Posted on 08/16/2020 7:54:08 PM PDT by Synthesist
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.
(Excerpt) Read more at independentsciencenews.org ...
Ancestral samples of earlier human virus infections in China show CLOSE relationship to SARS-CoV-2.
These samples (RaTG13) were sent to the Wuhan Institute of Virology maybe as early as 2012.
Alt link for article: http://archive.is/Brufs
the paper IGNORES the 4 HIV segments in the NOVEL virus
paid for by FauXi, wanted by GateXi and PeloXi,
and released by Xi.
the paper IGNORES the exact correspondence of the receptor
to Pangolin. It is the ONLY region that matches pangolin
and not bat.
0% likelihood this was natural unless pangolins’ have
a military bioweapons division.
The baseline virus was probably discovered in 2012, and the miners may actually have died from it. However, the point is that if this were the same virus, with such a high degree of contagion, it would have been more than just 3 miners in 2012. The pandemic would have started then, not in 2019.
It is still highly likely that the virus was genetically manipulated in the Wuhan lab, particularly in a manner to make it more contagious. And in 2019 the Chicoms released it on the world.
I find it totally unremarkable that of all the millions (billions or maybe trillions?) of existing viruses that they by pure chance of recombination and/or mutation share a few bits of genetic code.
Manufactured virus, manufactured crisis.
The authors do not say the workers fell ill/died of SARS-CoV-2. The samples taken about 2012 were identified as bat coronavirus variant RaTG13, VERY similar to SARS-CoV-2, but NOT the same.
This fact leads me to think that SARS-CoV-2 probably was not bio-engineered, just a natural viral evolution.
My opinion does NOT exclude the probability that SARS-CoV-2 may have leaked from that Wuhan lab, only that it was not a bio-engineered weapon, just merely a deadly accident.
Probably because that's been debunked. The claim came from a preprint paper from a team in India and was immediately debunked by others who looked into it. In short, there was only one insert even remotely similar to HIV and it was so short (6 AA) that its existence is easily within the boundaries of random chance.
"the paper IGNORES the exact correspondence of the receptor to Pangolin. It is the ONLY region that matches pangolin and not bat."
Here you're talking about the S protein. And it doesn't contain Pangolin DNA; it contains sequences similar to pangolin-CoV which is just a genetically similar coronavirus that infects pangolins. Yes, the S protein is similar between SARS-CoV-2 and pangolin-CoV. Yes, antibodies appear to be cross-reactive because of that. But all that suggests is that the SARS-CoV-2 virus is closely related to other coronaviruses circulating within animals. Bats aren't the only other creatures on Earth to harbor viruses that have jumped species. The 1918 Spanish flu we've been talking about so much since all this began likely was a cross between human Influenza and avian flu. Since they couldn't directly infect the other host at the time, the most likely candidate for an intermediate (an animal where both could infect and combine) would be pigs.
So a pig gets avian flu and human flu, and out pops a virus that's similar to both but have the right characters to enable infection of humans with a payload more similar to the avian variety. That's how species-jumping works; you get bits from different species.
Like most conspiracy theories, this is essentially a house of cards constructed from bits of misunderstood information.
#3. Red Chinese mines hide and bury a lot of people.
“The paper IGNORES the 4 HIV segments in the NOVEL virus”
Because that’s nonsense.
I repeat my opening post here:
Wuhan, in short, is a rather unlikely epicentre for a natural zoonotic transfer. In contrast, to suspect that Sars-CoV-2 might have come from the WIV is both reasonable and obvious.
In his statement, Petrovsky goes on to describe the kind of experiment that, in principle, if done in a lab, would obtain the same result as the hypothesised natural zoonotic transfer–rapid adaptation of a bat coronavirus to a human host.
“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.”
In other words, Petrovsky believes that current experimental methods could have led to an altered virus that escaped.
In this particular set of experiments the researchers combined “the spike of bat coronavirus SHC014 in a mouse-adapted SARS-CoV backbone” into a single engineered live virus. The spike was supplied by the Shi lab. They put this bat/human/mouse virus into cultured human airway cells and also into live mice. The researchers observed “notable pathogenesis” in the infected mice (Menachery et al. 2015). The mouse-adapted part of this virus comes from a 2007 experiment in which the Baric lab created a virus called rMA15 through passaging (Roberts et al., 2007). This rMA15 was “highly virulent and lethal” to the mice. According to this paper, mice succumbed to “overwhelming viral infection”.
