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22 Feb, 19 tweets, 12 min read
@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
@ydeigin @K_G_Andersen RacCS backbone to a “close wild backbone” derived from SARS-CoV-2 and RaTg13 to fabricate that sequence. vixra.org/abs/2010.0164
@ydeigin @K_G_Andersen No SRA exist to support the presence of EPi-ISLa610156 and it is a sequence from the GX cluster with identical primer binding locations as GX/P2V. It also came from the same GX sample batch and is likely sent to YNU for archiving process. They seems to be aware of a mass die-off
@ydeigin @K_G_Andersen And may have actually deduced that a lab Coronavirus have leaked and killed the entire captive colony. This way they kept all samples to a “medical institute” and may even actually either: kept a VERO E6 culture. kept a Human culture and made a cDNA clone library and spiked the
@ydeigin @K_G_Andersen samples with this cDNA.
@ydeigin @K_G_Andersen Lastly, RshSTT198/RshSTT200 have been manipulated—some human-derived RBM and N reads were integrated to replace the same positions in the bat sample. Both samples have human as the result.
@ydeigin @K_G_Andersen Fake backbone/S with real or partially real (mutagenized) RBM is commonly done with the WIV. The backbone is necessary to establish “similar in animal” while the RBM is extracted from an isolate (can be Sanger which causes sequencing error catastrophe with RaTG13)
@ydeigin @K_G_Andersen drive.google.com/file/d/1rpmEgw…
(The RBM have RaACE2 affinity slightly lower than hACE2 and much lower than SARS-CoV-2/hACE2 by flow cytometry staining, have better infectivity/entry capacity (drawn out by cell culture) on Rats than human or bat) is used to ensure that the S can bind
@ydeigin @K_G_Andersen it’s alleged “host”. archive.is/EiCQW
Just see how MN611520.1 got into SRR7896912 without that “bat”.
@ydeigin @K_G_Andersen Also, the GX Spike have very different NTD loop AA than SARS-CoV-2, and lacked insert 1 entirely.
@ydeigin @K_G_Andersen All HKU5 RBM bind P.abramus DPP4
@ydeigin @K_G_Andersen Just keep some RBM pulled out of a bank and add to a faux dataset. The backbone is PCRed or synthetic. zenodo.org/record/4064067…
The dataset is full of artefacts—banked RBM from improperly sequenced amplicon+4991+sun-dried SARS-CoV-2=RaTg13.
@ydeigin @K_G_Andersen Because the RBM is improperly sequenced, it contained prohibited positions and have poor binding affinity to all ACE2 ever tested.
@ydeigin @K_G_Andersen archive.is/CgQVj
The “positive antibodies” samples were 100% PCR negative using PREDICT primers targeting all Coronavirus sequences. This could either mean sera contamination by rabbit or civet positive control, intentional serology fabrication (PCR negative to not
@ydeigin @K_G_Andersen attempt sequence them—save then a headache on that dead RBM and to ensure that they don’t get exposed dropping rabbit or civet into the samples) or exposure to human circulating SARS-CoV or SARS-CoV-2 as these samples are collected well into the widespread human circulation of
@ydeigin @K_G_Andersen The human virus.

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More from @Daoyu15

22 Feb

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
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.
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.
Read 7 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
• 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


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.

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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