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. is in 2017, Rs4231. is in 2016, RsSHC014 and RsWIV16. is in 2013, RsWIV1. notice that this is before the beginning of the project
@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 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 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 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?
@franciscodeasis No other Betacoronaviruses have been isolated from R.blythi.
@franciscodeasis @garyruskin

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@franciscodeasis 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. 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
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. 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
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.
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.
in fact, the PRRARS, as opposed to other mutated cleavage sites--even the "perfect" H5CS--confers the greatest infectivity in CaLu-3 cells.
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
@AngloScot2 @WisdomRebel
PRRA is highly purified in the CaLu-3 cell line when FBS is added to inhibit trypsin. Stu lied about that in his defense on the FCS identity. the Gallaher article contain glaring

@WisdomRebel Mistakes and is completely impossible as HKU9 + RaTG13 only lead to a frameshift inactivated S and not a furin cleaved S.
The serological test the WIV claimed to be negative in Shi’s addendum is the exact same test they claimed positive in 2012 in the phD

@WisdomRebel thesis, and Stu once again lied about it. significant evidence in the form of contaminated SRA datasets suggest that the DEFUSE grant have been funded in China, as the full-length HKU4 is not a part of the 2016-2019 grant, but is found before the start

@WisdomRebel Date of the 2020-2024 grant of June 2020. The WIV also contained several HKU3-like Coronaviruses, particularly in mice in an 2017 GEO experiment, which is consistent with the published HKU3 and batified mice experiment in the DEFUSE document (evidence from an already conducted

@WisdomRebel Experiment). Either DEFUSE or fast-tracked form of the 2020-2024 grant in 2019 would have lead to full-length Sarbecovirus clones being used, leading to SARS-CoV-2 in the lab—they used HKU4 in stead of HKU5 for the MERS spike experiment indicating that backbone sequence distance

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1/ Here’s a list of conversational frameworks I’ve picked up that have been helpful.

Please add your own.

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“Gun to the head—what would you decide now?”

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“What does success look like in a world where you pick that path?”

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