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Post by Admin on Jun 2, 2021 4:18:41 GMT
To recapitulate Fig 2 from our vaccine paper, there are 6 inserts which make the SARS-CoV-2 Spike structurally special.They are unique fingerprints of the SARS-CoV-2 Spike which deserve to be highlighted in support of this view; and there are five salient features that strengthen the case for purposive manipulation in the laboratory.1. A major part of the spike protein has human-like domains with matured transmission adaption. Blasting the Spike protein with a rolling window of 6 amino acids showed that 78.4% of 6 amino acid windows are human like.This means that with nearly 80% of the spike protein has a built-in stealth property by having high human similarity. Therefore, it is remarkably well-adapted virus for human co-existence. Such high human similarity also implies a high risk for the development of severe adverse events/toxicity and even Antibody Dependent Enhancement (ADE) unless specific precautions are taken when using the Spike protein in any vaccine candidate:precautions that might not suggest themselves to designers employing conventional methodologies and innocent assumptions about the target virus, lacking our detailed anatomisation of it. Furthermore and significantly, Zhanet al also note that, surprisingly, this characteristic is present from the very first isolate (Zhan et al, 2020). This is something that does not sit well with an hypothesis of natural evolution.2. The Spike displays new amino acid inserts with condensed cumulative charge, all of which are surface exposed(please refer to the reproduced figure from the vaccine paper, above). This is a most significant finding as we mentioned in opening. Being physically located on the surface of the Spike protein greatly increases the infectivity and pathogenicity of the virus, enabling these inserts to participate in binding to co-receptors/negatively charged attachment receptors or even, as we have discovered, to the negatively charged phospholipid heads on the cell membrane. Such a result is typically the objective of gain of function experiments to create chimeric viruses of high potency. Therefore this is a strong indicator of manipulation3. The concentration of positive charge is on the receptor binding domain near the receptor binding motif at the top of the Spike protein. As with (2) this is more elegantly explained by an hypothesis of purposive manipulation than one of natural evolution. As can be seen in Figure 2 (side view) of the Spike trimer, the majority of the positive charged amino acids are located near or on the top of the spike protein giving the receptor binding domain apI=8.906, while the Cov-2 specific Cys538-Cys590 bridge brings in additional charge from 526-560 (with even higher pI=10.03) via the Cys391-Cys525 to positions right next to the receptor binding motif (where the ACE2 receptor is located). It is this which facilitates the dual mode capability, allowing binding to ACE2 and/or to co-receptors/attachments receptors. We posit that such ACE2 independent attachment and infectivity is happening and is evidenced clinically by the Covid-19 disease pattern. It is also reported by Zhou et al (2018). The receptors that are the most likely to be involved are CLEC4M/DC-SIGN (CD209) – see discussion point (5) below.
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Post by Admin on Jun 2, 2021 19:41:13 GMT
4. The Spike is so configured that it can bind to cell tissue without use of the ACE2 receptor. Clinically it is widely observed that the Covid-19 virus compromises the functions of olfaction and bitter/sweet receptors,erythrocytes, t-cells, neurons and various tissues such as intestine epithelia. These different targets do not engage and use ACE2 receptor binding. The concentration of high positive charge in and around the top of the Spike protein and the potential to use opposite charged attachment-/co-receptors can facilitate binding and infection in the general mode of action for infectivity that we published in detail in QRBD. In 2018 Zhou P et.al.2018 found that a new Corona virus which they named SADS (Swine Acute Diarrhoea Syndrome) could infect the intestine and kill piglets without use of ACE2, aminopeptidase N (APN) or dipeptidyl peptidase 4 (DPP4)receptors.[9] We have done a blast analysis of the SADS Spike S1 protein and could find no trace of ACE2 RBM.The significance of this will become clear in the next point and the next section.5. Location and concentration of charge on the attachment receptor CLEC4M/DC-SIGN (C-type Lectin domain family4 member M (CLEC4M)/ Dendritic Cell-Specific Intercellular adhesion molecule-3-Grabbing Non-integrin(DC-SIGNR) also known as CD209) (Marzi et al., 2004). Analysis of the CLEC4M attachment receptor shows an overallpI=5.23 where the C-type lectin tail 274-390 has a pI=4.4. However, due to the two disulfide bonds Cys296-Cys389 and Cys368-Cys381 the C-terminal part of the tail is pulled back to a domain around position 296. This condensed negatively charged domain is ready for formation of salt-bridges with similar condensed opposite charged amino acids structures on the S1 RBD of SARS-CoV-2. This finding is fascinating and significant for a different reason to the others. It is not about Spike manipulation itself: in the next section we will explain that and how we believe that these capabilities were developed between 2008 - 2015. This finding points to something else: a trial to demonstrate a newly discovered attachment/co-receptor by field testing and verification. The context was the 2018 Swine Acute Diarrhoea Syndrome (SADS) outbreak in Guangzhou province.