>>13311534
Oh sweetie~
A Bayesian analysis concludes beyond a reasonable doubt that SARS-CoV-2 is not a natural zoonosis but instead is laboratory derived
https://archive.is/eOJsU
''Evidence: Lack of seroconversion in Wuhan and Shanghai.''
"A hallmark of zoonotic infections (vertebrate animal host-to-human microbial infection) is repeated, abortive jumps into humans over time until sufficient ‘human-adapted’ mutations permit efficient human-to-human spread and further evolution"
''Evidence: Lack of posterior diversity for SARS-CoV-2 compared to MERS and SARS-CoV-1''
The earliest stages of human CoV-1 and MERS infections were characterized by viral genome base diversity as expected for multiple, independent jumps from a large and diverse intermediate host population into humans.
Combining MERS and CoV-1 studies, out of the earliest 255 human infections in which virus genome sequences are available, 137 could not be rooted in a prior human-to-human infection and so are attributed to an independent intermediate host-to-human infection.
That is about 54% non-human-to -human transmission.
On the other hand, Ralph Baric has written68 that CoV-2 is different: “SARS-CoV-2 probably emerged from bats, and early strains identified in Wuhan, China, showed limited genetic diversity, which suggests that the virus may have been introduced from a single source.” [emphasis added.]
With CoV-2, there are 249 viral genomes in GISAID from Hubei province, where Wuhan is located, collected between Dec 24, 2019 and Mar 29, 2020.
From Dec 24, 2019 to November 2020, there are 1001 genomes sequenced from all of China and 198,862 worldwide.
For CoV-2, every single genome sequence is rooted in the first sequence from the PLA Hospital in Wuhan.
Not one case of posterior diversity.
''Evidence: Opportunity.''
The Wuhan Institute of Virology has publicly disclosed that by 2017 it had developed the techniques to collect novel coronaviruses, systematically modify the receptor binding domain to improve binding or alter zoonotic tropism and transmission, insert a furin site to permit human cell infection, make chimera and synthetic viruses, perform experiments in humanized mice, and optimize the ORF8 gene to increase human cell death (apoptosis).
''Evidence and Motive for laboratory furin site insertion:''
A key to infectivity of coronaviruses is the addition, in nature or the laboratory, of a furin cleavage site (FCS) at the S1/S2 junction of the Spike Protein. Furin cleavage sites (FCS) have been widely understood to be important for many viral infections, including HIV, influenza, and others. It has also been widely understood before now that lineage B coronaviruses do not have FCS.It was therefore surprising when an examination of SARS-CoV-2 Spike Protein found an insertion of a 12-nt, 4-AA sequence near the junction of the S1/S2 subunits which creates a furin site that is essential to human infectivity and transmission. As expected from previous work, no lineage B (sarbecovirus) coronavirus has this feature. This is the most difficult “molecular fingerprint” of SARS-CoV-2 to explain having been acquired in the wild and for that reason there are no even passingly feasible theories. One database of whole genome sequences of 386 coronaviruses was devoid of furin cleavage sites.78 Another database of 2956 genomes of sarbecovirus strains sequences shows that none have a furin site.79 This is a highly significant finding with a probability that sarbecovirus has a furin site in the wild of one in about 985.
''Evidence: Codon usage can distinguish insertion events in the wild from those created in the laboratory.''
Decades of research has identified that all life forms, viruses, bacteria, and humans alike, use the codons in a signature pattern of frequency which can be used to identify a particular sequence of RNA or DNA as human or non-human; viral or non-viral.In this way, viruses in nature and scientists in the laboratory, with different goals and motivations, make distinguishing codon usage decisions which can sometimes provide a fingerprint of their source.
''Evidence. Laboratory codon optimization uses CGG for laboratory insertions of arginine residues 50% of the time.''
''Evidence: SARS-CoV-2 Spike Protein is Highly Optimized for ACE2 Binding and Human Cell Infectivity, a Finding that is Inconsistent with Natural Selection but is Consistent with Laboratory Creation''