The main post starts behind the divider bar, few updates upfront. AND THANK YOU for reading;)
Update 11/18/2023: Important interview with Dr. Michael Palmer on a planned genocide in regard to gene modifications via covid injections: https://www.bitchute.com/video/z5B7nGKZrEkh/ with a link to his book explaining more details of the new synthetic genes-based technology: https://doctors4covidethics.org/mrna-vaccine-toxicity/
Update 9/24/2023: Not quite the topic of this post, just some science history from Germany, related to the field of macromolecular biology, hidden behind every ‘variant’ of todays’ covid hell. A link to the 2017 interview with a German scientist: https://archive.embl.org/uploads/r/archive-of-european-molecular-biology-laboratory/1/3/7/137250e31a096f825c420a141e4aa13c842483849ff66f57f26399ca623bc897/2017_11_16_HeinrchStuhrmann_transcript.pdf
who summarizes all his scientific work achievements using only one name (in addition to his collaborators), his daughters name, despite of having the entire team of other highly qualified PhD students, who actually did all the technical work... The interview touches extremely important ribosomal work done by the Israeli researcher Ada Yonath, who got the Nobel prize for it https://www.nobelprize.org/womenwhochangedscience/stories/ada-yonath
We are always being told in advance what’s gonna happen, please read the above from the front cover of Time edition on 1/11/1999, in particular the small print. And remember the date, backwards… We are in that future, right now, and the reminder about this Time edition, comes from Dr. Bryan Ardis, whose interview can be found in the previous post
Update 9/15/2023: each scientist, each politician, health care specialist of all kinds, should be MANDATED to watch ALL the series at: https://www.bitchute.com/search/?query=sterben%20nach%20den%20impfungen&kind=video which have this one in common: injections of SYNTHETIC genetic material covering ALL the variants, from 0 to X, material is which falsely called ‘vaccine’, including ALL the most prestigious scientific journals out there! All on purpose, all with a goal, which even those participating criminals (scientists), do not seem to grasp.
Update 9/14/2023: Dr. DAVID MARTIN’S speech in EU just yesterday: https://www.brighteon.com/9fe23bf5-7a03-4c38-9305-1ef3c44b8115 title of it: ““Dr. David Martin at EU Parliament in Strasbourg:Expert Panel about WHO's power grab!Wed, Sept. 13th” talking about Barick’s publication analyzed in this post.
New 9/13: VERY IMPORTANT analysis of SARS-CoV-2 ‘variants’ publication from Feb 2022, at the end of this post.
Everyone remembers the admitted fact that “Pfizer did not know whether Covid vaccine stopped transmission before rollout, executive admits“, still available to watch at:
Months back, Kevin McKernan on his substack, answered the question about distinguishing the natural Spike (KV) from the injected Spike (PP): there is no method to detect the difference (Proline-Proline) between the synthetic injected Spike and the one coming from the natural SARS-CoV-2 infection, carrying the Lys-Val (KV) on the same position. That was hard to imagine, given todays genetic capabilities of producing point mutations in countless proteins and detecting them… That changed recently, in different way, working on proteins only. The consequences of a genetic modification treatments via injections of Spike gene coding for specific Proline-Proline(PP) mutation, were just published by Carlo Brogna et al. (https://doi.org/10.1002/prca.202300048) ”The specific PP-Spike fragment was found in 50% of the biological samples analyzed, and its presence was independent of the SARS-CoV-2 IgG antibody titer. The minimum and maximum time at which PP-Spike was detected after vaccination was 69 and 187 days, respectively.” (https://onlinelibrary.wiley.com/doi/epdf/10.1002/prca.202300048)
That injected gene and the amount of its produced Spikes (fragments containing the PP mutation in this study) to the resulting antibody independence, indicates many possible reasons, one of which is considered in this post. The extreme importance of that new study is the finding, that none of the covid jabbed study participants had the Spike with the PP mutation, meaning ‘the shedding phenomena’ must be Spike protein independent, including the gene shedding, which would continue producing the PP-mutated Spike. It is possible, it can be a detection limit issue of the MS (mass spectrometry) method though. The question how many of the covid non-jabbed did have the natural ‘KV’ mutation was not addressed in it, a great pity….