[10] Assuming that the Wuhan Institute of Virology team had discovered the functionalities of CLEC4M/DC-SIGN/CD209 receptors in the new SADS-CoV isolate and the fact that it could bind to positive charge(Ref: www.uniprot.org/uniprot/Q9NNX6 (CD209) and www.uniprot.org/uniprot/Q9H2X3) and that they wanted to do a field test of the described functionalities, the best conditions for doing so would be in connection with an ongoing viral infection. If this SADS originally did not have a ACE2 receptor binding motif 5(RBM), then a binding capacity verification of these attachment receptors could be done straightforwardly. But ifSADS did have an ACE2 RBM, then it would be necessary to remove or disable the RBM of the Spike protein on this CoV isolate and execute the experiment in piglets including the formal Cox postulate verification of infectionas described in the 2018 paper.We postulate that there are 2 charged domains on SADS that are likely to contribute to attachment receptor binding located in domains 330-360 and 540-560 respectively. Recollect that we have identified a similar highlycharged structure on SARS-CoV-2 within the edge of the RBD domain (526-560) with pI=10.03 which is brought right into the core of the RBD (to approximately position 400) by Cys-Cys bridging of the domain (538-590). This domain can contribute binding similar to that which can be observed for SADS. This new Cys-Cys property inserted into the SARS-CoV-2 Spike does not exist in SARS-CoV and hence could not provide such charge enhancement onto the RBD and co-receptor binding by natural evolution.Taken all together, we suggest that our research findings on the general mode of action for infectivity of SARS-CoV-2 andthe further puzzling features just mentioned, justify the question of the historical aetiology of these manipulations.We did not need to address this issue diachronically for the purposes of vaccine design. However, it is important for a soundly based understanding of the present and potential future epidemiology of the Covid-19 pandemic and for strategies for its management. Therefore to our earlier amino-acid level of biochemical analysis we now add here a forensic analysis of published research literature concerning SARS-CoV-2. We will extend this type of analysis to three other viruses in the companion article.Since, regrettably, international access has not been allowed to the relevant laboratories or materials, since Chinese scientists who wished to share their knowledge have not been able to do so and indeed since it appears that preserved virus material and related information have been destroyed, we are compelled to apply deduction to the published scientific literature, informed by our own biochemical analyses. We refute pre-emptively objection that this methodology does not result in absolute proof by observing that to make such a statement is to misunderstand scientific logic. The longer the chain of causation of individual findings that is shown, especially converging from different disciplines, the greater the confidence in the whole. We posit that the evidence below attains a high level of confidence.A sequence of four linked research papers is explaine dA comprehensive review of the relevant literature shows that a substantial amount of directly relevant gain-of function research has been undertaken. Four studies are especially noteworthy. They are linked in two ways: scientifically, in that the third and fourth build upon the results of the first and second, and in continuity of the institution and personnel across all four. The Wuhan Institute of Virology is a key collaborator in all these projects and Dr Zheng-Li Shi is one of the Institute's most experienced virologists and bat specialists. She is a common thread through all the key research projects.1. In 2008, Dr Shi was in the team whose research was an enabling pre-cursor to the two linked gain-of-function projects which lead to SARS-CoV-2's exact functionalities, including functionalities discovered via SADS and potentially field-tested in the 2018 study as suggested above. The 2008 Ren W et al project successfully demonstrated technical capabilities to interchange RBD’s between bat SARS-like and human SARS viruses: “... aminimal insert region (amino acids 310 to 518) was found to be sufficient to convert the SL-CoV S from non-ACE2 binding to human ACE2 binding, indicating that the SL-CoV S is largely compatible with SARS-CoV S protein both instructure and in function. The significance of these findings in relation to virus origin, virus recombination, and host switching is discussed" (Ren et al, 2008). Dr Shi is next a lead author of the second paper in this sequence,(Hou et al, 2010) and a co-author and the senior Chinese author of the third, (Menachery et al, 2015). She is also aco-author of the fourth (Zhou P. et al, 2018)2. In 2010 scientists from the 'Special Viruses' section of the Wuhan Institute of Virology were engaged in 'gain of function' experiments, jointly with international collaborators, to increase SARS-CoV infectiousness for humans.They used an HIV pseudo virus to express seven bat ACE2 receptors and compared their binding properties to human ACE2 receptors in order to pick the best for further optimizing a SARS-like coronavirus’s ability to bind to human cells. They also found that some bat ACE2 receptors are very close to human ACE2 receptors. This study provided a model system for testing the most infectious of SARS-CoV-like viruses which already had been selected in a vast survey of Chinese bat populations between 2005 – 2013.