In 2017, again with the intent of identifying bat viruses with ACE2 binding capabilities, the Shi lab at WIV reported successfully infecting human (HeLa) cell lines engineered to express the human ACE2 receptor with four different bat coronaviruses. Two of these were lab-made recombinant (chimaeric) bat viruses. Both the wild and the recombinant viruses were briefly passaged in monkey cells (Hu et al., 2017). Together, what these papers show is that: 1) The Shi lab collected numerous bat samples with an emphasis on collecting SARS-like coronavirus strains, 2) they cultured live viruses and conducted passaging experiments on them, 3) members of Zheng-Li Shi’s laboratory participated in GOF experiments carried out in North Carolina on bat coronaviruses, 4) the Shi laboratory produced recombinant bat coronaviruses and placed these in human cells and monkey cells. All these experiments were conducted in cells containing human or monkey ACE2 receptors. The overarching purpose of such work was to see whether an enhanced pathogen could emerge from the wild by creating one in the lab. (For a very informative technical summary of WIV research into bat coronaviruses and that of their collaborators we recommend this post, written by biotech entrepreneur Yuri Deigin).
It also seems that the Shi lab at WIV intended to do more of such research. In 2013 and again in 2017 Zheng-Li Shi (with the assistance of a non-profit called the EcoHealth Alliance) obtained a grant from the US National Institutes of Health (NIH). The most recent such grant proposed that:
“host range (i.e. emergence potential) will be tested experimentally using reverse genetics, pseudovirus and receptor binding assays, and virus infection experiments across a range of cell cultures from different species and humanized mice” (NIH project #5R01Al110964-04). Understanding the Risk of Bat Coronavirus Emergence
https://www.ecohealthalliance.org/?gclid=EAIaIQobChMI-M2esq3P6QIVBL7ACh3YaADkEAAYASAAEgJgO_D_BwE
https://grantome.com/grant/NIH/R01-AI110964-04
It is hard to overemphasize that the central logic of this grant was to test the pandemic potential of SARS-related bat coronaviruses by making ones with pandemic potential, either through genetic engineering or passaging, or both. Apart from descriptions in their publications we do not yet know exactly which viruses the WIV was experimenting with but it is certainly intriguing that numerous publications since Sars-CoV-2 first appeared have puzzled over the fact that the SARS-CoV-2 spike protein binds with exceptionally high affinity to the human ACE2 receptor “at least ten times more tightly” than the original SARS (Zhou et al., 2020; Wrapp et al., 2020; Wan et al., 2020; Walls et al., 2020; Letko et al., 2020).
This affinity is all the more remarkable because of the relative lack of fit in modelling studies of the SARS-CoV-2 spike to other species, including the postulated intermediates like snakes, civets and pangolins (Piplani et al., 2020). In this preprint these modellers concluded “This indicates that SARS-CoV-2 is a highly adapted human pathogen”.
Given the research and collection history of the Shi lab at WIV it is therefore entirely plausible that a bat SARS-like cornavirus ancestor of Sars-CoV-2 was trained up on the human ACE2 receptor by passaging it in cells expressing that receptor. [On June 4 an excellent article in the Bulletin of the Atomic Scientists went further. Pointing out what we had overlooked, that the Shi lab also amplified spike proteins of collected coronaviruses, which would make them available for GOF experimentation (Ge et al., 2016).]
Thank you for posting this. I believe we’re about to see more and more articles trying to push belief in a natural origin of the SARS-CoV-2 virus. It’s all attempts at misdirection and distraction IMHO.
“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).”
But the authors do not even discuss the analysis of these samples.
That’s all that matters in their theory.
It has not been debunked.
in fact the primary structure is near exactly
Pangolin RNA over the S protein
.... but not in any other part of the genome,
and there are several structural and non
structural proteins.
The HIV bit has been debunked. I posted multiple links showing it has been. Three of the four sequences pointed out by the team from India aren’t actually similar. The fourth is so short it’s meaningless that it’s similar. It would be like saying you and I have a very similar address because they both contain the same sequence of letter “Lane”. You could live in Maine and I could live in Peru and we still have that in common.
The S protein sequence isn’t Pangolin RNA; it’s just very similar to the spike protein on pangolin-CoV, which is a coronavirus that infects pangolins. The similarity isn’t really that significant. You can find similarities between similar viruses in different species all over the place.
It does not change the fact that the CCP lab in Wuhan screwed up.
“This fact leads me to think that SARS-CoV-2 probably was not bio-engineered, just a natural viral evolution.”
____________________________________________________________________________
That’s what the Chi-Coms and the US DS way everyone to believe...
The presence of unique HIV sequences in Covid-19 strongly suggests genetic manipulation...So says Luc Montagnier, Nobel Prize winner for discovery of HIV/AIDS...
I even doubt the storyline that Covid-19 was an accidental release from the Wuhan Institute...some poor Chi-Com janitor picking up a few Yuan selling some dead lab mice/bats to the wet market...
This is all psyops stuff...the human mind needs a narrative...
This event was planned by someone...I’ll leave it at that...
The article suggests that all the necessary passaging took place inside the lungs of the Majiong miners; that is was effectively SARS-Cov-2 while the Shi lab was experimenting with it.
The article is saying that the miners got infected by a form that was marginally infectious, by inhaling deeply a large viral load into their already damaged miner lungs. The virus then immediately and rapidly mutated into this pandemic virus within their lungs and because it was in their lungs.
Passaging the virus in monkey and human tissues would be an obvious experimental line of inquiry.
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