The main point here is, again, Spike related:
This post considers the possibility of ACE2 having nothing to do with SARS-CoV-2 infection(-rate) but rather, ‘just’ with the universally injected, patented Spike toxin binding that essential human MEMBRANE BOUND ACE2 protein, not even speaking about the integration of the synthetic Spike gene, for now. The consequences of this, are quite essential, because it would explain why the Spike design and its injections, in form of FOREIGN, SYNTHETIC GENETIC MATERIAL, with optimized features of binding to ACE2 via the RBD Spike domain, do nothing to the ‘viral transmission’, as confirmed in EU Parliament by the Pfizer rep. J.Small, but rather to take away from circulation the HUMAN ACE2 protein and its building blocks, while causing illness and death. That assumption would also affect the variants issue.
The VARIANTS.
The SARS-CoV-2 most out-sticking portion, the now by MANY companies PATENTED^1 universally injected Spike toxin (with venom-like sub-compounds..) and its versions, has 1273 amino acid (aa) residues. We are being told, the for decades developed Spike (with the oldest patent of its homolog going back to 1987 Duphar International for ‘new antigenicity active proteins and peptides and Infectious Bronchitis Virus vaccines) binds to the ACE2 receptor, which then leads to a viral entry and infection. Human ACE2 receptor NEVER CHANGES its sequence/folding, it is a zinc metalloprotease MEMBRANE FIXED HUMAN PROTEIN, given to you from your birth. So how something like the Spike on the viral surface, which constantly mutates, still manages to bind to the ALWAYS THE SAME ACE2 SURFACE, which first THEN causes OPENING of the cell membrane following the viral entry and infection??? ACE2 has only few residues participating in its catalytic action, Glutamic acid (proton acceptor) at position 375, that’s the E* in the TAHHE*MGHIQ motif, Hystidine505 (proton donor) in a string (ASLFH*VSNDY) and Histidine345 and arginine Arg273. All E, H and R are charged residues, which participate in cutting at the position of PF (see below) of very small peptides(examples at the end of this post). So how ACE2 suddenly cuts into a 1273 residues Spike monster^5?? ACE2 uniprot entry lists 13 publications which talk about ACE2 which “Acts as a receptor for human coronaviruses SARS-CoV and SARS-CoV-2, as well as human coronavirus NL63/HCoV-NL63.“ Here are the citations in regard how ACE2 participates in SARS-CoV-2 viral entry, from some of the abstracts:
-Collectively, our results in conjunction with those of previous studies indicate that TMPRSS2 and potentially related proteases promote SARS-CoV entry by two separate mechanisms: ACE2 cleavage, which might promote viral uptake, and SARS-S cleavage, which activates the S protein for membrane fusion.” (J. Virol. 88:1293-1307 (2014))
-Here, we demonstrate that SARS-CoV-2 uses the SARS-CoV receptor ACE2 for entry and the serine protease TMPRSS2 for S protein priming. A TMPRSS2 inhibitor approved for clinical use blocked entry and might constitute a treatment option. Finally, we show that the sera from convalescent SARS patients cross-neutralized SARS-2-S- driven entry. (Cell 181:1-10 (2020))
-”We determined cryo-EM structures of the SARS-CoV-2 S ectodomain trimer, providing a blueprint for the design of vaccines and inhibitors of viral entry. Finally, we demonstrate that SARS-CoV S murine polyclonal antibodies potently inhibited SARS-CoV-2 S mediated entry into cells, indicating that cross-neutralizing antibodies targeting conserved S epitopes can be elicited upon vaccination.” (Cell 180:1-12 (2020))
-”Here, using SARS-CoV-2 S protein pseudovirus system, we confirm that human angiotensin converting enzyme 2 (hACE2) is the receptor for SARS-CoV-2, find that SARS-CoV-2 enters 293/hACE2 cells mainly through endocytosis, that PIKfyve, TPC2, and cathepsin L are critical for entry, and that SARS-CoV-2 S protein is less stable than SARS-CoV S.” (Nat. Commun. 11:1620-1620 (2020))
- “crystal structure of the receptor-binding domain (RBD) of the spike protein of SARS-CoV-2 (engineered to facilitate crystallization) in complex with ACE2. In comparison with the SARS-CoV RBD, an ACE2-binding ridge in SARS-CoV-2 RBD has a more compact conformation; moreover, several residue changes in the SARS-CoV-2 RBD stabilize two virus-binding hotspots at the RBD-ACE2 interface.“(Nature 581:221-224 (2020))
