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#15104428
skinster wrote:NED/CIA is def not on my side. :lol:


Actually they kind of are. Or more accurately, it's you who's on the side of the NED/CIA. In the big picture the China-US relationship is more symbiotic than adversarial. The US ruling class created China(probably the most heinous crime against humanity the US has ever perpetrated) and while both vie for strategic advantage within an unholy alliance of hegemonic imperialism and fascistic gulag capitalism, there is far more cooperation than conflict between the two. So when you act as an apologist for the Chicom regime you are effectively aiding and abetting US imperialism which means you are on the side of organizations like the NED and the CIA.
#15104537
Sivad wrote:Actually they kind of are. Or more accurately, it's you who's on the side of the NED/CIA. In the big picture the China-US relationship is more symbiotic than adversarial. The US ruling class created China(probably the most heinous crime against humanity the US has ever perpetrated) and while both vie for strategic advantage within an unholy alliance of hegemonic imperialism and fascistic gulag capitalism, there is far more cooperation than conflict between the two. So when you act as an apologist for the Chicom regime you are effectively aiding and abetting US imperialism which means you are on the side of organizations like the NED and the CIA.


:lol:

Citations needed.
#15111173
A Proposed Origin for SARS-CoV-2 and the COVID-19 Pandemic

by Jonathan Latham, PhD and Allison Wilson, PhD

In all the discussions of the origin of the COVID-19 pandemic, enormous scientific attention has been paid to the molecular character of the SARS-CoV-2 virus, including its novel genome sequence in comparison with its near relatives. In stark contrast, virtually no attention has been paid to the physical provenance of those nearest genetic relatives, its presumptive ancestors, which are two viral sequences named BtCoV/4991 and RaTG13.

This neglect is surprising because their provenance is more than interesting. BtCoV/4991 and RaTG13 were collected from a mineshaft in Yunnan province, China, in 2012/2013 by researchers from the lab of Zheng-li Shi at the Wuhan Institute of Virology (WIV). Very shortly before, in the spring of 2012, six miners working in the mine had contracted a mysterious illness and three of them had died (Wu et al., 2014). The specifics of this mystery disease have been virtually forgotten; however, they are described in a Chinese Master’s thesis written in 2013 by a doctor who supervised their treatment.

We arranged to have this Master’s thesis translated into English. The evidence it contains has led us to reconsider everything we thought we knew about the origins of the COVID-19 pandemic. It has also led us to theorise a plausible route by which an apparently isolated disease outbreak in a mine in 2012 led to a global pandemic in 2019.

The origin of SARS-CoV-2 that we propose below is based on the case histories of these miners and their hospital treatment. This simple theory accounts for all the key features of the novel SARS-CoV-2 virus, including ones that have puzzled virologists since the outbreak began.

The theory can account for the origin of the polybasic furin cleavage site, which is a region of the viral spike protein that makes it susceptible to cleavage by the host enzyme furin and which greatly enhances viral spread in the body. This furin site is novel to SARS-CoV-2 compared to its near relatives (Coutard, et al., 2020). The theory also explains the exceptional affinity of the virus spike protein for human receptors, which has also surprised virologists (Letko et al., 2020; Piplani et al, 2020; Wrapp et al., 2020; Walls et al., 2020). The theory further explains why the virus has barely evolved since the pandemic began, which is also a deeply puzzling aspect of a virus supposedly new to humans (Zhan et al., 2020; van Dorp et al., 2020; Chaw et al., 2020). Lastly, the theory neatly explains why SARS-CoV-2 targets the lungs, which is unusual for a coronavirus (Huang et al., 2020).

We do not propose a specifically genetically engineered or biowarfare origin for the virus but the theory does propose an essential causative role in the pandemic for scientific research carried out by the laboratory of Zheng-li Shi at the WIV; thus also explaining Wuhan as the location of the epicentre.

Why has the provenance of RaTG13 and BtCoV/4991 been ignored?
The apparent origin of the COVID-19 pandemic is the city of Wuhan in Hubei province, China. Wuhan is also home to the world’s leading research centre for bat coronaviruses. There are two virology labs in the city, both have either collected bat coronaviruses or researched them in the recent past. The Shi lab, which collected BtCoV/4991 and RaTG13, recently received grants to evaluate by experiment the potential for pandemic pathogenicity of the novel bat coronaviruses they collected from the wild.

To add to these suggestive data points, there is a long history of accidents, disease outbreaks, and even pandemics resulting from lab accidents with viruses (Furmanski, 2014; Weiss et al., 2015). For these and other reasons, summarised in our article The Case is Building that COVID-19 Had a Lab Origin, we (a virologist and a geneticist) and others have concluded that a lab outbreak is a credible thesis. Certainly, a lab origin has at least as much circumstantial evidence to support it as does any natural zoonotic origin theory (Piplani et al., 2020; Segreto and Deigin, 2020; Zhan et al., 2020).

The media, normally so enamoured of controversy, has largely declined even to debate the possibility of a laboratory escape. Many news sites have simply labelled it a conspiracy theory.

The principal reason for media dismissals of the lab origin possibility is a review paper in Nature Medicine (Andersen et al., 2020). Although by Jun 29 2020 this review had almost 700 citations it also has major scientific shortcomings. These flaws are worth understanding in their own right but they are also useful background for understanding the implications of the Master’s thesis.

Andersen et al., a critique

The question of the origin of the COVID-19 pandemic is, in outline, simple. There are two incontrovertible facts. One, the disease is caused by a human viral pathogen, SARS-CoV-2, first identified in Wuhan in December 2019 and whose RNA genome sequence is known. Second, all of its nearest known relatives come from bats. Beyond any reasonable doubt SARS-CoV-2 evolved from an ancestral bat virus. The task the Nature Medicine authors set for themselves was to establish the relative merits of each of the various possible routes (lab vs natural) by which a bat coronavirus might have jumped to humans and in the same process have acquired an unusual furin site and a spike protein having very high affinity for the human ACE2 receptor.

When Andersen et al. outline a natural zoonotic pathway they speculate extensively about how the leap might have occurred. In particular they elaborate on a proposed residence in intermediate animals, likely pangolins. For example, “The presence in pangolins of an RBD [Receptor Binding Domain] very similar to that of SARS-CoV-2 means that we can infer that this was probably in the virus that jumped to humans. This leaves the insertion of [a] polybasic cleavage site to occur during human-to-human transmission.” This viral evolution occurred in “Malayan pangolins illegally imported into Guangdong province”. Even with these speculations there are major gaps in this theory. For example, why is the virus so well adapted to humans? Why Wuhan, which is 1,000 Km from Guangdong? (See map).


The authors provide no such speculations in favour of the lab accident thesis, only speculation against it:

“Finally, the generation of the predicted O-linked glycans is also unlikely to have occurred due to cell-culture passage, as such features suggest the involvement of an immune system.” (italics added).

[Passaging is the deliberate placing of live viruses into cells or organisms to which they are NOT adapted for the purpose of making them adapted, i.e. speeding up their evolution.]

It is also noteworthy that the Andersen authors set a higher hurdle for the lab thesis than the zoonotic thesis. In their account, the lab thesis is required to explain all of the evolution of SARS-CoV-2 from its presumed bat viral ancestor, whereas under their telling of the zoonotic thesis the key step of the addition of the furin site is allowed to happen in humans and is thus effectively unexplained.

A further imbalance is that key information needed to judge the merits of a lab origin theory is missing from their account. As we detailed in our previous article, in their search for SARS-like viruses with zoonotic spillover potential, researchers at the WIV have passaged live bat viruses in monkey and human cells (Wang et al., 2019). They have also performed many recombinant experiments with diverse bat coronaviruses (Ge et al., 2013; Menachery et al., 2015; Hu et al., 2017). Such experiments have generated international concern over the possible creation of potential pandemic viruses (Lipsitch, 2018). As we showed too, the Shi lab had also won a grant to extend that work to whole live animals. They planned “virus infection experiments across a range of cell cultures from different species and humanized mice” with recombinant bat coronaviruses. Yet Andersen et al did not discuss this research at all, except to say:

“Basic research involving passage of bat SARS-CoV-like coronaviruses in cell culture and/or animal models has been ongoing for many years in biosafety level 2 laboratories across the world”

This statement is fundamentally misleading about the kind of research performed at the Shi lab.

A further important oversight by the Andersen authors concerns the history of lab outbreaks of viral pathogens. They write: “there are documented instances of laboratory escapes of SARS-CoV”. This is a rather matter-of-fact allusion to the fact that since 2003 there have been six documented outbreaks of SARS from labs, not all in China, with some leading to fatalities (Furmanski, 2014).

Andersen et al might have also have noted that two major human pandemics are widely accepted to have been caused by lab outbreaks of viral pathogens, H1N1 in 1977 and Venezuelan Equine Encephalitis (summarised in Furmanski, 2014). Andersen could even have noted that literally hundreds of lab accidents with viruses have resulted in near-misses or very localised outbreaks (summarised by Lynn Klotz and Sam Husseini and also Weiss et al., 2015).

Also unmentioned were instances where a lab outbreak of an experimental or engineered virus has been plausibly theorised but remains uninvestigated. For example, the most coherent explanation for the H1N1 variant ‘swine flu’ pandemic of 2009/10 that resulted in a death toll estimated by some as high as 200,000 (Duggal et al., 2016; Simonsen et al. 2013), is that a vaccine was improperly inactivated by its maker (Gibbs et al., 2009). If so, H1N1 emerged from a lab not once but twice.

Given that human and livestock viral outbreaks have frequently come from laboratories and that many scientists have warned of probable lab escapes (Lipsitch and Galvani, 2014), and that the WIV itself has a questionable biosafety record, the Andersen paper is not an even-handed treatment of the possible origins of the COVID-19 virus.

Yet its text expresses some strong opinions: “Our analyses clearly show that SARS-CoV-2 is not a laboratory construct or a purposefully manipulated virus….It is improbable that SARS-CoV-2 emerged through laboratory manipulation of a related SARS-CoV-like coronavirus…..the genetic data irrefutably show that SARS-CoV-2 is not derived from any previously used backbone….the evidence shows that SARS-CoV2 is not a purposefully manipulated virus….we do not believe that any type of laboratory-based scenario is possible.” (Andersen et al., 2020).

It is hard not to conclude that what their paper mostly shows is that Drs. Andersen, Rambaut, Lipkin, Holmes and Garry much prefer the natural zoonotic transfer thesis. Their rhetoric is forthright but the evidence does not support that confidence.

Indeed, since the publication of Andersen et al., important new evidence has emerged that undermines their zoonotic origin theory. On May 26th the Chinese CDC ruled out the Huanan “wet” market in Wuhan as the source of the outbreak. Additionally, new research on pangolins, the favoured intermediate mammal host, suggests they are not a natural reservoir of coronaviruses (Lee et al., 2020; Chan and Zhan, 2020). Furthermore, SARS-CoV-2 was found not to replicate in bat kidney or lung cells (Rhinolophus sinicus), implying that SARS-CoV-2 is not a recently-adapted spill over Chu et al., 2020).

The Mojiang mine and the Master’s thesis

In our own search to resolve the COVID-19 origin question we chose to focus on the provenance of the coronavirus genome sequences BtCoV/4991 and RaTG13, since these are the most closely related sequences to SARS-CoV-2 (98.7% and 96.2% identical respectively). See FIG 1. (reproduced from P. Zhou et al., 2020).


