies are detectable during three years (estimate 2–3 years provided by WIV), with a rural population of 100 million in the provinces where the bat species in question live, that makes some 170,000 people infected each year. Now consider the number of occasions a virus gets to mutate in a petri dish with a cell culture, and the number of occasions it gets when infecting 170,000 people each year. In addition, we must take into account that a virus cannot optimize its adaptation to the human body by replicating in human cells. All SARS-like viruses are known to use various mechanisms to manipulate the immune system of their hosts, otherwise they could not successfully cause an epidemic. These mechanisms are different from one host to the next. If a virus is allowed to adapt to the cells of a new host in a cell culture, the virus cannot adapt to the immune system of the new host, simply because there are no cell cultures which provide a functioning human immune system. The claim that SARS-CoV-2 could have evolved into what it is now by being replicated in a cell culture is simply nonsense. Those SARS-like viruses circulating among bats which were somehow able to infect humans have probably been able to replicate in hundreds of thousands of people each year. That SARS-CoV-2 emerged in this way is by many orders of magnitude more likely than any lab hypothesis. But precisely the professor leading the lab which publishes such absurd theories is interviewed in the Times’ article.

Regarding the possibility of an infected person travelling thousands of kilometers without causing “a single noticeable outbreak” during his journey, we might also point to the example mentioned above of a South Korean businessman who was infected with MERS in the Middle East and travelled back to South Korea, causing a massive outbreak with more than 180 infected and 38 deaths.

All this shows to what extent the argumentation in the Times’ article, claiming that the most plausible explanation is that the WIV or some other research activity is linked to the emergence of SARS-CoV-2, is based exclusively on a flourishing fantasy and a skillful narrative ignoring plenty of scientific evidence.

Building a conspiracy theory based on the opinions of biased experts

If we put all the evidence presented here together, it becomes clear that the Times’ article builds some kind of conspiracy theory against the WIV or other research institutes in Wuhan, accusing them of having something to hide with regards to their role in the emergence of SARS-CoV-2. The problem is that virtually all their arguments are highly problematic; most of them are in contradiction with research published in influential peer-reviewed journals.

Published research is of course not “the truth”. More often than not, even in high-ranking journals, you can find papers which reach one conclusion and others which reach the opposite conclusion. However, journalism should not consist in finding all the information which nicely fits into your preferred narrative, and ignoring all the rest. In particular, if an important information contradicting your narrative is mentioned in an article your explicitly quote, there is definitely a problem.

One factor is certainly that the three authors of the article seem to have little or no experience in science reporting. Most of their other articles are related to politics. It is not necessary to be an expert in virology to investigate about SARS-CoV-2, but a general scientific background allows you to avoid many pitfalls.

Many academic experts are quoted in the article, but they don’t really contribute to a better information. One problem is that many of them don’t have a general scientific background either, only an extremely narrow expertise in their field. I have always been flabbergasted by the fact that apparently none of our eminent virologists, not even the most renowned experts in bat viruses, seem to be aware of the extremely frequent contacts in everyday life all over the world between bats and humans. In the Scientific American article (49) mentioned by the Times, Mr. Linfa Wang, a researcher from Singapore and longtime collaborator of Ms. Shi, is quoted as saying that the bats in themselves “are not the problem. The problem arises when we get in contact with them”. Peter Daszak, extensively quoted in the Times’ article, has recently written an opinion piece (58) in The Guardian claiming that the best prevention of new epidemics is the protection of rainforests and “ending wild meat trade in China”. Protecting the rainforest is definitely necessary. As to demanding an end to wild meat trade specifically in China, but not elsewhere in the world, is unacceptable and should be condemned, even if it comes from a highly regarded researcher.

It is obvious that if we stop going into rainforests, the chance of catching a new virus from chimpanzees and gorillas is strongly reduced. On the other hand, claiming that this would stop contacts between bats and humans is utter nonsense, but that’s what we get from the most influential academic experts on an almost daily basis. Bats are everywhere. Even in Western countries like Switzerland, bats live and hunt in rural areas, suburbs and inner cities. Everybody who knows where to look at the right moment of the day can easily see them. They roost in churches, old farmhouses and barns or other old buildings. Their viruses can contaminate humans through their droppings, through direct collisions (which happen on a regular basis (39)) or through other animals, e.g. cats which catch a bat, eat it raw and come to their owner to lick their hands or face. And this is not only a scenario for southwest China. Researchers have found that not only coronaviruses in general, but more specifically SARS-related viruses are common among Rhinolophus bats not only in parts of Asia, but also in parts of Europe and of the Americas (59) (60) (61) (62) (17). So where is the required worldwide search for the origin of SARS-CoV-2? Nowhere to be seen, for a number of reasons.