- “It is now well‑established that entry of SARS‑CoV‑2 into host cells is facilitated by its spike proteins mainly through binding to the angiotensin‑converting enzyme 2 (ACE‑2). Preclinical studies have suggested that neuropilin‑1 (NRP1), which is a transmembrane receptor that lacks a cytosolic protein kinase domain and exhibits high expression in the respiratory and olfactory epithelium, may also be implicated in COVID‑19 by enhancing the entry of SARS‑CoV‑2 into the brain through the olfactory epithelium. In the present study, we expand on these findings and demonstrate that the NRP1 is also expressed in the CNS, including olfactory‑related regions such as the olfactory tubercles and paraolfactory gyri. This furthers supports the potential role of NRP1 as an additional SARS‑CoV‑2 infection mediator implicated in the neurologic manifestations of COVID‑19. Accordingly, the neurotropism of SARS‑CoV‑2 via NRP1‑expressing cells in the CNS merits further investigation.“(Mol. Med. Report. 22:4221-4226 (2020))
-”Cleavage of S generates a polybasic Arg-Arg-Ala-Arg (RRAR=furin site) carboxyl-terminal sequence on S1, which conforms to a C-end rule (CendR) motif that binds to cell surface neuropilin-1 (NRP1) and NRP2 receptors. We used x-ray crystallography and biochemical approaches to show that the S1 CendR motif directly bound NRP1. Blocking this interaction by RNA interference or selective inhibitors reduced SARS-CoV-2 entry and infectivity in cell culture. NRP1 thus serves as a host factor for SARS-CoV-2 infection and may potentially provide a therapeutic target for COVID-19.”(Science 370:861-865 (2020))
None of these publications describe precisely how the MEMBRANE BOUND whole length ACE2 receptor opens the cell membrane and lets the SARS-CoV-2 viruses in, AFTER binding the Spike. The crystallographic structure at https://www.rcsb.org/fasta/entry/6M0J/display showing the ACE2 and the Spike has only pieces of both, NOT the two ENTIRE molecules, in particular the cell membrane anchored portions are NOT THERE. To crystallize a membrane protein, just one, is already a huge challenge, like real vaccine, it can take years, and here not even speaking about 2 proteins anchored on different membranes…. So the fact that ACE2 actually really binds Spike is proven by crystallographic data, of fragments, in soluble phase.
All this leads me to put the ACE2 based viral cell ENTRY, that, what happens AFTER binding to the SARS-CoV-2 Spike, into question.
Science 2022 Mar 4 edition describes how a chinese team did EM studies: https://pubmed.ncbi.nlm.nih.gov/35133176/
of many variants with, they say, full length ACE2 with supplemental material at : https://www.science.org/doi/10.1126/science.abn8863#supplementary-materials
in which the description about ACE2 states, quote: “The N-terminal peptidase domain of human ACE2 (residues Ser19–Asp615) with an N-terminal GP67 signal peptide for secretion and a C-terminal 8×His tag for purification was inserted into a modified pFastBac vector (Invitrogen).“
that’s NOT full length ACE2, which has 805 residues!! Further, quote: “The fractions for the peptidase domain of human ACE2 were collected, concentrated to about 2 mg/ml, and stored at− 80 °C until use.“
how the cell membrane was simulated"?? “10 nM ACE2 were attached to streptavidin-coated donor beads, and 10 nM His6-tagged Omicron spike ECD were attached to nickel-chelated acceptor beads.“
In the entire materials section there is no mention about the WHOLE length of MEMBRANE BOUND ACE2, yet, the protein data bank data show the ‘modeled’ ALL 805 residues of ACE2, bound to the trimer of Spikes, with NO MEMBRANES around, with coordinates at https://www.rcsb.org/structure/7WPA
while uniprot actually defining the 741-761 region of ACE2 being anchored in the membrane and the 762-805 residues being cytoplasmic portion, in which the section 778-786 ‘ENPYASIDI’ represents the ‘cell entry system’, located INSIDE of the cytoplasm, never reachable by the viral Spike coming from OUTSIDE of the cell, in natural infection.