For comparison, the next closest virus to SARS-CoV-2 is RmYN02 (not shown in Fig 1.) (H. Zhou et al., 2020). RmYN02 has an overall similarity to SARS-CoV-2 of 93.2%, making its evolutionary distance from SARS-CoV-2 almost twice as great.

BtCoV/4991 was first described in 2016. It is a 370 nucleotide virus fragment collected from the Mojiang mine in 2013 by the lab of Zeng-li Shi at the WIV (Ge et al., 2016). BtCoV/4991 is 100% identical in sequence to one segment of RaTG13. RaTG13 is a complete viral genome sequence (almost 30,000 nucleotides) that was only published in 2020, after the pandemic began (P. Zhou et al., 2020).

Despite the confusion created by their different names, in a letter obtained by us Zheng-li Shi confirmed to a virology database that BtCoV/4991 and RaTG13 are both from the same bat faecal sample and the same mine. They are thus sequences from the same virus. In the discussion below we will refer primarily to RaTG13 and specify BtCoV/4991 only as necessary.

These specifics are important because it is these samples and their provenance that we believe are ultimately key to unravelling the mystery of the origins of COVID-19.

The story begins in April 2012 when six workers in that same Mojiang mine fell ill from a mystery illness while removing bat faeces. Three of the six subsequently died.

In a March 2020 interview with Scientific American Zeng-li Shi dismissed the significance of these deaths, claiming the miners died of fungal infections. Indeed, no miners or deaths are mentioned in the paper published by the Shi lab documenting the collection of RaTG13 (Ge et al., 2016).

But Shi’s assessment does not tally with any other contemporaneous accounts of the miners and their illness (Rahalkar and Bahulikar, 2020). As these authors have pointed out, Science magazine wrote up part of the incident in 2014 as A New Killer Virus in China?. Science was citing a different team of virologists who found a paramyxovirus in rats from the mine. These virologists told Science they found “no direct relationship between human infection” and their virus. This expedition was later published as the discovery of a new virus called MojV after Mojiang, the locality of the mine (Wu et al., 2014).

What this episode suggests though is that these researchers were looking for a potentially lethal virus and not a lethal fungus. Also searching the Mojiang mine for a virus at around the same time was Canping Huang, the author of a PhD thesis carried out under the supervision of George Gao, the head of the Chinese CDC.

All of this begs the question of why the Shi lab, which has no interest in fungi but a great interest in SARS-like bat coronaviruses, also searched the Mojiang mine for bat viruses on four separate occasions between August 2012 and July 2013, even though the mine is a 1,000 Km from Wuhan (Ge et al., 2016). These collecting trips began while some of the miners were still hospitalised.

Fortunately, a detailed account of the miner’s diagnoses and treatments exists. It is found in a Master’s thesis written in Chinese in May 2013. Its suggestive English title is “The Analysis of 6 Patients with Severe Pneumonia Caused by Unknown viruses“.

The original English version of the abstract implicates a SARS-like coronavirus as the probable causative agent and that the mine “had a lot of bats and bats’ feces”.

The findings of the Master’s thesis

To learn more, especially about the reasonableness of this diagnosis, we arranged to have the whole Master’s thesis translated into English and are here making the translation available. To read it in full see the embedded document below (or download it here).


The six ill miners were admitted to the No. 1. School of Clinical Medicine, Kunming Medical University, in short succession in late April and early May 2012. Kunming is the capital of Yunnan province and 250 Km from Mojiang.

Of the descriptions of the miners and their treatments, which include radiographs and numerous CAT scans, several features stand out:

1) From their admission to the hospital their doctors informed the “medical office” of a potential “outburst of disease” i.e. a potential epidemic outbreak. Thus, the miners were treated for infections and not as if they had inhaled noxious gases or other toxins.

2) The symptoms (on admission) of the six miners were: a) dry cough, b) sputum, c) high fevers, especially shortly before death d) difficulty breathing, e) myalgia (sore limbs). Some patients had hiccoughs and headaches. (See Table 1).

3) Clinical work established that patients 1-4 had low blood oxygen “for sure it was ARDS” (Acute Respiratory Distress Syndrome) and immune damage considered indicative of viral infection. Additionally, a tendency for thrombosis was noted in patients 2 and 4. Symptom severity and mortality were age-related (though from a sample of 6 this must be considered anecdotal).

4) Potential common and rare causes of their symptoms were tested for and mostly eliminated. For patients 3 and 4 these included tests for HIV, Cytomegalovirus, Epstein-Barr Virus (EBV), Japanese encephalitis, haemorrhagic fever, Dengue, Hepatitis B, SARS, and influenza. Of these, only patient 2 tested positive for Hepatitis and EBV.

5) Treatment of the six patients included ventilation (patients 2-4), steroids (all patients), antivirals (all except patient 5), and blood thinners (patients 2 and 4). Antibiotics and antifungal medications were administered to counter what were considered secondary (but significant) co-infections.

6) A small number of remote meetings were held with researchers at other universities. One was with Zhong Nanshan at Sun Yat-Sen University, Guangdong. Zhong is the Chinese hero of the SARS epidemic, a virologist, and arguably the most famous scientist in China.

7) Samples from the miners were later sent to the WIV in Wuhan and to Zhong Nanshan, further confirming that viral disease was strongly suspected. Some miners did test positive for coronavirus (the thesis is unclear on how many).

8. The source of infection was concluded to be Rhinolophus sinicus, a horseshoe bat and the ultimate conclusion of the thesis reads “the unknown virus lead to severe pneumonia could be: The SARS-like-CoV from the Chinese rufous horseshoe bat.” Thus the miners had a coronavirus but it apparently was not SARS itself.

The significance of the Master’s thesis

These findings of the thesis are significant in several ways.

First, in the light of the current coronavirus pandemic it is evident the miners’ symptoms very closely resemble those of COVID-19 (Huang et al, 2020; Tay et al., 2020; M. Zhou et al., 2020). Anyone presenting with them today would immediately be assumed to have COVID-19. Likewise, many of the treatments given to the miners have become standard for COVID-19 (Tay et al., 2020).

Second, the remote meeting with Zhong Nanshan is significant. It implies that the illnesses of the six miners were of high concern and, second, that a SARS-like coronavirus was considered a likely cause.

Third, the abstract, the conclusions, and the general inferences to be made from the Master’s thesis contradict Zheng-li Shi’s assertion that the miners died from a fungal infection. Fungal infection as a potential primary cause was raised but largely discarded.

Fourth, if a SARS-like coronavirus was the source of their illness the implication is that it could directly infect human cells. This would be unusual for a bat coronavirus (Ge et al., 2013). People do sometimes get ill from bat faeces but the standard explanation is histoplasmosis, a fungal infection and not a virus (McKinsey and McKinsey, 2011; Pan et al., 2013).

Fifth, the sampling by the Shi lab found that bat coronaviruses were unusually abundant in the mine (Ge at al., 2016). Among their findings were two betacoronaviruses, one of which was RaTG13 (then known as BtCoV/4991). In the coronavirus world betacoronaviruses are special in that both SARS and MERS, the most deadly of all coronaviruses, are both betacoronaviruses. Thus they are considered to have special pandemic potential, as the concluding sentence of the Shi lab publication which found RaTG13 implied: “special attention should particularly be paid to these lineages of coronaviruses” (Ge at al., 2016). In fact, the Shi and other labs have for years been predicting that bat betacoronaviruses like RaTG13 would go pandemic; so to find RaTG13 where the miners fell ill was a scenario in perfect alignment with their expectations.

The Mojiang miners passaging proposal

How does the Master’s thesis inform the search for a plausible origin of the pandemic?

In our previous article we briefly discussed how the pandemic might have been caused either by a virus collection accident, or through viral passaging, or through genetic engineering and a subsequent lab escape. The genetic engineering possibility deserves attention and is extensively assessed in an important preprint (Segreto and Deigin, 2020).

We do not definitively rule out these possibilities. Indeed it now seems that the Shi lab at the WIV did not forget about RaTG13 but were sequencing its genome in 2017 and 2018. However, we believe that the Master’s thesis indicates a much simpler explanation.

We suggest, first, that inside the miners RaTG13 (or a very similar virus) evolved into SARS-CoV-2, an unusually pathogenic coronavirus highly adapted to humans. Second, that the Shi lab used medical samples taken from the miners and sent to them by Kunming University Hospital for their research. It was this human-adapted virus, now known as SARS-CoV-2­, that escaped from the WIV in 2019.

We refer to this COVID-19 origin hypothesis as the Mojiang Miners Passage (MMP) hypothesis.

Passaging is a standard virological technique for adapting viruses to new species, tissues, or cell types. It is normally done by deliberately infecting a new host species or a new host cell type with a high dose of virus. This initial viral infection would ordinarily die out because the host’s immune system vanquishes the ill-adapted virus. But, in passaging, before it does die out a sample is extracted and transferred to a new identical tissue, where viral infection restarts. Done iteratively, this technique (called “serial passaging” or just “passaging”) intensively selects for viruses adapted to the new host or cell type (Herfst et al., 2012).

At first glance RaTG13 is unlikely to have evolved into SARS-CoV-2 since RaTG13 is approximately 1,200 nucleotides (3.8%) different from SARS-CoV-2. Although RaTG13 is the most closely related virus to SARS-CoV-2, this sequence difference still represents a considerable gap. In a media statement evolutionary virologist Edward Holmes has suggested this gap represents 20-50 years of evolution and others have suggested similar figures.

We agree that ordinary rates of evolution would not allow RaTG13 to evolve into SARS-CoV-2 but we also believe that conditions inside the lungs of the miners were far from ordinary. Five major factors specific to the hospitalised miners favoured a very high rate of evolution inside them.

i) When viruses infect new species they typically undergo a period of very rapid evolution because the selection pressure on the invading pathogen is high. The phenomenon of rapid evolution in new hosts is well attested among corona- and other viruses (Makino et al., 1986; Baric et al., 1997; Dudas and Rambaut 2016; Forni et al., 2017).

ii) Judging by their clinical symptoms such as the CT scans, all the miner’s infections were primarily of the lungs. This localisation likely occurred initially because the miners were exerting themselves and therefore inhaling the disturbed bat guano deeply. As miners, they may already have had damaged lung tissues (patient 3 had suspected pneumoconiosis) and/or particulate matter was present that irritated the tissues and may have facilitated initial viral entry.

In contrast, standard coronavirus infections are confined to the throat and upper respiratory tract. They do not normally reach the lungs (Perlman and Netland, 2009). Lungs are far larger tissues by weight (kilos vs grammes) than the upper respiratory tract. There was therefore likely a much larger quantity of virus inside the miners than would be the case in an ordinary coronavirus infection.

Comparing a typical coronavirus respiratory tract infection with the extent of infected lungs in the miners from a purely mathematical point of view indicates the potential scale of this quantitative difference. The human aerodigestive tract is approximately 20cm in length and 5cm in circumference, i.e. approximately 100 cm2 in surface area. The surface area of a human lung ranges from 260,000-680,000 cm2 (Hasleton, 1972). The amount of potentially infected tissue in an average lung is therefore approximately 4500-fold greater than that available to a normal coronavirus infection. The amount of virus present in the infected miners, sufficient to hospitalise all of them and kill half of them, was thus proportionately very large.

Evolutionary change is in large part a function of the population size. The lungs of the miners, we suggest, supported a very high viral load leading to proportionately rapid viral evolution.

