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
“Gene Fragments are linear synthesized DNA sequences for direct cloning or larger gene assembly.”
Linear DNA, no vector, T7 can be included for run-off in-vitro transcription. Up to 5Kb. T7 polymerase just need to have a stretch of “GG” for transcription start and no promoter
Parts are required to be seen on the final RNA. Digest template with RNAse-free DNAse I after completion, and you get RNA that is indistinguishable from the real thing. Better, order by the TRS segments and use more RNA for the 3’-end of the genome to get even more realistic fake
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,
@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
@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
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.
@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.