COVID-19’s Biological Politics

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USMB software seems to be tweaking, though it could just be general russophobia. This is the originally found URL, and it sports the best snapshot of the virus that we have yet seen along with a good map of Ukraine biolabs:

sputniknews.com/20221017/just-why-boston-university-researchers-combine-omicron-wuhan-strains-to-make-deadliest-covid-ever-1101966140.html

 

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The Boston researchers say: We show that spike, the single most mutated protein in Omicron has an incomplete role in Omicron attenuation," they said. "This suggests that mutations outside the spike are major determinants of the attenuated pathogenicity of Omicron."

They conveniently don't mention the N969K mutation, where or not it is part of thende deadier virus. Furthermore, their claim is specious because the N969K mutation occurs in the heptad repeat region, which is used precisely to stabilize the protein for vaccine production.

So, scientific protocol would dictate that the naturally occurring N969K mutation must also be addressed in the heptad repeat of the spike protein as it relates to attenuation before dismissing the spike as inferior to those proteins outside the spike, which would require further experimentation.

 

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So the Boston lab's deadly (for mice) virus links to Eco Health collaboration:

2h

https://twitter.com/emilyakopp

' An Ecohealth collaborator who strongly opposed The Lancet's COVID origin investigation works at the Boston lab behind the controversial chimeric COVID experiment.'

 

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Here is Ralph Baric's video, the man working with bat viruses given to him by Peter Daszak, bat viruses that were growing in human Calu-3 cells. As we've already posted, Sorensen, Dalgleish and Susrud want to know where Baric got those cells:

 

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Above, the date is 25 Nov 2008. So Boston University's Omicron-Wuhan virus is mimicking Chapel Hill's previous project, though Baric would not receive RsSH014 via Daszak until Daszak collected it along the expressway on the southern shore of Lake Dian, Yunnan Province, China, in August of 2011.

 

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Omicron mutation N969K is the first SARS-CoV-2 mutation linked to the heptad repeat regions. If BU used this mutation with which to combine the Wuhan strain virus, then vaccines must be linked to the concept of gain-of-function.
"The statement from Boston University is disturbing in several ways. First, it denies that this is GOF.'

https://twitter.com/mlipsitch

 

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According to BU, this was LOF (loss of function) not GOF:

Boston University's Rebuttal

NEIDL Researchers Refute UK Article about COVID Strain

Boston University is refuting a series of misleading claims about research at the University’s National Emerging Infectious Diseases Laboratories (NEIDL). BU called the reporting “false and inaccurate,” and said, “this research made the virus replicate less dangerous.”

www.bu.edu

 

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Dr. Daniel Kuritzkes: "If you were going to find vaccines...."

Boston University lab did not create deadly new COVID strain, experts say

The goal of the study was to determine why the Omicron variant of COVID-19 seems to cause less severe disease than the original strain.

www.cbsnews.com

'....With the original strain, 100% of the mice died. With Omicron, none of the mice died. And with the combined strain, 80% of the mice died.'

 

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Boston University's report states (via Avian Flu Talk):

17 Oct Dutch Josh's Post

Complete madness - new strain of Covid created

This is complete madness. This is what scientists should be banned from doing. Just because you can...

www.avianflutalk.com

'....We generated chimeric recombinant SARS-CoV-2 encoding the S gene of Omicron in the backbone of an ancestral SARS-Cov-2 isolate and compared this virus with the naturally circulating Omicron variant. The Omicron S-bearing virus robustly escapes vaccine-induced humoral immunity, mainly due to mutations in the receptor binding motif (RBM)....This indicates that, while the vaccine-escape of Omicron is defined by mutations in S, major determinants of viral pathogenicity reside outside of S.'

We would question this claim. In the first place, the RBM is located in the RBD (receptor binding domain) which spans positions 319-541. The heptad-repeat region of interest for the N969K mutation, the mutation that is the first expression of the virus mutating according to a protein stretch that must be stabilized for vaccine production, is penultimate to the end of the repeat at position 970.

30 Nov 2021 Post #66

CDC approves fourth booster shot…

After the 20th booster.......Fauci Dr 666, promises that should do it :mad:

www.usmessageboard.com

 

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Another reason to question the Boston University report, is because of the origin of Omicron in mice: the N969K mutation happened in humans, and it's unlikely it happened first in mice. Thusfar, Boston lab has not mentioned N969K of Omicron.

 

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Scrutiny of Quay's concern about bronchiolar damage of the new Boston chimera:

https://twitter.com/Quay_dr @ 11h
'...."The 20-fold increased bronchiolar viral particles of the chimera was considered in the analysis. For me, the latter could make a case for increased human pathogenicity. This is the phenotype that will have the biggest clinical impact." '

Recalling porcine influenza transmission to humans, the Chinese engineered a chimera consisting of PRRSV (porcine reproductive respiratory syndrome virus) and PEDV (porcine epidemic diarrhea virus), the latter virus carrying the capability to subsist on steel surfaces for up to 28 days. This is the report of the chimera:

Ap 2019

Porcine epidemic diarrhea virus isolate XJ1904-34 spike (S) gene, comp - Nucleotide - NCBI

Thusfar, the only spike sequence found for PRRSV (which would be pertinent to the Baric Chapel Hill lab and introduced German wild boars) is this one which is only a segment lacking the heptad repeat region:

Sep 2008 PRRSV Partial Spike

Porcine respiratory and reproductive syndrome virus isolate SD-LC1 env - Nucleotide - NCBI

 

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We can, however, compare heptad regions of PEDV:

UniProt

uniprot.org

Heptad repeat region I spans positions 969 (the location of Omicron N969K mutation) to 1088. Position 969 is leucine (L). Position 1088 is also L.