Furthermore, according to the Master’s thesis, the immune systems of the miners were compromised and remained so even for those discharged. This weakness on the part of the miners may also have encouraged evolution of the virus.

iii) The length of infection experienced by the miners (especially patients 2, 3 and 4) far exceeded that of an ordinary coronavirus infection. From first becoming too sick to work in the mine, patient 2 survived 57 days until he died. Patient 3 survived 120 days after stopping work. Patient 4 survived 117 days and then was discharged as cured. Each had been exposed in the mine for 14 days prior to the onset of severe symptoms; thus each presumably had nascent infections for some time before calling in sick (See Table 2 of the thesis).

In contrast, in ordinary coronavirus infections the viral infection is cleared within about ten to fourteen days after being acquired (Tay et al., 2020). Thus, unlike most sufferers from coronavirus infection, the hospitalised miners had very long-term bouts of disease characterised by a continuous high load of virus. In the cases of patients 3 and 4 their illnesses lasted over 4 months.

iv) Coronaviruses are well known to recombine at very high rates: 10% of all progeny in a cell can be recombinants (Makino et al., 1986; Banner and Lai, 1991; Dudas and Rambaut, 2016). In normal virus evolution the mutation rate and the selection pressure are the main foci of attention. But in the case of a coronavirus adapting to a new host where many mutations distributed all over the genome are required to fully adapt to the new host, the recombination rate is likely to be highly influential in determining the overall speed of adaptation by the virus population (Baric et al., 1997).

Inside the miners a large tissue was simultaneously infected by a population of poorly-adapted viruses, with each therefore under pressure to adapt. Even if the starting population of virus lacked any diversity, many individual viruses would have acquired mutations independently but only recombination would have allowed these mutations to unite in the same genome. To recombine, viruses must be present in the same cell. In such a situation the particularities of lung tissues become potentially important because the existence of airways (bronchial tubes, etc.) allows partially-adapted viruses from independent viral populations to travel to distal parts of the lung (or even the other lung) and encounter other such partially-adapted viruses and populations. This movement around the lungs would likely have resulted in what amounted to a passaging effect without the need for a researcher to infect new tissues. Indeed, in the Master’s thesis the observation is several times made that areas of the lungs of a specific patient would appear to heal even while other parts of the lungs would become infected.

v) There were also a number of unusual things about the bat coronaviruses in the mine. They were abnormally abundant but also there were many different kinds, often causing co-infections of the bats (Ge et al., 2016). Viral co-infections are often more infectious or more pathogenic (Latham and Wilson, 2007).

As the WIV researchers remarked about the bats in the mine:

“we observed a high rate of co-infection with two coronavirus species and interspecies infection with the same coronavirus species within or across bat families. These phenomena may be owing to the diversity and high density of bat populations in the same cave, facilitating coronavirus intra- and interspecies transmissions, which may result in recombination and acceleration of coronavirus evolution.” (Ge et al., 2016).

The diversity of coronaviruses in the mine suggests that the miners were similarly exposed and that their illness may potentially have begun as co-infections.

Combining these observations, we propose that the miners’ lungs offered an unprecedented opportunity for accelerated evolution of a highly bat-adapted coronavirus into a highly human-adapted coronavirus and that decades of ordinary coronavirus evolution could easily have been condensed into months. However, we acknowledge that these conditions were unique. They and their scale have no exact scientific precedent we can refer to and they would be hard to replicate in a lab; thus it is important to emphasize that our proposal is fully consistent with the underlying principles of viral evolution as understood today.

In support of the MMP theory we also know something about the samples taken from the miners. According to the Master’s thesis, samples were taken from patients for “scientific research” and blood samples (at least) were sent to the WIV.

“In the later stage we worked with Dr. Zhong Nan Shan and did some sampling. The patient* tested positive for serum IgM by the WuHan Institute of Virology. It suggested the existence of virus infection” (p62 in the section “Comprehensive Analysis”.)

(*The original does not specify the number of patients tested.)

The Master’s thesis also states its regret that no samples for research were taken from patients 1 and 2, implying that samples were taken from all the others.

We further know that, on June 27th, 2012, the doctors performed an unexplained thymectomy on patient 4. The thymus is an immune organ that can potentially be removed without greatly harming the patient and it could have contained large quantities of virus. Beyond this the Master’s thesis is unfortunately unclear on the specifics of what sampling was done, for what purpose, and where each particular sample went.

Given the interests of the Shi lab in zoonotic origins of human disease, once such a sample was sent to them, it would have been obvious and straightforward for them to investigate how a virus from bats had managed to infect these miners. Any viruses recoverable from the miners would likely have been viewed by them as a unique natural experiment in human passaging offering unprecedented and otherwise-impossible-to-obtain insights into how bat coronaviruses can adapt to humans.

The logical course of such research would be to sequence viral RNA extracted directly from unfrozen tissue or blood samples and/or to generate live infectious clones for which it would be useful (if not imperative) to amplify the virus by placing it in human cell culture. Either technique could have led to accidental infection of a lab researcher.

Our supposition as to why there was a time lag between sample collection (in 2012/2013) and the COVID-19 outbreak is that the researchers were awaiting BSL-4 lab construction and certification, which was underway in 2013 but delayed until 2018.

We propose that, when frozen samples derived from the miners were eventually opened in the Wuhan lab they were already highly adapted to humans to an extent possibly not anticipated by the researchers. One small mistake or mechanical breakdown could have led directly to the first human infection in late 2019.

Thus, one of the miners, most likely patient 3, or patient 4 (whose thymus was removed), was effectively patient zero of the COVID-19 epidemic. In this scenario, COVID-19 is not an engineered virus; but, equally, if it had not been taken to Wuhan and no further molecular research had been performed or planned for it then the virus would have died out from natural causes, rather than escaped to initiate the COVID-19 pandemic.

Evidence in favour of the MMP proposal

Our proposal is consistent with all the principal undisputed facts concerning SARS-CoV-2 and its origin. The MMP proposal has the additional benefit of reconciling many observations concerning SARS-CoV-2 that have proven difficult to reconcile with any natural zoonotic hypothesis.

For instance, using different approaches, numerous researchers have concluded that the SARS-CoV-2 spike protein has a very high affinity for the human ACE2 receptor (Walls et al., 2020; Piplani et al., 2020; Shang and Ye et al., 2020; Wrapp et al., 2020). Such exceptional affinities, ten to twenty times as great as that of the original SARS virus, do not arise at random, making it very hard to explain in any other way than for the virus to have been strongly selected in the presence of a human ACE2 receptor (Piplani et al., 2020).

In addition to this, a recent report found that the spike of RaTG13 binds the human ACE2 receptor (Shang and Ye et al., 2020). We proposed above that the virus in the mine directly infected humans lung cells. The main determinant of cell infection and species specificity of coronaviruses is initial receptor binding (Perlman and Netland, 2009). Thus RaTG13, unlike most bat coronaviruses, probably can enter and infect human cells, providing biological plausibility to the idea that the miners became infected with a coronavirus resembling RaTG13.

Moreover, the receptor binding domain (RBD) of SARS-CoV-2, which is the region of the spike that physically contacts the human ACE2 receptor, has recently been crystallised to reveal its spatial structure (Shang and Ye et al., 2020). These authors found close structural similarities between the spikes of SARS-CoV-2 and RaTG13 in how they bound the human ACE2 receptor:

“Second, as with SARS-CoV-2, bat RaTG13 RBM [a region of the RBD] contains a similar four-residue motif in the ACE2 binding ridge, supporting the notion that SARS-CoV-2 may have evolved from RaTG13 or a RaTG13-related bat coronavirus (Extended Data Table 3 and Extended Data Fig. 7). Third, the L486F, Y493Q and D501N residue changes from RaTG13 to SARS CoV-2 enhance ACE2 recognition and may have facilitated the bat-to-human transmission of SARS-CoV-2 (Extended Data Table 3 and Extended Data Fig. 7). A lysine-to-asparagine mutation at the 479 position in the SARS-CoV-2 RBD (corresponding to the 493 position in the SARS-CoV-2 RBD) enabled SARS-CoV to infect humans. Fourth, Leu455 contributes favourably to ACE2 recognition, and it is conserved between RaTG13 and SARS CoV-2; its presence in the SARS CoV-2 RBM may be important for the bat-to-human transmission of SARS-CoV-2″ (Shang and Ye et al., 2020). (italics added)

The significance of this molecular similarity is very great. Coronaviruses have evolved a diverse set of molecular solutions to solve the problem of binding ACE2 (Perlman and Netland, 2009; Forni et al., 2017). The fact that RaTG13 and SARS CoV-2 share the same solution makes RaTG13 a highly likely direct ancestor of Sars-CoV-2.

A further widely noted feature of SARS-CoV-2 is its furin site (Coutard et al., 2020). This site is absent from RaTG13 and other closely related coronaviruses. The most closely related virus with such a site is the highly lethal MERS (which broke out in 2012). Possession of a furin site enables SARS-CoV-2 (like MERS) to infect lungs and many other body tissues (such as the gastrointestinal tract and neurons), explaining much of its lethality (Hoffman et al., 2020; Lamers et al., 2020). However, no convincing explanation for how SARS-CoV-2 acquired this site has yet been offered. Our suggestion is that it arose due to the high selection pressure which existed in the miner’s lungs and which in general worked to ensure that the virus became highly adapted to the lungs. This explanation, which encompasses how SARS-CoV-2 came to target lung tissues in general, is an important aspect of our proposal.

The implication is therefore that the furin site was not acquired by recombination with another coronavirus and simply represents convergent evolution (as suggested by Andersen et al., 2020).

An intriguing alternative possibility is that SARS-CoV-2 acquired its furin site directly from the miner’s lungs. Humans possess an epithelial sodium channel protein called ENaC-a whose furin cleavage site is identical over eight amino acids to SARS-CoV-2 (Anand et al., 2020). ENaC-a protein is present in the same airway epithelial and lung tissues infected by SARS-CoV-2. It is known from plants that positive-stranded RNA viruses recombine readily with host mRNAs (Greene and Allison, 1994; Greene and Allison, 1996; Lommel and Xiong, 1991; Borja et al., 2007). The same evidence base is not available for positive-stranded animal RNA viruses, (though see Gorbalenya, 1992) but if plant viruses are a guide then acquisition of its furin site via recombination with the mRNA which encodes ENaC-a by SARS-CoV-2 is a strong possibility.

A further feature of SARS-CoV-2 has been the very limited adaptive evolution of its genome since the pandemic began (Zhan et al., 2020; van Dorp et al., 2020; Starr et al., 2020). It is a well-established principle that viruses that jump species undergo accelerated evolutionary change in their new host (e.g. Baric et al., 1997). Thus, SARS and MERS (both coronaviruses) underwent rapid and readily detectable adaptation to their new human hosts (Forni et al., 2017; Dudas and Rambaut, 2016). Such an adaptation period has not been observed for SARS-CoV-2 even though it has now infected many more individuals than SARS or MERS did. This has even led to suggestions that the SARS-CoV-2 virus had a period of cryptic circulation in humans infections that predated the pandemic (Chaw et al., 2020). The sole mutation consistently observed to accumulate across multiple studies is a D614G substitution in the spike protein (e.g. Korber et al., 2020). The numerically largest analysis of SARS-CoV-2 genomes, however, found no evidence at all for adaptive evolution, even for D614G (van Dorp et al., 2020).