(Xu L et al, 2016). These viruses were potentially infectious to humans via the ACE2 receptor. Further new viruses were identified between 2012-2015 (Lin et al,2017).3. In 2015 scientists from the 'Special Viruses' section of the Wuhan Institute of Virology were engaged in 'gain of function' experiments jointly with a majority team from the University of North Carolina Chapel Hill. Together,they manipulated bat viruses to create a mouse adapted chimeric virus SHC014-MA15 which binds to and can proliferate on human upper airway cells (2B4 Calu-3 - a cell line contributed by Chapel Hill): ("group 2b viruses encoding the SHC014 spike in a wild type backbone can efficiently utilize multiple ACE2 receptor orthologs,replicate efficiently in primary human airway cells, and achieve in vitro titers equivalent to epidemic strains of SARS-CoV"). We suggest that it is a high priority in further investigations to ascertain precisely from Chapel Hilllab records the exact donor provenance of 2B4 Calu-3. The lead Wuhan scientist, who provided the CoV material,was Dr Zheng-Li Shi ("provided SHC014 spike sequences and plasmids"). We note that what is described here are, in fact, precisely SARS-CoV-2 properties. In vivo experiments at Chapel Hill replicated the chimeric virus in mouse lung which showed significant pathogenesis which was the opposite of what the team had expected ("the creation of chimeric viruses like SHC014-MA15 was not expected to increase pathogenicity"). Menachery et al reported that it may be hard to develop a vaccine against SHC014-MA15. We can see, therefore, that the 2015 experiment advanced the 2010 work by perfecting in animal trials a virus optimised to infect the human upper respiratory tract. The 2015 authors were well aware that the chimeric virus which they had created was very dangerous because they discussed this fact. Of the opportunity/costs of their research, they suggested that“while offering preparation against future emerging viruses, this approach must be considered in the context of the US government-mandated pause on Gain Of Function (GOF) studies” (which has since been lifted). They also speculated that " review panels may deem similar studies too risky to pursue as increased pathogenicity in mammalian models cannot be excluded." It is certainly the case that this experiment created a chimeric virus with very high infectivity potential targeted to the human upper respiratory tract. Yet a surprising observation is that the paper states that this research consortium has permission to continue this research. It appears that optimisation gain of function work on this chimeric virus did continue. We deduce from paper authorships that this was done in the Wuhan Institute of Virology.4. In 2018, as discussed earlier, Dr Shi's close colleague Peng Zhou, with others, investigated a coronavirus outbreakassociated with a fatal Swine Acute Diarrhoea Syndrome (SADS) in Guangdong Province. This paper relates that piglets had a tissue specific infection site located in the intestine and that verification of the Bat Covid nature of this new SADS as the disease-causing agent was confirmed. 25,000 piglets died. However, the really interesting part of this study reports that in order to identify the receptor(s) used by the SADS CoV, known coronavirus host cell receptors were investigated: Angiotensin Converting Enzyme 2 (ACE2), Amino Peptidase N (APN), and Di-Peptidyl Peptidase 4 (DPP4). None of these receptors worked. But indirectly in their paper, the authors revealed their ability to express and to test new receptors in the ways posited earlier. Recollect that the model to do this was proven and reported in the 2010 work. Thus it is plain that SADS is a CoV infection utilising new tissue-specific binding domains; but the authors provide no hint about which receptor the virus is using in piglets except that it is not any of the best known three. We have offered our deduction above. Pigs, of course, have immunesystems very similar to humans.Now recollect that Menachery V.D et al in 2015 had shown that their chimeric virus SHC014-MA15 could, against their prediction, very successfully infect primary human upper airway epithelial cells (HAE) from the cell-line 2B4 Calu-3. With this in mind, we next observed that in the Covid-19 pandemic, a well-reported symptom in the early phase of the infection is loss of taste, headache and a sore throat. We have discussed this issue in the QRBD article in detail. But to summarise: in2015 in a research review (Workman et al, 2015) discussed bitter/sweet taste receptors and the role these receptors play in mediating airway immune functions. They concluded thus: "Over the past several years, taste receptors have emerged as key players in the regulation of innate immune defenses in the mammalian respiratory tract. Several cell types in the airway, including ciliated epithelial cells, solitary chemosensory cells, and bronchial smooth muscle cells, all display chemoresponsive properties that utilize taste receptors."Therefore we hypothesise the reconstructed historical aetiology of the Spike as follows:In 