lrb.co.uk/the-paper/v25/…

dlnr.hawaii.gov/mk/files/2017/…

medcraveonline.com/JHVRV/chimpanz…
How dirty Biolabs and lack of understanding of nucleic acids(or classification of viruses) sparked multiple pandemic human pathogens from simian cell cultures and oral polio vaccines.
ncbi.nlm.nih.gov/pmc/articles/P…
Yes. That include Marburg as well.

ncbi.nlm.nih.gov/books/NBK22111…
Minor Pathogen that came from OPV in 1960: SV40. Known to cause cancer.

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More from @flavinkins

27 Sep
propublica.org/article/here-a…
On mice as a potential lab vector.
usatoday.com/story/news/201…
Mouse escapes are very common in Biolabs. Even BSL-3.
Read 6 tweets
25 Sep
cell.com/fulltext/S0092…
Yeast DICERs bypass dsRNA 5’ cap, 3’ overhangs(from the endoU of CoVs) and other viral modification to dsRNA ends, normally inhibiting RNAi for normal cells. The Yeast Argonautes also have a highly specific binding profile and cleaved ssRNA efficiently. Image
This kind of enzyme, if present, completely silences all transposons in that strain. This is only antagonized due to the presence of a dsRNA “killer” totivirus and the M satellite in S.Cerevisiae, responsible for the secretion of killer toxins in yeast. S.Cerevisiae lost the RNAi
Pathway due to the adavantage of the Killer. Despite being a Totivirus and perform all transcription and translation in virio, academic.oup.com/nar/article/48…

ncbi.nlm.nih.gov/pmc/articles/P…
The Killer is quickly lost if exogenous RNAi from another budding yeast strain was introduced.
Read 18 tweets
25 Sep
Like whatever lying in that deleted 61.5MB database of Shi? And whatever that was behind the password protected section, like the full length sequence of 7896 and the real 4991 with a working, rather than broken-in-the-fake-RaTG13, RBM?
Read 6 tweets
24 Sep
biorxiv.org/content/10.110…
Now it seems that RaTG13 was the ONLY full-length RBM that can't bind to human ACE2! (they made GX but not GD. confirming that the GD Spike is totallymessed up).
(Notice that the P2V was VERO cells while P3B have humans). this was also made well after the MP789 which indicate sample spiking with a live isolate of another yet unpublished bat Coronavirus sequence cultured in human/vero cells. the other datasets were composites that have Image
already been censored, most of the reads--including, human reads, removed. the GX Spike have high hACE2 entry capacity, and no outbreaks were recorded in 2017, which mean that this was also a Spike-in using some yet unknown Bat sequences. the GX can not be a precursor of CoV2 as
Read 8 tweets
24 Sep
biorxiv.org/content/10.110…
Bats constitutively expresses IFN-1. However CoV2 is far more susceptible to IFN-1 treatment then SARS. This mean that it couldn’t have came from bats. RaTg13 is even worse in this regards (removing PRRA make it CoV2 grow better in IFN-deficient cells).
Read 7 tweets
23 Sep
Shredding a "paper" who uses multiple fraudulent "evidence" to "debunk" the idea that SARS-CoV-2 is not a natural zoonosis.
centerforhealthsecurity.org/our-work/pubs_…
This "paper" was made by K_G Anderson, the creater of the fraudulent O-linked glycan claim to defend the WIV.
Claim 1: "e. SARS-CoV-1 and Middle East respiratory syndrome (MERS) have furin cleavage sites in their Spike protein." There are no furin cleavage sites in SARS-CoV-1, and MERS-CoV is a DPP4-using merbecovirus that have entirely different tropism and dynamics than Sarbecoviruses. Image
sciencedirect.com/science/articl…

fairdomhub.org/publications/5…
an absence of furin cleavage sites were found in Sarbecoviruses, the only ACE2-using beta-CoVs.
Read 62 tweets

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