The general observation is therefore that Sars-CoV-2 has remained functionally unchanged or virtually so (except for inconsequential genetic changes) since the pandemic began. This is a very important observation. It implies that SARS-CoV-2 is highly adapted across its whole set of component proteins and not just at the spike (Zhan et al., 2020). That is to say, its evolutionary leap to humans was completed before the 2019 pandemic began.

It is hard to imagine an explanation for this high adaptiveness other than some kind of passaging in a human body (Zhan et al., 2020). Not even passaging in human cells could have achieved such an outcome.

Two examples illustrate this point. In a follow up to Shang and Ye et al., (2020), a similar group of Minnesota researchers identified a distinct strategy by which the spike (S) protein (which contains the receptor bind domain; RBD) of SARS-CoV-2 evades the human immune system (Shang and Wan et al., 2020). This strategy involves more effective hiding of its RBD, but it implies again that the spike and the RBD evolved in tandem and in the presence of the human immune system (i.e. in a human body and not in tissue culture).

The Andersen authors, in their critique of a possible engineered origin for SARS-CoV-2, also stress the need for passaging in whole humans:

“Finally, the generation of the predicted O-linked glycans is also unlikely to have occurred during cell-culture passage, as such features suggest the involvement of an immune system” (Andersen et al., 2020).

The final point that we would like to make is that the principal zoonotic origin thesis is the one proposed by Andersen et al. Apart from being poorly supported this thesis is very complex. It requires two species jumps, at least two recombination events between quite distantly related coronaviruses and the physical transfer of a pangolin (having a coronavirus infection) from outside China (Andersen et al., 2020). Even then it provides no logical explanation of the adaptedness of SARS-CoV-2 across its whole genome or why the virus emerged in Wuhan.

By contrast, our MMP proposal requires only the one species jump, which is documented in the Master’s thesis. Although we do not rule out a possible role for mixed infections in the lungs of the miners, nor the possibility of recombination between closely related variants in those lungs, nor the potential acquisition of the furin site from a host mRNA, only mutation was needed to derive SARS-CoV-2 from RaTG13. Hence our attention earlier to the figure from P. Zhou et al., 2020 showing that RaTG13 is the most closely related virus to SARS-CoV-2 over its entire length. This extended similarity is perfectly consistent with a mutational origin of SARS-CoV-2 from RaTG13.

In short, the MMP theory is a plausible and parsimonious explanation of all the key features of the COVID-19 pandemic and its origin. It accounts for the propensity of SARS-CoV-2 infections to target the lungs; the apparent preadapted nature of the virus; and its transmission from bats in Yunnan to humans in Wuhan.

Further question

The hypothesis that SARS-CoV-2 evolved in the Mojiang miner’s lungs potentially resolves many scientific questions about the origin of the pandemic. But it raises others having to do with why this information has not come to light hitherto. The most obvious of these concern the actions of the Shi lab at the WIV.

Why did the Shi lab not acknowledge the miners’ deaths in any paper describing samples taken from the mine (Ge et al., 2016 and P. Zhou et al., 2020)? Why in the title of the Ge at al. 2016 paper did the Shi lab call it an “abandoned” mine? When they published the sequence of RaTG13 in Feb. 2020, why did the Shi lab provide a new name (RaTG13) for BtCoV/4991 when they had by then cited BtCoV/4991 twice in publications and once in a genome sequence database and when their sequences were from the same sample and 100% identical (P. Zhou et al., 2020)? If it was just a name change, why no acknowledgement of this in their 2020 paper describing RaTG13 (Bengston, 2020)? These strange and unscientific actions have obscured the origins of the closest viral relatives of SARS-CoV-2, viruses that are suspected to have caused a COVID-like illness in 2012 and which may be key to understanding not just the origin of the COVID-19 pandemic but the future behaviour of SARS-CoV-2.

These are not the only questionable actions associated with the provenance of samples from the mine. There were five scientific publications that very early in the pandemic reported whole genome sequences for SARS-CoV-2 (Chan et al., 2020; Chen et al., 2020; Wu et al., 2020; P. Zhou et al., 2020; Zhu et al., 2020). Despite three of them having experienced viral evolutionary biologists as authors (George Gao, Zheng-li Shi and Edward Holmes) only one of these (Chen et al., 2020) succeeded in identifying the most closely related viral sequence by far: BtCoV/4991 a viral sequence in the possession of the Shi lab at the WIV that differed from SARS-CoV-2 by just 5 nucleotides.

As we noted in our earlier article, the most important of the questions surrounding the origins of SARS-CoV-2 could potentially be resolved by a simple examination of the complete lab notebooks and biosafety records of relevant researchers at the WIV. Now that a credible and testable lab escape hypothesis exists this task becomes potentially much easier. This moment thus represents an opportune one to renew that call for an independent and transparent investigation of the WIV.

In requesting an investigation we are aware that no scientific institution anywhere has made a comparable request. We believe that this failure undermines public trust in a “scientific response” to the pandemic. Instead, the scientific establishment has labeled the lab escape theory a “rumor“, an “unverified theory” and a “conspiracy” when its proper name is a hypothesis. By taking this stance the scientific establishment has given the unambiguous message that scientists who take the possibility of a lab origin seriously are jeopardising their careers. Thus, while countless scientific publications on the pandemic assert in their introductions that a zoonotic origin for SARS-CoV-2 is a matter of fact or near-certainty (and Andersen et al has 860 citations as of July 14th), there is still not one published scientific paper asserting that a lab escape is even a credible hypothesis that deserves investigation.

Anyone who doubts this pressure should read the interview with Birger Sørensen in Norway’s Minerva magazine in which Sørensen discusses the “reluctance” of journals to publish his assessment that the existence of a virus that is “exceptionally well adjusted to infect humans” is “suspicious” and “cannot have evolved naturally”. The source of this reluctance, says Sørensen, is not rationality or scientific evidence. It results from conflicts of interest. This mirrors our experience. To find genuinely critical analysis of COVID-19 origin theories one has to go to Twitter, blog posts, and preprint servers. The malaise runs deep when even scientists start to complain that they don’t trust science.

We nevertheless hope that journalists will investigate some of the conflicts of interest that are keeping scientists and institutions from properly investigating the lab escape hypothesis.

https://www.independentsciencenews.org/ ... -pandemic/

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The article wrote:To find genuinely critical analysis of COVID-19 origin theories one has to go to Twitter, blog posts, and preprint servers.
The mantra of all conspiracy theorists. No wonder you like this version. :roll:
#15111182
The usual braindead commentary from the ponut gallery.

Jonathan R Latham, PhD is co-founder and Executive Director of the Bioscience Resource Project and the Editor of Independent Science News. Dr Latham is also the Director of the Poison Papers project which publicizes documents of the chemical industry and its regulators. Dr. Latham holds a Masters degree in Crop Genetics and a PhD in Virology. He was subsequently a postdoctoral research associate in the Department of Genetics, University of Wisconsin, Madison. He has published scientific papers in disciplines as diverse as plant ecology, plant virology, genetics and genetic engineering. Dr Latham talks frequently at international events and scientific and regulatory conferences on the research conducted by the Project. He has written for Truthout, MIT Technology Review, the Guardian, Resilience, Salon.com, and many other magazines and websites.

Allison K Wilson, PhD is co-founder and Science Director of the the Bioscience Resource Project; Editor of the Bioscience Resource Project website; Assistant Editor of Independent Science News; and a contributor to the Poison Papers project. Dr. Wilson holds a BA in Biology from Cornell University, a doctorate in Molecular Biology and Genetics from Indiana University, Bloomington, and was formerly a postdoctoral research associate at the Fred Hutchinson Cancer Research Center, Seattle and the John Innes Centre, Norwich, UK. Dr. Wilson has published scientific research on plant hormones and flowering time in Arabidopsis, Tetrahymena molecular biology, and plant genetic engineering. She was also a contributing author of the Encyclopedia of Molecular Biology (John Wiley and Sons Inc.,1999).
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Unthinking Majority wrote:That doesn't mean Trump's response and the the actions of governors and regular citizens especially in the southern states hasn't made things worse for them.

As opposed to the great success of New York, the richest city in the US, Democrat run, in a wealthy Democrat run State. Trump was almost universally hated by the New York Democratic Party and much of the business and administrative elite within New York. Liberals have admitted on this forum that if Trump said the world was round they would believe it was flat. In places like New York and New Jersey, nothing could be more likely to galvanise support for lockdown than Trump's opposition to it.

Before Trump there was widespread support for border walls amongst Democrats. Not now. While Obama hid his Liberalness or Leftness during his first term, during his time in office he never supported open borders. Now because Trump said America should get serious about immigration control, most Democrats oppose all measures of immigration control, they support open borders although of course most of the Democrat establishment lyingly pretends it doesn't.
#15111379
BeesKnee5 wrote:Makes you wonder why Jonathon Latham only published his research at independent science news instead of a peer reviewed journal.



The fight for a controversial article
Birger Sørensen and Angus Dalgleish failed to get an article about the origins of the coronavirus published in a scientific journal. The authors suspect foul play and political considerations. Not everything gets published, is the answer from the journals. Minerva has obtained a draft of the paper, to let readers and researchers decide.

In an interview with Minerva last week, the well-known Norwegian vaccine researcher and physical chemist Birger Sørensen argued that the novel coronavirus is not natural in origin.

Together with his colleagues Angus Dalgleish and Andres Susrud – the latter in a data analytical role as statistician and data miner – Sørensen has written a series of journal articles that put forward arguments for why the most likely explanation for the origin of the coronavirus is a laboratory.

If such findings were confirmed, there could be political ramifications. Naturally, therefore, Sørensen, Dalgleish and their unpublished paper have been mired in controversy ever since Sir Richard Dearlove, former head of the MI6, endorsed their conclusions. The authors themselves suspect that the controversial conclusions and the heated debate may have made journals reluctant to evaluate their paper objectively. However, tons of scientific articles are rejected for any number of reasons.

By tracing the writing of articles, the contact between the authors and the journals, and reviewing the findings, this article aims to shed light on a troubling question for the scientific community during the Corona crisis: One the one hand, there is an overabundance of papers and findings of highly variable quality – some of which fuel conspiracy theories. On the other hand, the question of the origin of the Corona virus has become a fraught political question, with the Chinese government clamping down on independent research, and president Donald Trump claiming that the virus originated in a Chinese lab without producing any evidence to back up the assertion.

With the consent of Mr. Sørensen and his co-authors (henceforth: Sørensen and Dalgleish), Minerva has obtained a full print of the article, to be read freely by our readers – and by scientists, who may then discuss and dissect the paper.

Searching for a vaccine

It started out with something less controversial: Originally, the authors were engaged in analysis of the virus with the aim to create a vaccine. The discoveries that the authors claim to be relevant for determining the origin of the virus came as a by-product of this research.

In fact, Sørensen and Dalgleish have managed to get a paper on the corona virus peer reviewed and published, in Quarterly Reviews of Biophysics Discovery. This article, which is more closely linked to their vaccine development, deals with observations of the virus and the receptors that the virus can attach to in humans. Sørensen and Dalgleish do indeed believe that these properties indicate a lab origin for the virus. However, the article itself avoids any mention of this implication of the discovered properties.

