Daoyu Profile picture
22 Feb, 7 tweets, 2 min read
archive.is/Oh9eD
Debunking virological’s latest fraudulent claim using “new sequences”. RacCSXXX are synthetic DNA that aren’t even viable, RshSTT198/200 used a human sample to replace the RBD/S2 and EPI-ISL-610156 had BACTERIA stuck to the ends.
ift.tt/3uhuzEF
Fabricating serology tests are easy—just take existing antisera and spike into sample sera. They intentionally did not perform metagenomic analysis because it will show that their sera have been tampered with. “were all negative”.
Rc-O319 lacked SRA support and is extremely distant, belonging to the European/African Cohort for RBM and S1-S2 that also lacked a FCS.
Remember that these Duke NUS and institute pasteur staff were zealots that were “only aware after November”. This is basically their collusion by Ecohealth alliance to fake sequences and publish them. The RacCSXXX are essentially synthetic sequence with bat backbone and RmYn02 S.
They have such a significant assembly error that all their 5’-UTR were inverted—all at the exact same location. This is from their first oligo acting as a negative strand in stead of the positive strand as the should be.

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More from @Daoyu15

22 Feb
biorxiv.org/content/10.110…

archive.is/iYWse
SARS-CoV-2 have mutations that are required for human infection, banned in non-humans and are favored in cell cultures—they only form without immune selection. The Absence of an immune system is required to explain all these sites.
T372 is found in all Sarbecovirus Spike proteins, and is required for the protein to be structurally stable and live in an animal. A372 is found in the very first SARS-CoV-2 and is thought to be required for in-vivo replication in humans. It causes a notable increase in human
Airway cell lines of the infectivity and replication. Animal Spike of the SARS-CoV-2 clade with QTQTNS cant go into a live human with T372. Human S with a A372 can’t survive in an animal without causing sterilizing and virus-extinguishing immunity. Cell lines, on the other hand,
Read 6 tweets
22 Feb
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola It have no effect in an animal (vero e6) and also kills off immunoevasion by removing a N glycan. This also arose long before the first sequences were created. The virus can’t infect a human lung without it and it is critical for replication in human lung cell lines (faster
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola kinetics). The terminal evolution before human introduction is done almost entirely in a state without all immune systems—RAG- type immunodeficiency with total lack of antibodies. Just like a cell culture in FBS. And it also involves very specifically human Lung cells. Other cell
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola types like the kidney or the intestines (all animals are infected in the intestines as this place is required for asymptomatic storage of the virus) does not show difference and are not affected by this change. This is a lung-specific and human-specific adaptations, not found
Read 21 tweets
22 Feb
@ydeigin @K_G_Andersen Japan bat don’t have RBD that bind human ACE2. Cambodia bat have it’s RBD tampered with. None of these “new” sequences, RmYN02 included, have an “insert” in the S1-S2, and no “partial furin site” exist in any of them. The Spike of RmYN02 is an altered version of RacCSXXX Spike
@ydeigin @K_G_Andersen With manipulated S1-S2 sequence to skew ClustalW alignment, inserted in to a simulated backbone and created as an in-silico sequencing dataset based on the limited Rm exome available. If the WIV found similar Spike sequences before, they could transplant it from the unrelated
Read 19 tweets
22 Feb
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Alignment here. None have a FCS nor they have any inserts.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola That EPi-ISL-610156 had bacteria stuck to the ends! Also there is no current SRA datasets that support it’s existence from anything made by the YunNan university. It is identical to GX-P2V on every site other than places where non-virus got into it.
Read 62 tweets
22 Feb
twistbioscience.com/sites/default/…
“KEY HIGHLIGHTS
• Fully synthetic RNA generated from Twist Gene Fragments
• >99.9% viral genome coverage
• NGS sequence verified
• Positive control for both RT-PCR and
NGS-based assays”
That is correct: fully synthetic, 29856nt-long, RNA controls,
indistinguishable from live virus, BSL-1 and can be used to generate realistic fakes of ANY sequences within weeks. Spike into animal sample, “intermediate host!” Spike into bat samples, “closely related!” Spike into pangolin samples, “pangolin coronavirus!” “Non-overlapping”
By the product sheet? Just order them in Overlapping fragments in stead. GeneFragments and ssRNA transcription service (include DNAse I digestion to clear away the templates, T7 run-off transcription to eliminate terminators) gives realistic RNA spiking forensically
Read 9 tweets
20 Feb
@EricTopol @firefoxx66 @carlzimmer That SHEDS it’s allegedly “protective glycans”. The immune system is NOT happy at that Pro in the PRRA! nuolan.net/motif.html

jvi.asm.org/content/82/12/…

biorxiv.org/content/10.110…
In Insect cells, the S1-S2 is glycosylated and can not be cleaved, forming a Heparan Sulfate binding
@EricTopol @firefoxx66 @carlzimmer Motif fit for binding to cells in a dish.

pubs.acs.org/doi/10.1021/ac…
In human cells, no O-linked glycosylation can be detected at significant quantities at any position on the Spike.
Read 8 tweets

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