2008, Dr Zheng-Li Si and WIV colleagues successfully demonstrated technical capabilities to interchange RBD’s between bat SARS-like and human SARS viruses. Building upon this, the 2010 work (Hou et al, 2010) perfected the ability to express receptors on human cells. On these foundations, the central Gain of Function work that underpins the functionalities of SARS-CoV-2 took place, carrying the WIV spike and plasmid materials to bond successfully to a UNC Chapel Hill human epithelial cell-line. This work (Menachery et al) produced a highly infectious chimeric virus optimised to the human upper respiratory tract. In convergent support of this hypothesis, both Lu (Lu et al, 2020) and Jia (Jia et al, 2020) have now, in January and April 2020, shown that SARS-CoV-2 has a bat SARS-like backbone but is carrying an RBD from a human SARSand Zhan et al have, like us, noted unusual adaption to humans from the first isolate. In the 2015 Chapel Hill work it was only ACE2 receptors that were discussed. However, in 2018 Zhou P. et al demonstrated capabilities to clone other receptors like APN and DPP4 and to test and compare these against the (intestine) tissue specific SADS-CoV identified.Then, in the 2019-20 Covid-19 pandemic, profuse symptoms indicating compromise of the bitter/sweet receptors are reported. Taken all together, this implies that by employing insights gained after 2015, as just deduced, a further optimization of the 2015 chimeric virus for additional binding to receptors/co-receptors such as bitter/sweet specific upper airway epithelia receptors occurred. That would help to explain the otherwise puzzling high infectivity and pathology associated with SARS-CoV-2 and hence also help to explain the social epidemiology of its spread. Conclusion We have deduced the internal logic of published research which resulted in the exact functionalities of SARS-CoV-2,including the convergence of agreement from difference classes of source, the timings of the stages of the research and the development of documented capabilities by named institutions and individuals. These meet the criteria of means,timing, agent and place in this reconstructed historical aetiology to produce sufficient confidence in the account to reverse the burden of proof. Henceforth, those who would maintain that the Covid-19 pandemic arose from zoonotic transfer need to explain precisely why this more parsimonious account is wrong before asserting that their evidence is persuasive, most especially when, as we have indicated, we note puzzling errors in their use of evidence. In our companion article, in asimilar forensic manner we will explore the primary evidence used to sustain the hypothesis of zoonotic transfer. In neither this article nor the next do we speculate about the motive.
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Post by Admin on Jun 3, 2021 3:08:00 GMT
The reason for the sudden shift in attitudes is clear: over the weeks and months of the pandemic, the pileup of circumstantial evidence pointing to the Wuhan lab kept growing—until it became too substantial to ignore. The people responsible for uncovering this evidence are not journalists or spies or scientists. They are a group of amateur sleuths, with few resources except curiosity and a willingness to spend days combing the internet for clues. Throughout the pandemic, about two dozen or so correspondents, many anonymous, working independently from many different countries, have uncovered obscure documents, pieced together the information, and explained it all in long threads on Twitter—in a kind of open-source, collective brainstorming session that was part forensic science, part citizen journalism, and entirely new. They call themselves DRASTIC, for Decentralized Radical Autonomous Search Team Investigating COVID-19. For a long time, DRASTIC's discoveries stayed confined to the strange world of Twitter, known only to a few nerdy followers. The sleuths ran into a fair number of dead ends, got into the occasional spat with scientists who disagreed with their interpretations, and produced a firehose of reporting. Gradually, the quality of their research and the rigor of their thinking drew a larger following, including many professional scientists and journalists. Thanks to DRASTIC, we now know that the Wuhan Institute of Virology had an extensive collection of coronaviruses gathered over many years of foraging in the bat caves, and that many of them—including the closest known relative to the pandemic virus, SARS-CoV-2—came from a mineshaft where three men died from a suspected SARS-like disease in 2012. We know that the WIV was actively working with these viruses, using inadequate safety protocols, in ways that could have triggered the pandemic, and that the lab and Chinese authorities have gone to great lengths to conceal these activities. We know that the first cases appeared weeks before the outbreak at the Huanan wet market that was once thought to be ground zero. None of this proves that the pandemic started in the Wuhan lab, of course: it's entirely possible that it did not. But the evidence assembled by DRASTIC amounts to what prosecutors call probable cause—a strong, evidence-based case for a full investigation. It's not clear that the best efforts of the U.S. and other nations to investigate the lab-leak hypothesis will ever turn up unequivocal evidence one way or another, at least without the full cooperation of China, which is unlikely.
