4-23/25-2020
Professor Petr Chumakov of Moscow said the Wuhan Laboratory team have been actively involved in the development of various coronavirus variants for more than 10 years, possibly in the name of HIV vaccine research.“They did absolutely crazy things, in my opinion,” he told a Moscow newspaper. “The picture of the possible creation of the current coronavirus is slowly emerging.
“It is interesting that the Chinese and Americans who worked with them published all their works in the open (scientific) press. I think that an investigation will nevertheless be initiated, as a result of which new rules will be developed that regulate the work with the genomes of such dangerous viruses. It’s too early to blame anyone.”
https://torontosun.com/news/world/wuhan-lab-did-crazy-things-in-covid-19-research ………………………………………..….
4-23-20 He told the newspaper Moskovsky Komsomolets, "There are several inserts, that is, substitutions of the natural sequence of the genome, which gave it special properties." https://www.dailymail.co.uk/news/article-8249875/Wuhan-laboratory-scientists-did-absolutely-crazy-things-alter-coronavirus.html ………………………………………………………......................................... To me, the authors (Baric and Shi Zhengli) followed a familiar path: they took the spike-like protein from RsSHC014, which Shi Zhengli isolated from Yunnan bats in 2011, and inserted it into a murine-adapted variant of SARS-CoV for subsequent in vivo experiments. They also tested it in human cells, and almost as an aside created a recombinant clone of the same RsSHC014 strain….The researchers also uncovered that it was not only the binding of spike protein to the receptor that determined the virus’s potential for transition from one animal species to another, because the SHC014-MA15 chimera was more virulent than SHC014 itself, even in human cells:
Notably, differential tropism in the lung as compared to that with SARS-MA15 and attenuation of full-length SHC014-CoV in [human epithelial airway cell] cultures relative to SARS-CoV Urbani suggest that factors beyond ACE2 binding--including spike processivity, receptor bio-availability or antagonism of the host immune responses--may contribute to emergence.
I especially want to highlight the spike processivity in the quote, because this is not the first time that virologists have mentioned that the ability of a spike protein to be cleaved by proteases (including furin) can have an impact on virulence….
One quick aside regarding the “murine virus MA15” from the above paper. That was not some kind of natural murine coronavirus, as one might think. It was a laboratory-modified human SARS-CoV, which back in 2007 the Baric group--possibly in competition with the Shi Zhengli group (remember their article from 2007)--turned into a real beast. To do this, they first iteratively “improved” it in mice, and when after several iterations it became maximally “effective”, they reproduced the observed mutations in a synthetic clone, and once again checked that it really does have increased virulence and lethality:
We adapted the SARS-CoV (Urbani strain) by serial passage in the respiratory tract of young BALB/c mice. Fifteen passages resulted in a virus (MA15) that is lethal for mice following intranasal inoculation. Lethality is preceded by rapid and high titer viral replication in lungs, viremia, and dissemination of virus to extrapulmonary sites accompanied by lymphopenia, neutrophilia, and pathological changes in the lungs. Abundant viral antigen is extensively distributed in bronchial epithelial cells and alveolar pneumocytes, and necrotic cellular debris is present in airways and alveoli, with only mild and focal pneumonitis. These observations suggest that mice infected with MA15 die from an overwhelming viral infection with extensive, virally mediated destruction of pneumocytes and ciliated epithelial cells. The MA15 virus has six coding mutations associated with adaptation and increased virulence; when introduced into a recombinant SARS-CoV, these mutations result in a highly virulent and lethal virus (rMA15), duplicating the phenotype of the biologically derived MA15 virus. Intranasal inoculation with MA15 reproduces many aspects of disease seen in severe human cases of SARS.
Baric-2008
Here is another example of the potential scientific rivalry between the Baric and Shi Zhengli groups. In 2008, the Baric group took the Bat-SCoV strain and replaced its RBD with an RBD from human SARS. That is, they essentially reproduced the work of Shi Zhengli’s group from 2007, except they didn’t limit themselves to pseudo-viruses, but created a real chimeric virus.
Baric-2016
The Baric group does seem to have its share of similar papers. For example, in 2016, they essentially repeated their collaboration with Shi Zhengli from 2015 to create a chimeric virus, only this time they inserted a spike protein segment into their mouse-adapted SARS not from RsSCH014, but from another strain Shi Zhengli found in Yunnan--its close relative Rs3367. Or, to be exact, from WIV1--the laboratory clone of Rs3367 isolated at the Wuhan Institute of Virology in 2013….Baric has been creating mutant viruses for over 30 years….Baric and Shi Zhengli, 2015, wrote: Thus, relative to the Urbani spike–MA15 CoV, SHC014-MA15 shows a gain in pathogenesis.
…Here is an example of the work of the Baric group from 2008, where they took Bat-SCoV and replaced its RBD by an RBD from human SARS….Today, genetic manipulation techniques are so advanced and have become so routine that the October 2019 Beijing paper which had inserted a new furin site into the chicken coronavirus, only devoted a couple of sentences to their methodology…
I hope this post is not used to prematurely assign blame or propagate one-sided theories. What I do hope it highlights is the scale of dangerous gain-of-function research that has been and is going on in virology. -Y. Deigin https://yurideigin.medium.com/lab-made-cov2-genealogy-through-the-lens-of-gain-of-function-research-f96dd7413748
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