Originally, the findings which are now published in Quarterly Reviews of Biophysics Discovery were part of a more condensed article, which included the lab origin hypothesis. To make this argument, the three have now instead written a second article, “The Evidence which Suggests that This Is No Naturally Evolved Virus”, that puts forward their arguments on why they believe the virus is likely to be a laboratory construct, by combining insights from the first paper with what is known from lab work on corona viruses.

However, this second article is yet to be accepted by a scientific journal – having been rejected at different times and formats by three leading journals. Sørensen states that he is presently in dialogue with other journals regarding publication. A third paper on a related topic also taken from the original argument, is yet to be submitted.

Endorsed and criticized

Before we move on, let’s take a look on some of the reactions from within the scientific community. Sørensen has received both severe criticism and partial support.

Professor Kristian Andersen at the department of immunology and microbiology at Scripps Research, a medical research facility in California, was lead author on the article “The proximal origin of SARS-CoV-2” where he states that his “analyses clearly show that SARS-CoV-2 is not a laboratory construct or a purposefully manipulated virus”.

Andersen last week told Sky news that Sørensen’s and Dalgleish’s work was “complete nonsense, unintelligible, and not even remotely scientific – leading the authors to make unfounded and unsupported conclusions about the origin of SARS-CoV-2”. However, Andersen has not had an opportunity to read the second, unpublished article.

Minerva has, however, shared that second article with Birgitta Åsjö, a professor emerita in virology at the university of Bergen. She is puzzled by Andersen’s comments, and rejects the notion that Sørensen’s and Dalgleish’ work is unscientific nonsense. “Andersen is harsh, I don’t know why he’s so harsh. I don’t want to dismiss it completely”, she told Minerva in an interview.

Åsjö does not consider the article to contain conclusive evidence that the novel coronavirus has a lab origin, but adds that she considers the article to contain “interesting findings”. She is herself critical of some of the arguments presented in Andersen’s own article on the origin of the virus.

In particular, Åsjö is interested in Sørensen’s and Dalgleish’ findings concerning properties of a swine corona virus detected in connection with an outbreak among piglets in Guandong in 2016–2017, and its possible significance for the present SARS-CoV-2 virus. So far, the controversy seems to resemble other controversies between academics who rarely hesitate to describe rivalling theories in the harshest possible terms. Indeed, Sørensen and Dalgleish originally intended to publish their arguments as a stark critique of the article by Andersen et al in Nature and what they describe “as puzzling errors in their use of evidence”.

Self-confident scientists and strict journals

With this aim, Angus Dalgleish wrote a letter to the editor in Nature on April 2, requesting that journal to publish an earlier version of these arguments.

This article was rejected by Nature five days later, on April 7. Announcing the rejection, João Monteiro, chief editor in Nature Medicine, wrote to Dalgleish:

First rejection from Nature Medicine

“While we appreciate that the points you have raised extend the discussion about the origin of SARS-CoV2 further our opinion is that the content complements other viewpoints that have been considered and published elsewhere, and therefore would be as appropriate for publication in the specialized literature. Please note that this is not a criticism regarding the importance of the matter or the quality of your analyses, but rather an editorial assessment of priority for publication, in a time when there are many pressing issues of public health and clinical interest that take precedence for publication in Nature Medicine, and limited space in the journal.”

Monteiro ended the email by encouraging Dalgleish to post his comments in one of “the accepted preprint repositories so that it remains visible and adds to the discussion about the origin of the virus.”

A clearly angered Dalgleish then wrote a response stating: “Thank you for your extraordinarily unhelpful replies. We can only conclude that the Nature editorial team does not understand that there is no scientific issue in the world at present more important than establishing with scientific precision the aetiology of the Covid-19 virus.”

After the first rejection by Nature, the authors approached another premier journal, Journal of Virology. However, by April 20, the first version of the paper had been rejected there as well. A few days later, this version of the paper was put to death by a rejection from bioRxiv, a non-peer-reviewed preprint repository. The stated reason for rejection was that the format of the paper did not conform to a normal, full research paper, with sections such as «Methods» and «Results».

The first iteration of rejections thus seem to fit into a typical pattern: Scientists with overconfidence not only in the quality of their own research, but also its relevance and significance, encountering journals with strict guidelines for format, each with its own mission and focus, and not very patient with professors that flaunt formal requirements.

Still, it seems that the actual arguments put forward might not have been properly evaluated, or could not be properly evaluated in this setting. And the findings, if correct, would seem to merit some sort of scientific attention. How to proceed?

A publication and new rejections

After the initial round of rejections, the authors made several revisions to their original article, with the arguments sectioned into separate articles. The first article – an analysis of the novel coronavirus, for the purpose of vaccine design, without making the argument that the virus is engineered – was published June 2 in the Quarterly Reviews of Biophysics Discovery which is one of the top peer-reviewed science journals in the world.

Having achieved this publication, and presumably regained confidence that the scientific quality of the work was all right, Sørensen and Dalgleish again reached out to several of the world’s most prestigious scientific journals. Now they wanted to publish the second article, which builds on the first, already accepted article, and presents their arguments for why the coronavirus is of a non-natural origin.

However this article was again rejected by Nature on June 24 – without being sent out to peer review. The rejection, written by Senior Editor Clare Thomas, states: .

Second rejection from Nature Medicine
It is our policy to decline a substantial proportion of manuscripts without sending them to referees so that they may be sent elsewhere without further delay. In making this decision, we are not questioning the technical quality or validity of your findings, or their value to others working in this area, only assessing the suitability of the study based on the editorial criteria of the journal. In this case, we do not believe that the work represents a development of sufficient scientific impact such that it might merit publication in Nature. We therefore feel that the study would find a more suitable audience in another journal.

On July 1, Sørensen and his colleagues therefore challenged Science, another scientific journal to publish his article. Arguing for the publication of the article Sørensen wrote in an e-mail to editor Professor Holden Thorp:

“Now that Dr. Tedros Adhanom Ghebreyesus has indicated that WHO will pursue a long-overdue inquiry into the aetiology of the SARS-CoV-2 virus, which we welcome, we hope that you will support the very necessary debate that is now breaking in a second wave, following the publication of our vaccine. We are aware of significant responsible mainstream media interventions that are imminent. We are glad that this important question will now be addressed where it should be, in mainstream media and science journals, and not left to internet speculations, some of which have been both uninformed and therefore unhelpful, in our view.”

However, Sørensen was rebuffed also by Science the very next day. In an email to Sørensen, Professor Throp wrote that the article was unfit for publishing in Science, due to the fact that it criticizes work published in another journal:

Rejection from Science
Dr. Sorenson,

Thank you for your interest. We do not publish papers that are critiques of works in other journals, so we cannot consider something along these lines.

Holden

Holden Thorp

Editor-in-Chief

On the rejections from the scientific journals co-author Angus Dalgleish told Sky News: “I thought the whole point of a scientific journal was that you put forward some speculation and you opened it up to debate”, said Professor Dalgleish.

Agree or disagree with Dalgleish’s description of what a scientific journal does, the new round of rejections complicate the picture from the first round. A major part of the argument was accepted by a respectable journal – the one that didn’t spell out the implications for the origin of the virus. The article that did spell it out, was now rejected twice, without peer review, and the second rejection on purely formal grounds that the authors vehemently contest, arguing that the paper in its current form is not first and foremost a critique of the Andersen et al. paper.

Minerva has asked both Nature and Science to elaborate on the reasons for why the articles by Sørensen and his co-authors have been rejected. Both Science and Nature have declined to comment on the specific rejection of the article as they view this information as confidential. However, Executive Director of the Science Press Package Meagan Phelan, replied that “Science receives upwards of 11,000 manuscripts per year, and the acceptance rate is 6%, so the vast majority of papers are rejected for one reason or another. Science’s acceptance rate for COVID-19-related submissions is even lower, at 4%. The journal continues to receive an exceptionally high volume of COVID-19-related submissions each week.”

At press time, the second article is still in search of a scientific journal willing to publish – or, at least, to subject it to peer review.


https://www.minervanett.no/angus-dalgle ... cle/362519
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The most logical explanation is that it comes from a laboratory
The well-known Norwegian virologist Birger Sørensen and his colleagues have examined the corona virus. They believe it has certain properties which would not evolve naturally. These conclusions are politically controversial, but in this interview he shares the findings behind the headlines.

“I understand that this is controversial, but the public has a legitimate need to know, and it is important that it is possible to freely discuss alternate hypotheses on how the virus originated” Birger Sørensen starts to explain when Minerva visits him in his office one morning in Oslo.

Despite the explosiveness of his statements and research, Sørensen remains calm and collected.

Sørensen has been a point of controversy ever since former MI6 director Richard Dearlove cited a yet to be published article by Sørensen and his colleagues in an interview with The Daily Telegraph. The article claims that the virus that causes Covid-19 most likely has not emerged naturally.

“It’s a shame that there has already been so much talk about this, because I have yet to publish the article where I put forward my analysis”, Sørensen says in the form of an exasperated sigh.

Together with his colleagues, Angus Dalgleish and Andres Susrud have authored an article that looks into the most plausible explanations regarding the origins of the novel coronavirus. The article builds upon an already published article in the Quarterly Review of Biophysics that describes newly discovered properties in the virus spike protein. The authors are still in dialogue with scientific journals regarding an upcoming publication of the article.

[...]

On May 18th, WHO decided to conduct an inquiry into the coronavirus epidemic in China. Sørensen believes that it is important that this inquiry looks into new and alternate explanations for how the virus originated, beyond the already well-known suggestion that the virus originated in the Wuhan Seafood Market.

“There are very few who still believe that the epidemic started there, so as of today we have no good answers on how the epidemic started. Then we must also dare to look at more controversial, alternative explanations for the origin,” Sørensen says.

Birger Sørensen and one of his co-authors, Angus Dalgleish, are already known as HIV researchers par excellence.

In 2008, Sørensen’s work came to international attention when he launched a new immunotherapy for HIV. Angus Dalgleish is the professor at St. George’s Medical School in London who became world famous in 1984 after having discovered a novel receptor that the HIV virus uses to enter human cells.

The purpose of the work Sørensen and his colleagues have done on the novel coronavirus, has been to produce a vaccine. And they have taken their experience in trialling HIV vaccines with them to analyse the coronavirus more thoroughly, in order to make a vaccine that can protect against Covid-19 without major side effects.

[...]

“We have examined which components of the virus are especially well suited to attach themselves to cells in humans. And we have done this by comparing the properties of the virus with human genetics. What we found was that this virus was exceptionally well adjusted to infect humans.”

He pauses for a second.

“So well that it was suspicious,” he adds.

Perfected to infect humans

It is already known that the novel coronavirus, like the virus that caused the SARS epidemic in Southeast Asia in 2002-2003, could attach itself to the ACE-2 receptors in the lower respiratory tract.

“But what we have discovered is that there are properties in this new virus which enables it to use an additional receptor, and create a binding to human cells in the upper respiratory tract and the intestines which is strong enough to produce an infection,” Sørensen elaborates.

Sørensen says that it is the use of this additional receptor that most likely results in a different illness in Covid-19 patients than the one resulting from SARS.

“This is what enables the virus to transmit to a greater degree between humans, without the virus having attached itself to the ACE-2 receptors in the lower respiratory tract, where it causes deep pneumonia.

“That is also why so many of the Covid-19 patients have mild symptoms at the start of the illness, and are contagious before they develop severe symptoms,” he adds.

It might also explain why some people are ‘super spreaders’ without being ill themselves, Sørensen says.