That chinese study cites the no 1 source for their MODELS: https://pubmed.ncbi.nlm.nih.gov/33271067/ , Cell Host Microbe. 2020 Dec 9;28(6):867-879.
This 2020 publication in turn states: “Overall, our findings provide structural definition for the binding of up to three ACE2 molecules per SARS-CoV-2 spike trimer and define a key structural transition between pH 5.5 and 4.5, highlighting the crucial role of a refolding region with multiple aspartic acid residues—a pH-dependent switch—that mediates positioning of RBDs, by twisting the relative orientation of disulfide-linked helices and coordinating the interprotomer movement of domains.“
How much of ACE2 was in this ‘models’?? The methods section says, quote:”Human ACE2 proteins were prepared in monomeric form (residues 1-620) and in dimeric form (residues 1-740). The expression plasmids were constructed and the protein purified as described previously (Zhou et al., 2020b).”
Again, that study does NOT INCLUDE the FULL LENGTH of the entire MEMBRANE ANCHORED ACE2.
Transmembrane protease serine 2 (TSMPRSS2) which is also said to be involved in pre-proteolytic cleavage of the spike, has the N-terminal 84 residues in the cytoplasm, 85-105=20 residues anchored in the membrane, and 106-492 outside of the cell, with 3 residues 296-345-441 (His-Asp-Ser) representing s.c. CHARGE-RELAY-system, thus performing the proteolytic cuttings outside of the cell, like ACE2. So what the papers describing that feature say? Uniprot on TSMPRSS2 at: https://www.uniprot.org/uniprotkb/O15393/entry#O15393-1 points to 6 publications on it, here just one of them:
-The demonstration of T-ex5 PPMO efficacy in the present study suggests that reducing TMPRSS2 expression by use of an mRNA-directed approach in general and by PPMO in particular is worthy of further consideration. PPMO are highly selective inhibitors of target gene expression. They bind to a complementary sequence in target mRNA and can affect gene expression by steric blockage of translation initiation or pre-mRNA splicing. (TMPRSS2 and furin are both essential for proteolytic activation of SARS- CoV-2 in human airway cells. Life. Sci Alliance 3:1-14 (2020)) => not a proof of enzymatic digestion of ACE2, but rather inhibition of the protease by manipulating its mRNA.
The ACE2 uniprot entry has just one section related to its special membrane features, quote:”In addition, ACE2 C-terminus is homologous to collectrin and is responsible for the trafficking of the neutral amino acid transporter SL6A19 to the plasma membrane of gut epithelial cells via direct interaction, regulating its expression on the cell surface and its catalytic activity (PubMed:18424768, PubMed:19185582).” Both of the here 2 cited publications, indicate that the ACE2 activates the expression of neutral SINGLE amino acid transporter on the cell membrane, and do not indicate opening of the cell membrane by ACE2…
What would be the advantage of actually proving, that the natural ACE2 (whole length and membrane bound) contributes to viral spread by BINDING the SARS-CoV-2 Spike first (given) and THEN (questionable) opening the cell membrane and allowing the SARS-CoV-2 in? It would justify the application of covid injection materials, reprogramming human bodies so it produces the Spike which then suppose to generate antibodies to it, it would justify the current ‘scenario’. And what if ACE2 does not open the cell walls, and all what the injected Spike is doing is to ‘just’ bind to ACE2? Well, no effect on transmission.. Also every Spike bound ACE2 is a lost ACE2, thus still affecting the blood and circulation system by its very functional properties, but it had little to do with viral load! Also, will a synthetic gene, mimicking the behavior of a human gene (because it is allowed to express the Spike), suddenly cause the body to reject it?? Not even talking about the mimick while using FOREIGN genetic material here..
And if the natural, membrane fixed ACE2 is just binding the Spike, will the countless Spike mutations have any effect on infection, determined mainly by the viral load, i.e. number of replicating viruses which CROSSED the cellular membrane, ‘opened’ by ACE2, something what ACE2 does not seem to do??