From reading the research papers of the academic experts quoted in the Times’ article and from what they state in the media, it becomes quite obvious that many of them have got a preferred narrative of their own. One expert is obviously fiercely anti-communist; one is a known activist against gain-of-function experiments; one has dedicated his life to the preservation of the habitat of wild animals in developing countries. And one thing is common to all academic researchers: they are always in search of funding for their lab. This in turn requires tuning in to the preferred narratives of the media, since media reporting about research results is vital for the “visibility” of a lab and the university which hosts it.

In Western countries, the fact that China has been able to control the outbreak in Wuhan/Hubei province and to prevent it from causing large scale outbreaks in other provinces, when many Western countries ended up having hundreds of thousands of cases, has led to fierce hostility towards China. In consequence, news reports accusing China are hugely popular and all information contradicting the anti-Chinese argumentation will be ignored.

For many decades, the West has seen a rise in mistrust towards technology. In consequence, the fact that gain-of-function research and other related technologies have allowed to issue early warnings about the potential threats from SARS-like viruses will be ignored. On the other hand, experts coming up with purely speculative theories that gain-of-function research in the WIV has led to the creation and escape of SARS-CoV-2 from this lab will be highly welcome. The fact that the creation of SARS-CoV-2 from RaTG13 in a lab is virtually impossible with present-day technology is ignored. All you need is an expert passionately opposed to gain-of-function experiments claiming that it is possible.

Likewise, the fact that massive spillovers from bat viruses to humans have been documented in academic research is ignored, even though the journalists who wrote the article in the Times knew about this information. This is certainly linked to the fact that in the Western preferred narrative, nature is basically good and should be left untouched by humans. The fact that in most Western countries, virtually every single square kilometer is used for agriculture, cutting wood, hunting or tourism (hiking, etc.) is deemed irrelevant. The story that SARS-CoV-2 emerged because the Chinese don’t “respect” nature or because they led “irresponsible” lab experiments fits so well into the preferred Western narrative that it must simply be true.

A last example illustrates how the journalists from the Times use the available information. They allege that the Chinese government clung to the theory that the virus jumped from animals to humans at the Huanan market in Wuhan for months (until May) in order to divert attention from its true origin. The fact is that after most experts considered a spillover event at the Huanan market as a plausible explanation (63) (64), on Feb. 22–23, several media from mainland China (65) (66) (67) (68), Hong Kong (69) and other countries (70) (71) reported that new research had revealed that this was not the case, that the market had only been a place where intense spreading took place, but that the virus had circulated among humans well before it arrived there.

Virtually all influential Western media outlets ignored this information and some of them, among which the BBC (72), The Guardian (73) and Business Insider (74), immediately published stories reemphasizing that the spillover was thought to have taken place at this market. All the three articles were published between Feb. 25 and 26. None of them provided any reason for ignoring the Chinese research results. All three emphasize the importance of finding the origin of the virus and blame capturing wild life (BBC), fur farming (The Guardian) and wet markets (Business Insider) for the origin of the epidemic. In mid-April, the Business Insider article added the information (75) that the Huanan market is no more believed to be the place of the SARS-CoV-2 spillover, but keeps its headline unchanged, which claim: “Both the new coronavirus and SARS outbreaks likely started in Chinese ‘wet markets.’” The Times’ article is not the first one to accuse China of trying to hide something by clinging to the hypothesis of a spillover at the Huanan market. An article from May 17 in the New Zealand Herald (76) claimed that new research contradicts “Beijing’s claim” that the virus spillover happened at the Huanan market. The article then goes on accusing China of preventing research into the origin of the virus, when Chinese scientists and media tried for almost three months to explain that this is not where the spillover happened.

Other inconsistencies in the Times’ article are not addressed here because they would make the present text too long. All in all, the whole article perfectly illustrates the mechanisms leading to the emergence of a conspiracy theory. The fact that this narrative prevents us from doing the necessary research to find the origin of SARS-CoV-2 and to prevent other future epidemics is obviously considered irrelevant.

We need more accountability among the media and the academic community. In recent times, there have been too many high profile articles in influential media outlets which are not based on sound investigative research, but on picking all the information which fits into a well-selling narrative and on discarding the rest. If the resulting article is in contradiction with information from reliable sources, there should be ways of holding journalists and academic experts accountable. Unfortunately, these tools don’t exist. The result is a long-term decreasing trend in trust into our media. The present COVID-19 crisis shows the consequences of this confidence crisis and should be considered a wake-up call. So far, nobody seems to be aware of this danger.

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