Heptad repeat region II spans position 1240 (P), a proline, to 1336 (I).

As was mentioned in post #1,249 (for the 30 Nov 2021 post #66): It is by manipulating branched-chain amino acids either by varying among the three branched-chain aminos (isoleucine, leucine, and valine) or by creating multiples of these when it mutates.'

PEDV spike position L969, is preceded by a 4-alanine stretch. The Chinese chimera above also may have had the increased bronchiolar damage, though it's not possible to determine what role PRRSV may have had in the construction of this chimera.

 

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Emily Kopp has just posted a Science article on monkeypox that shows photos of two of the vectors, Cricetomys and Funisciurus. It does not show a suspected monkeypox vector, Malacomys longipes, which is also documented for coronaviruses, as we have already shown here at USMB (search).

https://twitter.com/emilyakopp

Moving Target: The Global Monkeypox Outbreak

Science | AAAS

www.science.org

A photo of the coronavirus/monkeypox suspect is here:

Malacomys longipes

Big-eared Swamp Rat (Malacomys longipes)

The big-eared swamp rat (Malacomys longipes) is a species of rodent in the family Muridae. It is found in Angola, Cameroon, Central African Republic, Republic of the Congo, Democratic Republic of the Congo, Equatorial Guinea, Gabon, Nigeria, Uganda, and Zambia. Its natural habitat is subtropical...

www.inaturalist.ca

 

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Quay: "Here I perform an analysis of the number, location, genome pattern and sequences of two restriction sites, Bsal and Bsmbl, that helps distinguish natural viruses from synthetic viruses....and part of Baric's "No See 'Em" technology.
....
The conclusion of this analysis is that SARS-CoV-2 has all the hallmarks of a laboratory-constructed synthetic virus....The likelihood SARS-CoV-2 is a natural sarbecovirus is less than one in a billion according to this analysis."

https://twitter.com/Quay_dr

Restriction Site Analysis of SARS-CoV-2 Demonstrates the signature of a synthetic virus

Two hypotheses of the origin of SARS-CoV-2 exist: • A spillover from an animal host somewhere outside a laboratory • A laboratory-related accident • Finding features within the genome to address these hypotheses would advance the investigation without requiring the cooperation of third-parties •...

www.zenodo.org

 

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Quay: "Here I perform an analysis of the number, location, genome pattern and sequences of two restriction sites, Bsal and Bsmbl, that helps distinguish natural viruses from synthetic viruses....and part of Baric's "No See 'Em" technology.
....
The conclusion of this analysis is that SARS-CoV-2 has all the hallmarks of a laboratory-constructed synthetic virus....The likelihood SARS-CoV-2 is a natural sarbecovirus is less than one in a billion according to this analysis."

https://twitter.com/Quay_dr

Restriction Site Analysis of SARS-CoV-2 Demonstrates the signature of a synthetic virus

Two hypotheses of the origin of SARS-CoV-2 exist: • A spillover from an animal host somewhere outside a laboratory • A laboratory-related accident • Finding features within the genome to address these hypotheses would advance the investigation without requiring the cooperation of third-parties •...

www.zenodo.org

The first noteworthy item is on p. 33 of Quay's 19 Oct 2022 report:

p.33 "The leucine amino acid in the restriction site is not found in 56 out of 58 sarbecoviruses."

Here seems another clue to the modus operandi of the virus we have mentioned in the use of branched-chain aminos (leucine, isoleucine and valine). Un-naturally placing a leucine at this position gives the sequence RDL.

 

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Quay's Talking Points

* The inframe restriction site CGTCTC is found only in RaTG13 and in no other sarbecoviruses.

* The SARS-CoV-2 sequence CGT-CTT is found in Banal-52, -103 and -236 but in no other sarbecoviruses.

*The finding of a restriction site in an amplicon that is not found in nature and its removal in an overlapping amplicon is consistent with reverse genetics workflow.

* A BLAST of amplicon #1 identifies onl RaTG13 and SARS-CoV-2, both with the GTTCTC non-restriction site sequence.

* Only 5 out of 58 sarbecoviruses do not have this restriction site, including SARS-CoV-2.

*This out-of-frame GAGACG restriction site is found in only three of 58 sarbecoviruses, including SARS-CoV-2. It is absent in RaTG13.

P. 39 "No sarbecovirus has a restriction site at this position, suggesting this was a laboratory-designed restriction site.

 

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Quay: "What is the probability that the five restriction site changes between SARS-CoV-2 and BANAL-52 occurred randomly?

Assumptions

*The viruses differ by five restriction sites of six nucleotides each.

*Random probability of six NTs being identical is (0.969) to the 6th power or 0.828.

* Probability of at least one NT difference in one restriction site is 1.0-0.828=0.172.

*Probability of all 5 restriction sites with at least 1 mutation is (0.172) to the 5th power = 0.000151 or one in >6,600.

*This pattern of restriction site changes could not have been random.

 

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Trouble in Paradise

About an hour ago, another report from a different team using the same restriction sites as did Quay:

60m

https://twitter.com/julienpotet

'....Whaough. Fascinating work. This is going to trigger a lot of discussions. Get the popcorn.
...."A collaborative product by @VBruttel, @tony_vandongen, and myself (Alex Washburne).'

Yes, a lot of discussions.

 

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3h

https://twitter.com/BallouxFrancois

'...."To me, this is by far the strongest piece of evidence to date against a simple scenario of strict zoonotic origin for SARS-CoV-2." '

 

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Thusfar, it appears that this new report is extremely similar to Quay's:

18 Oct 2022 Bruttel, Washburne and VanDongen

https://www.biorxiv.org/content/10.1101/2022.10.18.512756v1.full.pdf