In the already published article Sørensen and his colleagues Angus Dalgleish and Andres Susrud describe what they claim is curious about the spike protein of the coronavirus, which makes it especially well suited to infect humans. These findings are the foundation for the hypothesis Sørensen and his colleagues develop in the new article, where they claim that the virus is not natural in origin.

FACT BOX – Spike Protein
A spike protein is a part of the virus attached to the surface of the virus. The spike protein is used by the virus when it enters cells, enabling it to stick in humans. The properties of the spike determines which receptors a virus can utilise and thus which cells the virus can enter to create illness.

“There are several factors that point towards this,” says Sørensen. “Firstly, this part of the virus is very stable; it mutates very little. That points to this virus as a fully developed, almost perfected virus for infecting humans.

“Secondly, this indicates that the structure of the virus cannot have evolved naturally. When we compare the novel coronavirus with the one that caused SARS, we see that there are altogether six inserts in this virus that stand out compared to other known SARS viruses,” he goes on explaining.

Sørensen says that several of these changes in the virus are unique, and that they do not exist in other known SARS coronaviruses.

“Four of these six changes have the property that they are suited to infect humans. This kind of aggregation of a type of property can be done simply in a laboratory, and helps to substantiate such an origin,” Sørensen points out.

An artificially created virus

Asked about whether this implies that the virus is not natural, Sørensen goes on to explain the laboratory process that leads to the creation of new viruses.

“In a sense it is natural. But the natural processes have most likely been accelerated in a laboratory,” he explains. “It’s also possible for a virus to attain these properties in nature, but it’s not likely. If the mutations had happened in nature, we would have most likely seen that the virus had attracted other properties through mutations, not just properties that help the virus to attach itself to human cells.”

Sørensen vividly explains this argument:

“Imagine that you have cultivated a billion coronaviruses you have gathered from nature, then you take this mass of viruses and inject them into a human cell culture from for example the upper respiratory tract. As a result, a few of these viruses will change in order to better attach themselves to this type of cell in the nose and throat region and therefore to infect humans more easily. You end up with a virus with a spike protein which is perfect for attaching to and penetrating human cells.” Sørensen explains.

Asked about the particular mutations in the virus that lead to this conclusion, Sørensens says:

“What we see is that an area that you could observe in the first SARS coronavirus has been moved, so that the parts of the virus that are particularly well suited to attach to humans, have become part of the spike protein that the virus uses to penetrate human cells. And it is this moving of the area of the virus which makes the virus, together with the injected areas explained above, able to utilise an additional receptor to infect humans.”

On a board in the meeting room where Sørensen is hosting our meeting, he illustrates what he is trying to explain, and how a component of the virus which previously was situated on another part of the shell of the virus, now has become a part of the spike protein of the virus.

More than ninety percent confident

Sørensen is therefore quite confident that the virus has originated in a laboratory.

“I think it’s more than 90 percent certain. It’s at least a far more probable explanation than it having developed this way in nature”, Sørensen responds.

Sørensen also highlights other data than those related to the virus’ properties:

“The properties that we now see in the virus, we have yet to discover anywhere in nature. We know that these properties make the virus very infectious, so if it came from nature, there should also be many animals infected with this, but we have still not been able to trace the virus in nature.

“The only place we are aware of where an equivalent virus to that which causes Covid-19 exists, is in a laboratory. So the simplest and most logical explanation is that it comes from a laboratory. Those who claim otherwise, have the burden of proof,” Sørensen says.

https://www.minervanett.no/corona/the-m ... ory/361860

#15111427
Excellent article from The Bulletin of Atomic Scientists detailing the circumstantial evidence for a lab origin:

Did the SARS-CoV-2 virus arise from a bat coronavirus research program in a Chinese laboratory? Very possibly.

But long before Trump, Pompeo and Co. sought a Chinese scapegoat for the president’s gross and willful incompetence, researchers understood that the possibility of laboratory escape of the pathogen was a plausible, if unproven, possibility. It is most definitely not “a conspiracy theory.”


The circumstantial evidence for a lab escape. By way of introduction, there are two virology institutes in Wuhan to consider, not one: The Wuhan Center for Disease Control and Prevention (WHCDC) and the Wuhan Institute of Virology (WIV). Both have conducted large projects on novel bat viruses and maintained large research collections of novel bat viruses, and at least the WIV possessed the virus that is the most closely related known virus in the world to the outbreak virus, bat virus RaTG13. This virus was isolated in 2013 and had its genome published on January 23, 2020. Seven more years of bat coronavirus collection followed the 2013 RaTG13 isolation.

One component of the novel-bat-virus project at the Wuhan Institute of Virology involved infection of laboratory animals with bat viruses. Therefore, the possibility of a lab accident includes scenarios with direct transmission of a bat virus to a lab worker, scenarios with transmission of a bat virus to a laboratory animal and then to a lab worker, and scenarios involving improper disposal of laboratory animals or laboratory waste.

Documentary evidence indicates that the novel-bat-virus projects at Wuhan CDC and the Wuhan Institute of Virology used personal protective equipment and biosafety standards that would pose high risk of accidental infection of a lab worker upon contact with a virus having the transmission properties of the outbreak virus.

In assessing the possibility of a lab accident, one must take into consideration each of the following eight elements of circumstantial evidence:

1. Official Chinese government recognition early in the SARS-CoV-2 outbreak of biosafety inadequacies in China’s high containment facilities. In February 2020, several weeks after the outbreak of the disease in Wuhan, China’s President Xi Jinping stressed the need to ensure “biosafety and biosecurity of the country.”2 This was followed immediately by a China Ministry of Science & Technology announcement of new guidelines for laboratories, especially in handling viruses.3 Almost at the same time, the Chinese newspaper Global Times published an article on “chronic inadequate management issues at laboratories, including problems of biological wastes.”4

A PBS NewHour presentation on May 22, 2020 provided the following information:

On January 1, Wuhan Institute of Virology’s director general, Yanyi Wang, messaged her colleagues, saying the National Health Commission told her the lab’s COVID-19 data shall not be published on social media and shall not be disclosed to the media. And on January 3, the commission sent this document, never posted online, but saved by researchers, telling labs to destroy COVID-19 samples or send them to the depository institutions designated by the state. Late Friday [May 16, 2020] the Chinese government admitted to the destruction … but said it was for public safety.

The Chinese government explanation for the destruction of SARS-CoV-2 samples has no scientific credibility. For purposes of “public safety” any samples would surely be stored and studied, exactly as with the ones that were isolated from patients, and their RNA genomes decoded and published.

2. Recognition by Zhengli Shi, a renowned scientist who leads a research team at the Wuhan Institute of Virology, that a laboratory escape was a possibility. Shi took the possibility of a laboratory escape perfectly seriously. Jonna Mazat of the University of California-Davis, a collaborator with Dr Shi, told Josh Rogin of the Washington Post, “Absolutely, accidents can happen.” In an interview with Scientific American, Shi admitted that her very first thought was “If coronaviruses were the culprit, she remembers thinking ‘Could they have come from our lab?’”

Meanwhile she frantically went through her own lab’s records from the past few years to check for any mishandling of experimental materials, especially during disposal. She breathed a sigh of relief when the results came back: none of the sequences matched those of the viruses her team had sampled from bat caves. ‘That really took a load off my mind,’ she says. ‘I had not slept a wink for days.’

3. Questions surrounding Chinese government attribution of the Wuhan’s Huanan South China Seafood Market as the source of the SARS-CoV-2 virus. Many China scholars noted that it was quite unusual for Chinese government authorities to identify Wuhan’s Huanan South China Seafood Market so quickly as the source of the outbreak. They thought this behavior so uncharacteristic that it raised suspicions in their minds. The authors of a newly published paper wrote that

…we were surprised to find that SARS-CoV-2 resembles SARS-CoV in the late phase of the 2003 epidemic after SARS-CoV had developed several advantageous adaptations for human transmission. Our observations suggest that by the time SARS-CoV-2 was first detected in late 2019, it was already pre-adapted to human transmission to an extent similar to late epidemic SARS-CoV. However, no precursors or branches of evolution stemming from a less human-adapted SARS-CoV-2-like virus have been detected…. It would be curious if no precursor or branches of SARS-CoV-2 evolution are discovered in humans or animals….Even the possibility that a non-genetically-engineered precursor could have adapted to humans while being studied in a laboratory should be considered, regardless of how likely or unlikely.5

It is important to note that no intermediary host has yet been identified for the SARS-CoV-2 virus. The authors also noted that “[n]o animal sampling prior to the shutdown and sanitization [of the Wuhan fish market] was done.”


The question of whether the index case appeared in the Wuhan fish market appears to be moot in any case. Chinese researchers have published data showing that there were 41 cases of SARS-CoV-2 between December 1, 2019 and January 2, 2020. Fourteen of these had no contact with the Huanan seafood market, including the very first recorded case on December 1, 2019.6 And that supposes that the true index case was December 1, which is doubtful.

On May 26, the Chinese government scrapped the previous official story about the Wuhan fish market:

China’s top epidemiologist said Tuesday that testing of samples from a Wuhan food market, initially suspected as a path for the virus’s spread to humans, failed to show links between animals being sold there and the pathogen. Gao Fu, director of the Chinese Center for Disease Control and Prevention, said in comments carried in China state media.7

No SARS-CoV-2 isolates were detected in any of the animals or fish sold at the market, only in environmental samples, including sewage. Gao Fu added, “At first, we assumed the seafood market might have the virus, but now the market is more like a victim. The novel coronavirus had existed long before.”8

4. Suppression of information and individuals by Chinese authorities. A publication by two Chinese university academics discussed both the WHCDC and the WIV and concluded that “the killer coronavirus probably originated from a laboratory in Wuhan”; the publication was removed from the internet by Chinese government officials. The paper had been posted on Research Gate but was blocked after 24 hours. After being placed on an archive file by internet users, it was again blocked after a week, and the two Chinese authors were pressured to retract the paper. However, it is still available on Web archives.9

The Chinese government closed the laboratory in Shanghai that first published the genome of COVID-19 on January 10, explaining that it had been shuttered for “rectification”; the closure happened on January 11. The government then permitted the same genome to be published by Shi on January 12.10 Chinese citizens who reported on the coronavirus were censured and, in some cases, “disappeared.”11 These have included businessman Fang Bin, lawyer Chen Qiushi, former state TV reporter Li Zehua and, most recently, Zhang Zhan, a lawyer. They are reportedly being held in extrajudicial detention centers for speaking out about China’s response to the pandemic. They are usually accused of “picking quarrels and provoking trouble.”12

Another aspect of Chinese government secrecy involved in the SARS-CoV-2 pandemic relates to official reporting by Chinese government officials on the severity of the outbreak in China and on levels of mortality. The number of cases and deaths are suspected of being undercounted by at least an order of magnitude, and possibly two, meaning that the reported figures could be as little as one percent of the actual totals. In the last week of April 2020, Caixin, one of the most reliable publications in China, reported that a serological study had been carried out in Wuhan on 11,000 inhabitants. Extrapolating from its results, which showed that five to six percent of the sample of 11,000 persons carried antibodies for SARS-CoV-2, Caixin estimated that 500,000 people in the city had been infected, or 10 times the level of official Chinese government reporting. The publication was quickly deleted by Chinese government censors.13

The Chinese government has also attempted to obscure the origins of the pandemic with disinformation. On March 13, Chinese Foreign Ministry spokesperson Zhao Lijian suggested that the United States might have introduced the coronavirus to Wuhan.14 A month later, Zhao Lijian again posted Russian coronavirus and biowarfare-related disinformation, this time followed by online posts from Chinese ambassadors in 13 countries spread across the world.15 This was unprecedented diplomatic behavior for China, but not an accident. It was a concerted, deliberate, and preposterous disinformation campaign, repeated in May by CGTN, the China Global Television Network, which reposted the disinformation to the social media sites Weibo, Facebook, and Twitter.16 The history of Soviet and then Russian government biowarfare disinformation suggests that a country spreading such disinformation has or may have something to hide.17

5. Laboratory accidents and the escape of highly dangerous pathogens from laboratories are frequent occurrences worldwide. The accidental infection of researchers in the highest containment biosafety facilities—labelled BSL-2, BSL-3 and BSL-4—occurs worldwide, as do accidental releases by other means. In an excellent review published in February 2019, Lynn Klotz of the Center for Arms Control and Non-Proliferation noted that three releases of Ebola and Marburg viruses from BSL-4 and lower-containment facilities in the United States had occurred due to incomplete inactivation of cultures. Releases via infection of researchers took place in the highest containment facilities in the United States—at the Centers for Disease Control and Prevention (CDC) in Atlanta and at the US Army Medical Research Institute of Infectious Diseases (USAMRIID)—but in all cases only the researcher became ill, and there was no further transmission of the pathogen.

