SC2 = Synthethic Pathogen?
Funding
Features
Virulence
SC2 was already highly infectious in Wuhan! points to it being a lab product
Features
Virulence
It is physiological for a natural virus to lose its strength every time it infects a host, this process is called deletion.
But SC2 is a zoonotic / chimeric virus, developed in the laboratory, and its viral envelope, composed of numerous highly infectious pathogens, does not undergo deletion but remains unaltered in its RNA.
Mutation rates/cycle
RNA viruses replicate using their own RNA-dependent RNA polymerase (RdRp), which lacks proofreading mechanisms and is prone to mutate at high rates (10−3 / 10−5 substitutions/nucleotide/replication cycle), lending the virus a quasispecies structure.
Previous studies with severe acute respiratory syndrome coronavirus (SARS-CoV) and mouse hepatitis viruses have reported moderate mutation rates of 9.06×10−7 and 2.5×10−6 subs/site/cycle respectively, below the expected range for RNA viruses.
This is consistent with a role for non-structural protein (nsp) 14 in RNA proofreading or repair functions because of its 3’-5’ exonuclease (ExoN) activity.
Nonetheless, the large size of the CoV RNA genome increases the probability that deletions will be generated and recombination events will take place, which could facilitate adaptation to new host environments, as occurs with jumping between species.
One naturally occurring deletion on 29 nucleotides in the open reading frame Right pointing backhand index(ORF) 8 of SARS-CoV after human-to-human transmission was found to be associated with attenuation of replication.
The low mutation rate, high human-to-human transmissibility (R0=2.2), and absence of human pre-existing immunity against SARS-CoV-2 could explain its rapid spread through the human population, with very high sequence identity (99.9%) between isolates recovered all over the world.
All RNA viruses, even zoonotic / chimeric ones, created in the laboratory, such as SC2, have a virulence that diminishes with each passage in human clades.
If on the one hand the variants are formed, on the other hand the same variants are weakened
The Spike GlycoProtein has:
Glycan Shield for Immune Evasion
IUPAC defines glycan and polysaccharide as synonymous i.e.:
- "compounds consisting of a large number of monosaccharides linked glycosidically".
In practice, "Glycan" may also be used to refer to the carbohydrate portion of a glycoconjugate, such as a glycoprotein, glycolipid, or a proteoglycan, even if the carbohydrate is only an oligosaccharide.
Glycan reactive anti-HIV-1 antibodies bind the SARS-CoV-2 spike protein but do not block viral entry
Why?
To get the real picture of how the #SARSCoV2 spike protein works, you need to include the glycans.
Glycans appear to drive form, function, and evolution of the spike nearly as much as the protein itself.
An Evidence Based Perspective on mRNA-SARS-CoV-2 Vaccine Development:
"Therefore overcoming the highly glycosylated viral envelope is another challenge of SARS-CoV-2 vaccine development.
SARS-CoV-2 includes highly glycosylated spherical particles and has a large structure containing at least 66 N-linked glycan sites, of which 54 sites show similarity with SARS-CoV [56].
In contrast, the glycan sites of HIV are between three times and six times that of the influenza virus, which is one of the major reasons why an HIV vaccine has not been successfully developed at this time [57].
However, SARS-CoV-2 has more than twice the glycan sites of HIV [58]. This unusual degree of glycosylation means that SARS-CoV-2 may mutate quickly, making the development of a vaccine extremely difficult."
1) The Furin Cleavage Site (FCS)
This the location where the Spike Protein fuses with a human host cell to release its genetic material to infect cells.
The short segment of amino acids with the sequence PRRA on the spike protein
where by being exposed to furin, an ubiquitous human protease enzyme
dissolve the spike protein's coating
cleave in two
fuse
(Note: It is also called a Poly or Multi-Basic Cleavage Site as many other enzymes can do the work of furn in cleaving the viral spike protein)
What SC2's FCS?* 1) no other human coronaviruses have it SARS-CoV, the virus that caused the 2002 SARS epidemic,
does not have the sequence, so it was not as infectious as SARS-CoV-2.
its closest relatives of SARS-CoV-2 do not have The F does not arise at all in bats. [Q: Do bats have the furin protease?]
1) It has been inserted in precisely the best place in the spike protein to give it the ability to become highly infectious.8,9,10,11
2) FCSs tend to be more infectious than cleavage sites that use other enzymes.
It is highly improbable that the FCS revolved naturally as there is no sign of it evolving in any of SARS-CoV-2’s relatives in its clade (ie mutated fr Viruses are sequenced, analyzed and grouped into clades. The viruses evolved (mutated) from the same ancestor.8
The SC2's is different from the FCS in other coronaviruses in that its SC2's combination of amino acids makes it more efficient at infecting people.
This unique amino acid combination explains why: 1) SC2 is considerably more infectious than related coronaviruses. 2) SC2 infects multiple organs and attacks the nervous systems.9,10
Patents
Patent # US7223390B2 - Insertion of furin protease cleavage sites in membrane proteins and uses thereof https://patents.google.com/patent/US7223390B2/en
WO 03/083095 A1 - Viral Mutants, manipulated in the furin cleavage sites of glycoproteins
https://patentimages.storage.googleapis.com/61/a8/2b/ef357afa077a7a/WO2003083095A1.pdf
2) The Math:
https://threadreaderapp.com/thread/1339682907732905984.html
No See'm Technology (i.e. "No See Them" or "Not Noticeable"/ "No Seam" or "Seamless") Invented by
SC2's Spike Protein
cleaves at the furin cleavage site (FCS): PRRAR cct cgg cgg gca cgt
into 2 sub-units:
S1: freed & circulated by the blood stream
S2: which may/may not remain anchored
Toxin-like motifs (on both S1 & S2) become exposed and disrupt the normal functioning of surrounding receptors & proteins by binding / interacting with them:
Triggers hyperinflammation ie Severe COVID, in patients with skewed T-Cell Receptors repertoire, due to its super-antigenic character (in silico study)
Interacts with nicotinic acetylcholine receptors (nAChRs) (in silico study)
Interacts with amyloidogenic proteins
Induces degradation of junctional proteins that maintain endothelial barrier integrity
Induces paracrine senescence and leukocyte adhesion in endothelial cells
The Lancet’s special committee on the virus’s origins is headed by Peter Daszak.
Severe acute respiratory syndrome corona virus 2 ( SARS-CoV-2) causes severe acute respiratory syndrome. mRNA vaccines directed at the SARS-CoV-2 spike protein resulted in development of Abs and protective immunity.
To determine the mechanism, we analyzed the kinetics of induction of circulating exosomes with SARS-CoV-2 spike protein and Ab following vaccination of healthy individuals.
Results demonstrated induction of circulating exosomes expressing spike protein on day 14 after vaccination followed by Abs 14 d after the second dose.
Exosomes with spike protein, Abs to SARS-CoV-2 spike, and T cells secreting IFN-γ and TNF-α increased following the booster dose.
Transmission electron microscopy of exosomes demonstrated spike protein Ags on their surface.
Exosomes with spike protein and Abs decreased in parallel after 4 months.
These results demonstrate an important role of circulating exosomes with spike protein for effective immunization following mRNA-based vaccination.
This is further documented by induction of humoral and cellular immune responses in mice immunized with exosomes carrying spike protein.
revision by EddieC— view source
