Daoyu Profile picture
22 Feb, 21 tweets, 40 min read
@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
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Anywhere else even including alleged animal lung isolates. This poses two mysteries—Coronaviruses, especially food borne as claimed from “wildlife trade origin”, infect primarily the intestines and does not adapt to the lungs unless by accident (intestine-primary with spillover
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola To lungs as in MERS and SARS), as the intestines are functional, efficient and minimally impacting reservoir organs. intestinal infections are seldom symptomatic even in humans, and efficient fecal-oral spread is present in all species incuding humans. The only place you see this
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Specific adaptation is with unnatural intranasal inoculation route seen in all animal serial passages—and also in cultures of human lung cells from A549, CaLu-3 to HAE. All these changes were highly specific adaptation to human Lung cells. Things that are Prohibited in animals.
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola ALL other isolates that is not SARS-CoV-2 have a T372. That when present, bans the virus from the lungs. A SARS-CoV-2 precursor without A372 likely won’t even survive in a human—they can’t infect live humans. A372 can’t infect animals in reservoirs, T372 can’t infect humans. No
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Isolate from human have T372 indicating A372 is necessary for human infection by this clade. Only human cell cultures bridge this gap (or serial passage using swabs up ferret noses). The very first human SARS-CoV-2 have fully lost it’s ability to survive in a wild animal
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Reservoir. This is before it have entered humans. The glycan motif is conserved in all Sarbecoviruses that have a putative animal reservoir. This indicate that it is necessary for survival in a non-human lung environment, most probably through RBD locking stability (it fits in a
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Pocket in the S). Which in turn affect Spike immunogenicity and may have been necessary to block binding of a RBD-targeting neutralizing Antibody. Human ACE2 and human lung cell cultures are specifically required for this particular site adaptation—it have no effect in VERO E6.
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Loss of multiple shielding glycans except when it blocks a Protease, 10+ fold enhanced lethal immunogenicity through enhanced RBD up display, binding to cellular heparan sulfate by mean of a conditionally O-glycosylated (in certain cell cultures, but not actual humans) XBBXBX
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola motif that require glycosylation to prevent cleavage, loss of Spike stability and dramatically enhanced neutralization of the S by separating S1 and S2 (create lethal cross-reactive antibodies that the virus can’t escape)—early adaptation of SARS-CoV-2 is characterized by a
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Complete absence of humoral and cellular immunity, with all the immunoevasiveness completely gone, to the point that animals can’t even host the virus in a real reservoir (minks burn out and have 0 reinfections, vaccines provide 100% protection)—opposite of anderson immune
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola selection, incompatible with zoonosis (which have strong immune pressure at all stages of adaptation—signs of which were completely missing in SARS-CoV-2) and optimal adaptation to human ACE2—it is literally full of signatures of cell culture adaptation.
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola Also, guess what—the S1 inserts provide optimal cell co-receptor binding, contribute to enhanced infectivity—But is getting killed off in humans as the B1.1.7 and many modern immune-selected variants deletes exactly at those inserts. Remember that VERO E6 is prone to insertion.
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola GX-P2V inserted different sequences at these. VERO.
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola For those who claim that “P384 allow partial escape to CR3022 and permit FCS emergence”—that position is conserved all the way down to ZC45. Not a new feature yet none of the P384 carriers have a FCS.
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola This also mean that any animal carrying a precursor strain would already have a P384-specific CR3022 homologue—sciencedirect.com/science/articl… ZC45 sera cross-neutralize SARS2 so clearly this is not a “permissive mutation”.
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola sciencedirect.com/science/articl…
And it didn’t do it’s job well. Freshly prepared CR3022 neutralizes live SARS-CoV-2.
@lab_leak @sai_suryan @virological_org @Ayjchan @ydeigin @Rossana38510044 @Harvard2H @emmecola journals.plos.org/plospathogens/…
And A372 does not influence CR3022 binding even with decayed commercial CR3022–P384 is the sole contributer to the difference.

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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
@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
@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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