https://t.co/OuQaBRFPu7
Unfortunately the "This work includes the identification of viral sequences in bat samples, and has resulted in the isolation of three bat SARS-related coronaviruses that are now used as reagents to test therapeutics and vaccines." were BEFORE the

@franciscodeasis chimeric infectious clone grants were there.https://t.co/DAArwFkz6v is in 2017, Rs4231.
https://t.co/UgXygDjYbW is in 2016, RsSHC014 and RsWIV16.
https://t.co/krO69CsJ94 is in 2013, RsWIV1. notice that this is before the beginning of the project https://t.co/HPJhwq7NgH
@franciscodeasis starting in 2016. Also remember that they told about only 3 isolates/live viruses. RsSHC014 is a live infectious clone that is just as alive as those other "Isolates".
@franciscodeasis P.D. somehow is able to use funds that he have yet recieved yet, and send results and sequences from late 2019 back in time into 2015,2013 and 2016!
@franciscodeasis https://t.co/4wC7k1Lh54 Ref 3: Why ALL your pangolin samples were PCR negative? to avoid deep sequencing and accidentally reveal Paguma Larvata and Oryctolagus Cuniculus?
@franciscodeasis Ref.5: "However, inspection of Figure 4 shows that clade B is connected to viruses lacking T8782C and C28144T by single mutational steps via other human isolates, so this explanation requires not only positing two markets with two progenitors differing by just two mutations,
@franciscodeasis but also the exceedingly improbable evolution of one of these progenitors towards the other after it had jumped to humans."
@franciscodeasis in fact, both T8782C without C28144T and C28111T without T8782C have been found in humans. clearly these are impossible to be "two separate markets" as A and B have been found to be connected by single mutations in humans--requiring the exceedingly improbable event of one
@franciscodeasis progenitor evolving toward the other in humans.
@franciscodeasis https://t.co/4gQ4cwKyGk
@franciscodeasis As for ref 4? Why ALL the closest bat-borne backbones for SARS-CoV-2 LACKED the Spike that is necessary for infection of anything that isn't it's own species? RpYN06 had ZC45 S, which infect only R. Pusillus and R. Blythi. RpACE2 have been experimentally confirmed to be not
@franciscodeasis Usable by any RBD/RBM from the clade SARS-CoV or SARS-CoV-2, and could not have been able to recombine with any of these because of physical isolation between R. Pusillus and SARS-CoV-2-like Spike and RBD.
@franciscodeasis https://t.co/3vdIBEBA1k
@franciscodeasis Ref 6? Why the “full-length genomes” claimed by the RaTG15 paper were DISCONTIGUOUS with the RdRp sequences deposited under the title “Origin and cross-species transmission of bat coronaviruses in China” in 13-Aug-2019? https://t.co/gBfRmGcTf4 https://t.co/2E63NmRjTE
@franciscodeasis No other Betacoronaviruses have been isolated from R.blythi.
@franciscodeasis @garyruskin

More from Daoyu

@franciscodeasis https://t.co/Sd9IslUCH5 a FCS need a FCS in the inoculum to exist. It can not arise de-novo as it will be destroyed instantly by the immune system.

https://t.co/UgXygDjYbW a fourth Sars-like CoV is live at the WIV. This fourth virus is an infectious clone, where engineering of the S1-S2 is used regularly as mean to generate a culturable virus in HAE cells. No VERO E6 here, and HeLa-hACE2 is the new VERO of the WIV

https://t.co/DtjyycKy1v
https://t.co/PG7LVnHfsy
Even with VERO E6, only half the time does passage lead to the loss of the FCS—smaller plaques need to be explicitly picked for that to be a certainty.

Marburg virus is a novel virus that escaped from the lab. https://t.co/OGQM6qV27l the only reason why it did not become a pandemic is due to it being too lethal to sustain asymptomatic transmission in humans.

The highest reported number of cases were in WuChang right on top of the old WIV headquarters, In contrast to the population density data of Wuhan—note that the place near the market had the highest population density in all of Wuhan, which make it the most optimal location for
https://t.co/hXlo8qgkD0
Look like that they got a classical case of PCR Cross-Contamination.
They had 2 fabricated samples (SRX9714436 and SRX9714921) on the same PCR run. Alongside with Lung07. They did not perform metagenomic sequencing on the “feces” and they did not get


A positive oral or anal swab from anywhere in their sampling. Feces came from anus and if these were positive the anal swabs must also be positive. Clearly it got there after the NA have been extracted and were from the very low-level degraded RNA which were mutagenized from

The Taq.
https://t.co/yKXCgiT29w to see SRX9714921 and SRX9714436.
Human+Mouse in the positive SRA, human in both of them. Seeing human+mouse in identical proportions across 3 different sequencers (PRJNA573298, A22, SEX9714436) are pretty straight indication that the originals

Were already contaminated with Human and mouse from the very beginning, and that this contamination is due to dishonesty in the sample handling process which prescribe a spiking of samples in ACE2-HEK293T/A549, VERO E6 and Human lung xenograft mouse.

The “lineages” they claimed to have found aren’t mutational lineages at all—all the mutations they see on these sequences were unique to that specific sequence, and are the result of RNA degradation and from the Taq polymerase errors accumulated from the nested PCR process
https://t.co/TVXC4QOjt0
https://t.co/QnMiOrdNhx
https://t.co/ZK2vfwYEFj
in fact, adaptation in CaLu-3 actually reverses changes that happened in VERO E6. P681 and RRAR is fine-tuned to growth in CaLu-3 cell cultures. P681 guards the cardin-weintraub motif against cleavage in

cell lines.

https://t.co/vytn6YVRYQ
https://t.co/fjg6ZXc2KN
the FCS is perfectly stable in anything that isn't VERO E6 classic or 293T-ACE2. anything that had TMPRSS2 and grown in trypsin-free media stably maintains the FCS.

https://t.co/NUrJ8AndTx
in fact, the PRRARS, as opposed to other mutated cleavage sites--even the "perfect" H5CS--confers the greatest infectivity in CaLu-3 cells.

https://t.co/TVXC4QOjt0
in fact, even P681R or S686G changes were less fit in CaLu-3 compared to PRRA virus--the P681R virus show either no difference or is slightly less effective compared to the P681 virus, and the S686G virus
https://t.co/DNtIR17r4S
https://t.co/nDNNw9OaWd
https://t.co/SvP0tfbDki


https://t.co/k9mmL9e5kn


https://t.co/7fR13yb3qJ


https://t.co/EXerlaiG9u


https://t.co/iNCdLY1Pzn

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