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Post by Admin on Jun 3, 2021 5:13:35 GMT
Strange coincidences The young Indian man who calls himself The Seeker is in his late-20s, lives somewhere in eastern India, and uses a piece of tribal art from his home region of West Bengal for his Twitter logo, he said via email. His career has been a melange of architecture, painting, and filmmaking—a khichdi, his mother and sister call it, meaning a stew of disparate ingredients that adds up to something surprising and delightful. A voracious autodidact, he'd become an expert at searching the back alleys of the web, far beyond the well-lit places patrolled by Google, for information on whatever topic interested him. He often posted on Reddit, where he had accumulated a massive 750,000 karma points. That's all The Seeker revealed to Newsweek through email and messaging; he maintains his anonymity. Like most people following the news back when the pandemic started, The Seeker initially believed that the virus had jumped from wild animals to humans at a Wuhan wet market. (On March 27 he tweeted, "Nobody wants to see their parents or grandma and grandpa die over a stupid virus from an exotic animal market.") He believed this because that's what the mainstream press told him, and the mainstream press believed it because that is what a handful of scientists had said. Chief among these scientists was a biologist named Peter Daszak, president of EcoHealth Alliance, a non-profit research group that ran a large international program to survey natural pathogens with the potential to cause a pandemic. Daszak had been collaborating for years with Shi Zhengli, the director of the Wuhan Institute of Virology and a renowned bat virologist. Daszak co-authored nearly a dozen papers with Shi and funneled at least $600,000 of U.S. government grants her way. When the pandemic happened to break out on the doorstep of the lab with the largest collection of coronaviruses in the world, fueling speculation that the WIV might be involved, Daszak and 26 other scientists signed a letter that appeared in The Lancet on February 19, 2020. "We stand together to strongly condemn conspiracy theories suggesting that COVID-19 does not have a natural origin," it stated. We now know, thanks to a Freedom of Information Act request, that Daszak orchestrated the letter to squelch talk of a lab leak. He drafted it, reached out to fellow scientists to sign it, and worked behind the scenes to make it seem that the letter represented the views of a broad range of scientists. "This statement will not have the EcoHealth Alliance logo on it and will not be identifiable as coming from any one organization or person," he wrote in his pitch to the co-signatories. Scientists whose work had overlapped with the WIV agreed not to sign it so they could "put it out in a way that doesn't link it back to our collaboration." At the time, however, there was no hint of Daszak's organizing role. The letter helped make Daszak a ubiquitous presence in the media, where he called a lab-leak "preposterous," "baseless," and "pure baloney." He also attacked scientists who published evidence pointing to the lab. Part of the reason the lab theory made no sense, he argued, was because the Wuhan lab wasn't culturing any viruses remotely similar to SARS-CoV-2. (Daszak has not responded to Newsweek's request for comment.) For a long time, Daszak was astonishingly influential. Few in the media questioned him or pointed out that his career and organization would be deeply damaged if it turned out his work had indirectly played a role in the pandemic. His unwitting accomplice was Donald Trump, who embraced the theory, turning what should have been a scientific question into a political one.
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Post by Admin on Jun 3, 2021 18:40:59 GMT
A Whiff of Censorship
By early 2020, The Seeker was beginning to question that viewpoint. He had begun to interact with people who were poking holes in the conventional wisdom.
One important piece was an extensive Medium post by the Canadian longevity entrepreneur Yuri Deigin that discussed RaTG13, a virus Shi Zhengli had revealed to the world in a February 3 paper in the journal Nature. In that paper, Shi presented the first extensive analysis of SARS-CoV-2, which had seemed to come from nowhere—the virus was unlike any that had been seen before, including the first SARS, which had killed 774 people from 2002 to 2004. In her paper, however, Shi also introduced RaTG13, a virus that is similar in genetic makeup to SARS-CoV-2, making it the only known close relative at the time.