“In an analysis circulated at the 2017 meeting for the Biological Weapons Convention, a conservative estimate shows that the probability is about 20 percent for a release of a mammalian-airborne-transmissible, highly pathogenic avian influenza virus into the community from at least one of 10 labs over a 10-year period of developing and researching this type of pathogen,” Klotz wrote. “This percentage was calculated from FSAP [US Federal Select Agent Program] data for the years 2004 through 2010. Analysis of the FOIA NIH (National Institutes of Health) data gives a much higher release probability—that is, a factor five to 10 times higher, based on a smaller number of incident reports.”18

Between 2009 and 2015, the FSAP recorded 749 incidents in seven categories—not solely releases or researcher infections—from 276 facilities. In addition, Klotz recorded 11 confirmed releases of select agents that resulted in a laboratory-acquired infection in roughly 280 specifically approved laboratories in the United States between 2003 and 2017, a rate of just under one per year.19 A second publication in the Bulletin that covered closely-related subject matter and a personal communication from its author suggested that federally reported cases involving select agents were likely to be substantially undercounted:20

There is a fundamental problem of using the defined select agents as a surrogate for potential pandemic agent releases from research labs. The vast majority of ‘classical BW agents’ that initially defined select agents in the US were selected specifically to be NOT capable of sustained transmission so as to better define the military tactical limits of a military employment and because the establishment of progressive transmission was considered unpredictable and possibly counterproductive in military operations, at least on the US side of offensive development in the 1940s-1960s.

As my historical review of lab escapes that resulted in pandemics or wide area epidemics published in the BAS found, most pandemic, continental or large scale community outbreaks originating from lab escapes came from civilian labs working with public or veterinary pathogens of non-military interest.

It takes only one superspreading graduate student or maintenance worker to start a pandemic.

It is known that a very large percentage of the individuals infected with the SARS-CoV-2 virus show no symptoms and do not become clinically ill, which would facilitate an unrecognized infection of one or more laboratory researchers.

6. There have been laboratory accidents and escapes of highly dangerous pathogens in China in general and biosafety issues at the Wuhan Institute of Virology in particular. After the SARS epidemic in 2002-2003, which originated naturally in China and which China initially kept secret, work on the coronavirus pathogen that was responsible for the outbreak was undertaken in laboratories around the world. This research led to six cases of infection in laboratory workers: four in the National Institute of Virology in Beijing and one each in laboratories in Singapore and Taiwan.

A second case of infected researchers in China resulted in brief outbreaks of disease in early December 2019. An outbreak of brucellosis began in an agricultural laboratory in Lanzhou (Gansu Province, central China) and spread to China’s premier bird flu laboratory in Harbin (Heilongjiang Province, northeast China). It was linked to index cases involving graduate students who were exposed while conducting research and included at least 96 people.22

7. Under what biosafety conditions was bat coronavirus research carried out at the Wuhan Institute of Virology? Most work—including all published work using live bat coronaviruses that were not SARS-CoV and MERS-CoV—was conducted under BSL-2 conditions.23 This was consistent with both WHO and CDC recommendations.24 BSL-2 provides only minimal protection against infection of laboratory researchers, and these regulations were almost certainly too lenient for working with bat coronaviruses. All such work should have been carried out under BSL-3 conditions. However, extremely high-risk gain of function (GoF) studies with bat SARS-related coronaviruses were carried out at BSL-3 or BSL-4. Statements made by various commentators claiming that the WIV worked only with RNA isolates and not with live viruses are untrue (as discussed in further detail in a following section).

In regard to the Wuhan Institute of Virology in particular, relevant information is again available from both Chinese and Western sources. Information from official Chinese government sources appeared in a Voice of America report which noted:

[T]here is Chinese evidence that the lab had safety problems. VOA has located state media reports showing that there were security incidents flagged by national inspections as well as reported accidents that occurred when workers were trying to catch bats for study.

About a year before the corona virus outbreak, a security review conducted by a Chinese national team found the lab did not meet national standards in five categories.

The document on the lab’s official website said after a rigorous and meticulous review, the team gave a high evaluation of the lab’s overall safety management. “At the same time, the review team also put forward further rectification opinions on the five non-conformities and two observations found during the review.”
In addition to problems in the lab, state media also reported that national reviewers found scientists were sloppy when they were handling bats.

One of the researchers working at the Wuhan Center for Disease Control & Prevention described to China’s state media that he was once attacked by bats, and he ended up getting bat blood on his skin.

In another incident, the same researcher forgot to take protective measures, and the urine of a bat dripped “like rain onto the top of his head,” reported China’s Xinhua state news agent.25

Also, information was leaked from the US Department of State and published in the Washington Post on April 14:

Two years before the novel coronavirus pandemic upended the world, U.S. Embassy officials visited a Chinese research facility in the city of Wuhan several times and sent two official warnings back to Washington about inadequate safety at the lab, which was conducting risky studies on corona viruses from bats. The cables have fueled discussions inside the U.S. government about whether this or another Wuhan lab was the source of the virus – even though conclusive proof has yet to emerge.

In January 2018, the U.S. Embassy in Beijing took the unusual step of repeatedly sending U.S. science diplomats to the Wuhan Institute of Virology, which had in 2015 become China’s first laboratory to achieve the highest level of international bioresearch safety (known as BSL-4). WIV issued a news release in English about the last of these visits, which occurred on March 27, 2018. The U.S. delegation was led by Jamison Fouss, the consul general in Wuhan, and Rick Switzer, the embassy’s counselor of environment, science, technology and health. Last week, WIV erased that statement from its website, though it remains archived on the Internet.

What the U.S. officials learned during their visits concerned them so much that they dispatched two diplomatic cables categorized as Sensitive But Unclassified back to Washington. The cables warned about safety and management weaknesses at the WIV lab and proposed more attention and help. The first cable … also warns that the lab’s work on bat coronaviruses and their potential human transmission represented a risk of a new SARS-like pandemic.

“During interactions with scientists at the WIV laboratory, they noted the new lab has a serious shortage of appropriately trained technicians and investigators needed to safely operate this high-containment laboratory,” states the Jan. 19, 2018, cable, which was drafted by two officials from the embassy’s environment, science and health sections who met with the WIV scientists.

“Most importantly,” the cable states, “the researchers also showed that various SARS-like coronaviruses can interact with ACE2, the human receptor identified for SARS-coronavirus. This finding strongly suggests that SARS-like coronaviruses from bats can be transmitted to humans to cause SARS-like diseases. From a public health perspective, this makes the continued surveillance of SARS-like coronaviruses in bats and study of the animal-human interface critical to future emerging coronavirus outbreak prediction and prevention.26

The US government had supplied a portion of the funds to build the Wuhan Institute of Virology and these cables were an appeal for funds to support additional training in biosafety and biosecurity. There were similar concerns about the nearby Wuhan Center for Disease Control and Prevention lab, which operates entirely at BSL-2. Chinese government authorities did not provide the US government with samples of the virus obtained from either the earliest cases or from the Wuhan fish market. A US intelligence official commented: “The idea that it was just a totally natural occurrence is circumstantial. The evidence it leaked from the lab is circumstantial. Right now, the ledger on the side of it leaking from the lab is packed with bullet points, and there’s almost nothing on the other side.”27

8. What is the nature of the research being carried out in Zhengli Shi’s laboratory at the Wuhan Institute of Virology? Details of the most recent National Institute of Allergy and Infectious Diseases (NIAID) grant for WIV bat coronavirus surveillance and WIV bat coronavirus gain of function research are publicly available. The key activity for bat coronavirus surveillance is “Aim 1 … We will sequence receptor binding domains (spike proteins) to identify viruses with the highest potential for spillover which we will include in our experimental investigations (Aim 3).” The key activity for bat coronavirus gain of function investigation is “Aim 3…. We will use S protein sequence data, infectious clone technology, in vitro and in vivo infection experiments, and analysis of receptor binding to test the hypothesis that % divergence thresholds in S protein sequences predict spillover potential.”28

Translated into something approaching lay language, Aim 3 states that de novo synthesis is to be used to construct a series of novel chimeric viruses, comprising recombinant hybrids using different spike proteins from each of a series of unpublished natural coronaviruses in an otherwise-constant genome of a bat coronavirus. The ability of the resulting novel viruses to infect human cells in culture and to infect laboratory animals would be tested. The underlying hypothesis is that a direct correlation would be found between the receptor-binding affinity of the spike protein and the ability to infect human cells in culture and to infect laboratory animals. This hypothesis would be tested by asking whether novel viruses encoding spike proteins with the highest receptor-binding affinity have the highest ability to infect human cells in culture and laboratory animals.

The WIV began its gain of function research program for bat coronaviruses in 2015. Using a natural virus, institute researchers made “substitutions in its RNA coding to make it more transmissible. They took a piece of the original SARS virus and inserted a snippet from a SARS-like bat coronavirus, resulting in a virus that is capable of infecting human cells.”29 This meant it could be transmitted from experimental animal to experimental animal by aerosol transmission, which means that it could do the same for humans. In other words, gain of function techniques were used to turn bat coronaviruses into human pathogens capable of causing a global pandemic.

There have been three publications, in 2015,30 2016 and 2017, describing the WIV gain of function research. The WIV, having learned both basic and traceless infectious-clone technology from joint research with a laboratory at the University of North Carolina (UNC) in 2015, initiated construction of novel chimeric coronaviruses without UNC immediately thereafter. WIV’s first publication on the use of basic infectious-clone technology to construct novel chimeric coronaviruses at WIV appeared in 2016.31 WIV’s first publication on the use of traceless, signature-free infectious-clone technology also appeared in 2016.32

As this article was being edited, two excellent publications appeared that provide greater technical detail on WIV’s gain of function research, and readers should certainly examine these with care.33 The two papers strongly support the argument that the SARS-CoV-2 outbreak was the results of an escape from one of the two Chinese virology laboratories in Wuhan.

