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22 Feb, 62 tweets, 103 min read
@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.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola drive.google.com/drive/folders/…
The human RBD of the cambodian bats are the result of fabrication by adaptation in human cell cultures. They are then specifically sequenced and merged with the rest of the bat sequences for fake “natural origin”.
Folder contains two ERR accessions with
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Literally their only evidence of “independent validation” was another example of the useless and non-identical GX-CoV, how could this be applied to the GD-CoV which they claim that alina’s claim is invalid? NO virus sequences from pangolins were obtained from the Thai bat article
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola and they literally Skipped mNGS for those samples. If you don’t sequence, how can you ensure that the “pangolin sera” didn’t contain rabbits? Spiked with rabbit antisera to fake serology positive.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola archive.is/V4Nh8
With all these datasets created so lately, HOW could you distinguish them from synthetic RNA like the twist SARS-CoV-2 RNA controls? NO need for cell culture and no human sequences will be necessary. NO need for vector so no fusions to impossible sequences
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola NO contamination from T7 promoter or terminator as that RNAP only need to start with a G, which can be removed by lightly digesting with exonuclease. neb.com/-/media/nebus/… linear DNA run-off by the T7 polymerase and leave perfect RNA amplicon attached to nothing else.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Coverage to virus genome >99.99%, suitable for both PCR, Short and Long read sequencing. Indistinguishable from real virus and can create variants within weeks. rapidmicrobiology.com/news/fda-recom… Available since 16 April.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola In addition, the claim that “all sequences are determined after the ourbreak” is completely fake as RaTG13 is sequenced in 2018, MP789 is sequenced in september 2019 as a contaminant, RmYN02 is also sequenced in 2019.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola The alleged virus isolation are all from destructively sampled individuals, which are illegal unless the animal is already dead. Both GX and the 610156 “muscle” indicating that the GX-CoV is highly pathogenic in all species of pangolins and kills them before transmission,
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola This “MP20” have the same date as the GX cluster by sampling, so they may even be the exact same batch—some bat CoV in lab contaminated the captive colony and all of them were dead. Samples were then sent to other institutions—possibly for studies and cover-up.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola GX-P3B have some human, GX-P2V is a culture in vero cells.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola They are not “genuine and accurate” and are fabricated with specific intent that have encountered repeated failures on the GD—they just can’t get their dirty human+mouse cell hands out of the samples.
The synthetic DNA for the RacCS203/264/271/entire cluster had the SL1 motif of
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola The 5’-UTR cut in the middle and joined to an inverted copy of itself. This is the result of errors in the polymerase/ligase based DNA oligo assembly approaches used in GeneFragments, which result in a (-) strand Oligo to anneal onto the (+) strand and invert the 5’-UTR.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Inversion of the 5’-UTR renders the RacCS cluster non-viable as they can’t even be replicated properly by the RdRp.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola The fact that they used a GX for EPI-ISL-610156 is exactly because the only sample of GX-CoV that is live and can be purified by repeated passage in primary M.pentadactyla cells ncbi.nlm.nih.gov/biosample/1689… for realistic fake samples that don’t contain other sequences like human+mouse
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Is GX-P2V. This is also the only sample of their alleged “pangolin coronavirus” that is live and can be purified by culture in this way.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola The alleged “RacCS cluster” was created by the Ecohealth alliance for the express purpose of defending RmYn02. This virus is so hastily fabricated and the DNA synthesized without verification, that the 5’-UTR is inverted and curls onto itself. This is fraudulent to the very core.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola This “virus”, if recreated, is not even viable. The remains of the SL1 after truncating the 5’-UTR is not a RdRp promoter and is not capable of replication. This is specifically created using GeneFragments and assembled by the mean of polymerase cycling assembly. Again, one
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Possibility can not be ruled out that is a bat-derived Spike have been in-silico stitched onto a SARS-CoV-2 derived Backbone for fraudulently claiming that there is a “close wild backbone”. Most notably, the bat-derived Spike have been subjected to transition mutagenesis to skew
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Alignment to convert a 6nt deletion in the RacCS203 Spike into an alleged “insertion”. arxiv.org/abs/2012.00627 and a fraudulent SRA is contrived to create a fake virus with a much closer backbone than the actual RacCSxxx sequences.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola vixra.org/abs/2010.0164
Considered that Synthetic RNA control sequences and other mean of virus fabrication have been perfected to the point that it becomes impossible to distinguish genuine samples from contrived samples using NGS data alone, NO datasets, sequences or any such
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Claimed “natural viruses” from a time-point that is well after the current global doubt into the so-called “natural origin” theories of SARS-CoV-2 can be assumed legitimate, and ALL such datasets must automatically be considered highly suspect and defaulted to fabrication unless
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola proven by another non-Ecohealth Alliance lab from a non-Ecohealth Alliance or CCP-affiliated institution.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola EPI-ISL-610156 additionally contained sequences from bacteria that are encountered directly fused to many of the sites for primer binding, bacteria are not hosts of Sarbecoviruses and can not be infected by a Coronavirus to recombine with it.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola These are PCR artifects that are generated during cDNA amplicon isolation and fraudulent NGS sequencing. They are direct fabrication.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola ncbi.nlm.nih.gov/biosample/SAMN…