The paper was vague about where RaTG13 had come from. It didn't say exactly where or when RaTG13 had been found, just that it had previously been detected in a bat in Yunnan Province, in southern China.
The paper aroused Deigin's suspicions. He wondered if SARS-CoV-2 might have emerged through some genetic mixing and matching from a lab working with RaTG13 or related viruses. His post was cogent and comprehensive. The Seeker posted Deigin's theory on Reddit, which promptly suspended his account permanently.
That early whiff of censorship piqued Seeker's curiosity, so he read more of the Twitter group's ideas. "I found a lively group of people eager to debate and explore the topic," he told Newsweek by email.
It was an eclectic group. There were entrepreneurs, engineers, and a microbiologist from the University of Innsbruck named Rossana Segreto. None of them had known each other in advance; they gravitated to the forum after independently concluding that the conventional wisdom of the origins of COVID-19 didn't make sense. Conversations were kept on track by a wisecracking coordinator living somewhere in Asia who went by the pseudonym Billy Bostickson, and whose Twitter icon was a cartoon of a beat-up lab monkey.
The Seeker fit right in. "They helped me catch up on the debate, and I started to educate myself," he says. "Before I knew it, I got hooked into the mystery." He was driven in part by curiosity, but also by a growing sense of civic duty. "COVID has taken the lives of countless people and devastated so many others. But it has also left so many clues that haven't been followed up. Humanity deserves answers."
The Seeker and the rest of the group became increasingly convinced that RaTG13 might hold the key to some of those answers. In a crackling thread, half a dozen participants hashed out its mysteries, combing the internet and the WIV's previous papers for clues.
If there is a moment when the DRASTIC team coalesced into something more than its disparate parts, it would be this thread. In real time, for all the world to see, they worked through the data, tested various hypotheses, corrected each other, and scored some direct hits.
The key facts quickly came together. The genetic sequence for RaTG13 perfectly matched a small piece of genetic code posted as part of a paper written by Shi Zhengli years earlier, but never mentioned again. The code came from a virus the WIV had found in a Yunnan bat. Connecting key details in the two papers with old news stories, the DRASTIC team determined that RaTG13 had come from a mineshaft in Mojiang County, in Yunnan Province, where six men shoveling bat guano in 2012 had developed pneumonia. Three of them died. DRASTIC wondered if that event marked the first cases of human beings being infected with a precursor of SARS-CoV-2—perhaps RaTG13 or something like it.
In a profile in Scientific American, Shi Zhengli acknowledged working in a mineshaft in Mojiang County where miners had died. But she avoided connecting it to RaTG13 (an omission she had made in her scientific papers as well), claiming that a fungus in the cave had killed the miners.
That explanation didn't sit well with the DRASTIC group. They suspected a SARS-like virus, not a fungus, had killed the miners and that, for whatever reason, the WIV was trying to hide that fact. It was a hunch, and they had no way of proving it.
At this point, The Seeker revealed his research powers to the group. In his online explorations, he'd recently discovered a massive Chinese database of academic journals and theses called CNKI. Now he wondered if somewhere in its vast circuitry might be information on the sickened miners.
Working through the night at his bedside table on phone and laptop, fueled by chai and using Chinese characters with the help of Google Translate, he plugged in "Mojiang"—the county where the mine was located—in combination with every other word he could think of that might be relevant, instantly translating each new flush of results back to English. "Mojiang + pneumonia"; "Mojiang + WIV"; "Mojiang + bats"; "Mojiang + SARS." Each search brought back thousands of results and half a dozen different databases for journals, books, newspapers, master's theses, doctoral dissertations. He combed through these results, night after night, but never found anything useful. When he ran out of energy, he broke for arcade games and more chai.
He was on the verge of calling it quits, he says, when he struck gold: a 60-page master's thesis written by a student at Kunming Medical University in 2013 titled "The Analysis of 6 Patients with Severe Pneumonia Caused by Unknown Viruses." In exhaustive detail, it described the conditions and step-by-step treatment of the miners. It named the suspected culprit: "Caused by SARS-like [coronavirus] from the Chinese horseshoe bat or other bats."
The Seeker dropped the link, without fanfare, on May 18, 2020, then followed up with a second thesis from a PhD student at the Chinese CDC confirming much of the information in the first. Four of the miners had tested positive for antibodies from a SARS-like infection. And the WIV had been looped in to test samples from them all. (Shortly after The Seeker posted the theses, China changed the access controls on CNKI so no one could do such a search again.)
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