The Chinese government has proudly stated that the WIV “preserves more than 1,500 strains of virus,” the largest collection in Asia of bat and other coronaviruses.34 (The government statement probably should have said 1,500 isolates rather than “strains.”) The 2019 interview with Shi in Scientific American reports that the WIV had at least hundreds of individual strains.35 These numbers have been reported by Chinese government authorities, and they are being taken at face value here.

From 2004 on, the WIV published many dozens of partial or full genome sequences of coronaviruses in their collection. On June 1, Daszak and Shi published partial genetic sequences of 781 Chinese bat coronaviruses, more than one-third of which had never been published previously.36 There are also multiple published records of animal infection research with bat coronaviruses at the WIV. In order to carry out the research program described above, the WIV laboratory needs to use live viruses, and not just RNA fragments. This contradicts two of the assertions, made by some commentators, that Shi worked only with RNA fragments and that her laboratory did not maintain live viruses. On May 24, 2020, the director of the WIV acknowledged that the laboratory did have “three live strains of bat corona viruses on site,” but implied only three.37 Knowledgeable virologists assume that the number must be much higher, probably hundreds of live viral isolates.38

It is precisely in the course of the kind of gain of function research that the WIV conducted that there would be the greatest likelihood of infection of a laboratory researcher. Many commentators have noted that millions of people in several western Chinese provinces, as well as in other South Asian countries, live their lives in daily proximity to bat caves and that serological testing has shown a fraction of these villagers to have antibodies to bat coronaviruses, showing that natural infection had occurred. The commentators argue therefore that “the odds” are in favor of SARS-CoV-2 having arisen in the field, and that a laboratory escape is so implausible that it is out of consideration. The logic of “the odds” is specious: It would take only a single laboratory infection to overcome “the odds,” if such could in fact be reckoned. That is essentially what happened in the four SARS laboratory infections that occurred in the Beijing laboratory in 2004; “the odds” for exposure of villagers in Yunnan province were irrelevant.

Since the SARS-CoV-2 genome was decoded and published, there have been numerous statements from virologists that the genome shows no indication of genetic manipulation, and that this too supports the argument that it arose in the field and did not escape from a laboratory. Although this argument implicitly recognizes that the WIV laboratory was using genetic engineering technology, there is no reason to arbitrarily assume that only a bat coronavirus that was genetically modified might have escaped from the laboratory. Nevertheless, the second portion of the NIAID research grant design made absolutely clear that the WIV would be applying genetic engineering techniques to bat coronaviruses. Using the current standard genetic engineering technology, many alterations of several bases in the RNA genome would be undetectable, including construction of a chimeric coronavirus encoding an unpublished spike protein in an unpublished genome. This would be the equivalent of a natural mutation in several bases that coded for the spike proteins.

An article in Independent Science News by Jonathan Latham and Allison Wilson discusses another mechanism, described by Nikolai Petrovsky of Flinders University in Australia, that could have resulted in the SARS-CoV-2 virus that produced the pandemic:

Take a bat coronavirus that is not infectious to humans, and force its selection by culturing it with cells that express human ACE2 receptor, such cells having been created many years ago to culture SARS coronaviruses and you can force the bat virus to adapt to infect human cells via mutations in its spike protein, which would have the effect of increasing the strength of its binding to human ACE2, and inevitably reducing the strength of its binding to bat ACE2.

Viruses in prolonged culture will also develop other random mutations that do not affect its function. The result of these experiments is a virus that is highly virulent in humans but is sufficiently different that it no longer resembles the original bat virus. Because the mutations are acquired randomly by selection there is no signature of a human gene jockey, but this is clearly a virus still created by human intervention.39

Final comments. On April 30, Newsweek described a report produced by the US Defense Intelligence Agency which stated that “in early February, China’s Academy for Military Medical Sciences ‘concluded that it was impossible for them to scientifically determine whether the Covid-19 outbreak was caused naturally or accidentally from a laboratory incident.’” The author of a newly published paper analyzing the genome of SARS-COV-2 reported that “the COVID-19 virus is exquisitely adapted to infect humans… The virus’s ability to bind protein on human cells was far greater than its ability to bind the same protein in bats, which argues against bats being a direct source of the human virus.”40

Overall, the data indicates that SARS-CoV-2 is uniquely adapted to infect humans, raising important questions as to whether it arose in nature by a rare chance event or whether its origins might lie elsewhere.


Milton Leitenberg is a senior research associate at the Center for International and Security Studies at the University of Maryland (CISSM). His research is concentrated in three disparate areas of study: biological weapons; actual wars and conflicts of the past two decades and the issue of international intervention in these; and the history of nuclear weapons between the United States and Soviet Union and Russia between 1945 and 1995. CISSM published his major monograph, Biological Weapons Arms Control, in 1996. Since 1992, he has published over 30 papers in the area of biological weapons. Several of these papers concern the biowarfare program of the former Soviet Union, and The Soviet Biological Weapons Program: A History was published by Harvard University Press in 2013. Leitenberg published two other recent books on the subject of biological weapons: The Problem of Biological Weapons (National Defense College, Stockholm, 2004) and Assessing the Biological Weapons and Bioterrorism Threat (US Army War College, December 2005).



https://thebulletin.org/2020/06/did-the ... possibly/#


NEXUS EXTRA: Wuhan Lab - DEEP ANALYSIS with leading arms control expert Milton Leitenberg

Milton Leitenberg has decades of experience when it comes to biosafety and biosecurity and he outlines the evidence for the Wuhan lab leak theory.


_________________________________________________________

Another top expert on the lab origin hypothesis:

No known animal host and 'almost perfect' human adaption: Top Australian vaccine scientist reveals how COVID-19's unique structure means it's either man-made - or a 'complete fluke' of nature
Professor Nikolai Petrovsky said virus was better at attaching itself to human cells than to any other animal

It is so 'perfectly adapted' to infect humans that the possibility it was made in a Chinese lab can't be ignored

Wuhan Institute of Virology studied bat coronaviruses and is theorised to have accidentally leaked COVID-19

Virus could have been formed naturally by mixing bat and pangolin versions, but this is statistically unlikely

Professor Petrovsky said the inquiry into virus origins needed urgently and should have started months ago

How COVID-19's unique structure means it could be man-made

Coronavirus is so 'perfectly adapted' to infect humans that the possibility it was made in a Chinese lab can't be ignored, Australian vaccine researchers conclude.

Professor Nikolai Petrovsky said the virus was better at attaching itself to human cells than to any other animal, explaining why it has infected five million people.

The vaccine expert warned the investigation into where COVID-19 started, as proposed by Prime Minister Scott Morrison, was as a result urgently needed and should have begun months ago.

The startling results of his research were first revealed by the Mail on Sunday on the weekend - and on Wednesday his team gave Daily Mail Australia fresh details about why it must be considered a possibility the virus escaped from a lab in Wuhan.

The team at Flinders University in Adelaide and Latrobe University in Melbourne studied how well SARS-CoV-2, the virus that causes COVID-19, infected different animals.

Coronavirus binds itself to the ACE2 receptor molecule in lung cells using a spike protein - the tighter it can attach itself, the less likely it is to be washed away and the sicker it makes its host.

Professor Petrovsky expected to find an animal that was most susceptible to this, such as bats, and was likely the original source of the virus - but was shocked when humans came out on top.

Furthermore, viruses tend to get better at infecting new species as they adapt over time, but COVID-19 started 'completely optimised from day one without the need to evolve'.

'This is a new virus that has never been in humans before, but it has an extraordinarily high binding to human receptors, which is very surprising,' he told Daily Mail Australia.

'It is almost perfectly human adapted, it couldn't do any better.

'We have to ask how that happened. Was it a complete fluke? It can be as nature has many shots at goal and you only see the ones that land.

'Another possibility which still cannot be excluded is that SARS-CoV-2 was created by a recombination event that occurred inadvertently or consciously in a laboratory handling coronaviruses, with the new virus then accidentally released into the local human population.'

The Wuhan Institute of Virology, a short trip from the city's wet markets, is the lab known to study several bat coronaviruses and is theorised to be where it was actually created.

Most scientists believe COVID-19 started naturally in an exotic animal market in Wuhan and was not man-made, and the WIV has rubbished claims it caused the outbreak.

However, Professor Petrovsky said no one had properly disproved the lab theory and his research showed it was plausible and there was just as little evidence for it to have naturally occurred.

The closest disease to COVID-19 is BatCoV RaTG1, found in bats, that is 96 per cent similar to the strain rampaging around the world in humans.

The Wuhan Institute of Virology, a short trip from the city's wet markets, is the lab known to study several bat coronaviruses and is theorised to be where it was actually created

However, its spike protein is considerably less effective than COVID-19's and would need significant adaptation to become something that would easily infect humans.

The next most susceptible animal to humans were pangolins, a small scaly animal found in many Chinese wet markets, but a coronavirus that affects its species is only 90 per cent similar to SARS-CoV-2.

Professor Petrovsky said while it was possible the wrong bat met the wrong pangolin 'thereby conferring the bat CoV with high binding for both pangolin and human ACE2' - this was statistically improbable.

'The probability of one pangolin creating the virus and that then comes into close contact with a human to infect them is ridiculously low,' he said.

'We would expect it would have to be in lots of infected pangolins and we've not found any.'

Such pangolins would be an 'intermediate host' - a species that caught it from the originators of the virus and gave it to humans.

An example of this is Middle Eastern Respiratory Syndrome (MERS) that began with bats who infected camels who then pass it on to humans by spitting on them

Not only have researchers not found an intermediate host for COVID-19, they haven't even found the disease rife in any animal species - not even in bats, the leading suspected culprit.

Professor Petrovsky said animals didn't move between communities as much as humans so it was possible we just haven't 'found the right bat cave' yet. Until that happens, the Wuhan lab theory had to be considered, he said.

'Viruses don't come out of nowhere, so we have to look harder to find the natural source, or we need to investigate further to find the unnatural source,' he said.

Richard Ebright, one of the world's top biosecurity experts, told the Mail on Sunday that the odds of COVID-19 containing such unusual features and occurring naturally were 'possible – but improbable'.

The professor of chemical biology at Rutgers University, in New Jersey, said scientists at the WIV were creating chimeric coronaviruses (new hybrid micro-organisms) and seeking funding to test their ability to infect human cells while using procedures that leave no sign of human manipulation.

China has stubbornly resisted calls for an inquiry as it is accused of covering up the severity of the epidemic, and only agreed to a watered-down version of Mr Morrison's proposal last week.


Professor Petrovsky argued the investigation should have begun months ago to give it the best chance of gathering evidence that may now be lost for good.

He said his research added to a body of 'circumstantial evidence' and coincidences, but was nowhere near proving the that the WIV had anything to do with the pandemic.

'There's no smoking gun inside the virus as they evolve and pick up genetic material from everywhere, just studying the virus itself won't tell us anything further,' he said.

'I don't think we'll have definitive proof either way, so we have to investigate to determine what is more probable.

'No one can say a laboratory leak is not a possibility.'

Professor Petrovsky claimed scientists were reluctant to discuss the possibility of botched lab experiments or leaks since any backlash could lead to research restrictions and threaten crucial research.

https://www.dailymail.co.uk/news/articl ... -made.html



Now think back to all those lying fucking liars from very serious expert officialdom that told you they had completely ruled out a lab origin and anyone who doubts that is a conspiracy theorist. Yeah, all those dirty fucking fakers were all just lying their lying fucking asses off. Science!
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