Primary fibroblast (“muscle”) cell culture of both species are available for the CCP to inoculate with GX-P2V and fabricate metagenomes out of since 20/03/2020 and 08/04/2020 ncbi.nlm.nih.gov/biosample/SAMN… respectively. Because they does not have a live isolate
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola of GD-1 that they could then perform repeated passage inoculation to purify away from human sequences, they chose the GX-P2V (which the EPI-ISL-610156 sequence is identical to except on the bacteria-fused ends) for this purpose and it is complete fabrication.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola In addition, none of the recorded animal infections lab or farm, except for hACE2 mice, have developed severe pathogenesis as seen in humans, evident by multiple in-vitro and real virus infection tests repeatedly revealing that human ACE2 have the absolute highest binding
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Affinity in all ACE2 from all animals when the ACE2 is expressed without tag.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola In fact, all prolonged infections in animals result in rapid RBD adaptation that either result in lowered or abolished human re-infection, even in minks.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola In addition, the RBM variants arose over a year into the human population and they all arose from immune selection, which is absent in a dish of cells and consequently no pressure exist in serial human cell passage that would have favored any of these “variants” that are cited as
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola “Evidence that it is not specifically adapted to humans”. This phrase is only correct if the term “In-Vivo” is added to the end. In the absence of an immune system, SARS-CoV-2 is perfectly and specifically adapted to the human cell lines A549 and HAE.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola N501Y, cited as “specific adaptation to humans” is in fact a variant that escapes 2 out of 3 the neutralizing Abs in an immune individual, and is a variant that arose in MOUSE not human. Same as all the other mutations. All of them were antibody escape variants that may or may
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Not accidentally cross the barrier that prevented all natural or cell passaged CoVs from further increasing binding—N501Y is also never found before in nature. This indicate that selection using Receptor-derived passage alone does not have sufficient drive force for N501Y.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola End to all Gain-Of-Function study. Also mean end to all Virology-related grants. This is guaranteed to happen if SARs-CoV-2’s lab origin is confirmed in any way. Therefore, ALL the “sampling virologists” under PREDICT programs have their lives and grant money at stake if they
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola D614G, another mutation cited for “evolution”, arose as a counterrevolution to compensate for the newly artificially inserted Furin site (FCS). This also arose sufficiently late that serial passage in Cell cultures are unlikely to uncover it right away—it adapts to VERO E6 and
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola HEK293T cells, which will rather delete the FCS in stead of having the slow way. In A549, CaLu-3 and other human ACE2 native cell lines, jvi.asm.org/content/82/12/… the Furin site is more likely to undergo an alternate adaptation pathway—through gain of P681, the P1’ is blocked by
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola O-linked glycosylation and is no longer efficiently cleaved in these cell lines, making is a Heparan Sulfate binder and render D614G no longer necessary.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola These cell lines also does not receive boosts from delFCS mutation and is unlikely to even select for G614 at all.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola The other “more transmissible mutations” seen recently ALL arise by antibody escape—they are all related to epitope targets on the S which bind neutralizing and cross-neutralizing antibodies, and are not even remotely related to receptor binding.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Therefore, all the claimed “adaptation in humans” are in-vivo specific adaptations that are related to an immune system, non-existent in a cell culture, and all the “infect without change” are invalidated by the rapid changes (ferrets, minks, cats) after initial infection the
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Soon as passage of any length is performed. “Can infect” and “is optimal” are two very different things.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Both RmYN02 and RacCSXXX are contrived—RmYN02 have a highly anomalous SRA that can not be from any known Transcriptome , being nearly half human 3’-ETS by content, and RacCSXXX was created in an attempt to rescue RmYN02 due to it’s critical role in the “natural FCS” claim. This
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Sequence is hastily fabricated with GeneFragments and short 200nt primers corresponding to sgRNA junctions are added for realism. The assembly is done so hastily and the sequences were unverified before spiking into samples, result in two separate recurring assembly errors
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecolaarchive.is/ujRT2 a non-random foresplice in nsp3 and a non-random inversion of the 5’-UTR—which resulted in all 5 sequences being non-viable.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Both are the result of oligos being improperly annealed when the GeneFragments are assembled.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola drive.google.com/file/d/1Xrgovg…
RaTG13 can’t infect a pangolin at all. The RBD don’t bind to it’s ACE2. Can’t bind at all and it can’t enter a pangolin’s cells. It can’t ever meet it’s recombination partner and can’t enter it’s cells.
@sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola A “recombination event” that literally can’t ever happen in nature.

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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 5 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 17 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
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.
Read 7 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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