If the Spikes JUST bind and never release all the ACE2, what consequences that may have? The answer was already proven, in a publication at https://www.nature.com/articles/s41467-020-18880-0 titled “ACE2 mouse models: a toolbox for cardiovascular and pulmonary research”. Table 1 describes what will happen with a mouse not producing ACE2 receptors (equivalent with a situation of releasing ‘just’ the SPIKE with ACE2 binding capacity on all accessible cells, and later penetrating them, a part done by the nanos, in both directions), here just one of the listed 4 models:
Table 1 Global ACE2 KO (so called knockout mouse) models and associated phenotypes.
Country of origin Canada (Source Life Science Institute, The University of British Columbia)
Phenotypes Source
Cardiovascular: Enhanced susceptibility to Ang-II or pressure overload-induced heart failure23,24, cardiac hypertrophy and myocardial fibrosis14 , myocardial infarction25 , vascular dysfunction and atherosclerosis26,27, abdominal aortic aneurysm28
Metabolic: Lipodystrophy and steatosis29 , obesity-induced epicardial adipose tissue inflammation and insulin resistance31 , diabetic cardiovascular complications 32, reduced intestinal uptake of tryptophan and altered serotonin metabolism37,38
Liver: Hepatic steatosis and fibrosis29,30
Lung: Resistant to SARS-CoV infection39 , exacerbated ALI/ARDS due to acid aspiration, lipopolysaccharide or pseudomonas aeruginosa infection41–43 , impaired inactivation of des-Arg9 -bradykinin43 , exacerbated lung fibrosis with a sex dichotomy44, increased susceptibility to respiratory viral infection45–47
Kidney: Renal fibrosis and inflammation33,34 and diabetes or hypertension associated nephropathy3
The options in molecular biology, which the eyes can’t see, are limitless, it appears there is another peptidase, which can do the ACE2 cutting job, quote: ”The type II transmembrane serine proteases TMPRSS2 and HAT can cleave and activate the spike protein (S) of the severe acute respiratory syndrome coronavirus (SARS-CoV) for membrane fusion. In addition, these proteases cleave the viral receptor, the carboxypeptidase angiotensin-converting enzyme 2 (ACE2), and it was proposed that ACE2 cleavage augments viral infectivity.”
Assume there is no infecting virus around, will TMPRSS2 still cut and destroy ACE2 in a healthy body, when actually both of them are anchored/fixed in cell membranes??? Uniprot lists only one 2011 publication describing this issue only in presence of SARS-CoV. What does it say? Quote (https://journals.asm.org/doi/10.1128/jvi.02062-10):”ACE2 and TMPRSS2 colocalized on cell surfaces and enhanced the cell entry of both SARS S-pseudotyped HIV and authentic SARS-CoV. Enhanced entry correlated with TMPRSS2-mediated proteolysis of both S and ACE2. These findings indicate that a cell surface complex comprising a primary receptor and a separate endoprotease operates as a portal for activation of SARS-CoV cell entry.” Entry while using HIV??
No, lets’ forget the TMPRSS2 for a moment, and go back to Barick’s in Sep 2015 to PNAS submitted article titled:”SARS-like WIV1-CoV poised for human emergence” with that one sentence, quote: ”The identification of WIV1-CoV and its capacity to use ACE2 orthologs offers a warning for possible reemergence and provides an opportunity to prepare for a future CoV outbreak.” (https://www.pnas.org/doi/10.1073/pnas.1517719113 )
That work didn’t produce new viruses but rather concentrated on ‘production’ of the Human ACE2 Expressing Mice, with consequences described in this quote from that work:”In the context of both the SARS-CoV and MERS-CoV outbreaks, focus had been primarily directed to spike binding as the key component of emergence and pandemic potential. Supported by adaption at Y436H in mouse-adapted SARS spike (10), improved binding to host receptor cannot be discounted as a crucial component in emergence. This fact is supported by improved replication of WIV1-CoV in mice expressing human ACE2 compared with control (Fig. 2D versus Fig. 3B).” One also should ask, is it reversible what Baric says: “we generated a mouse that expresses human ACE2 receptor under control of HFH4, a lung ciliated epithelial cell promoter”?? Improved replication by expressing more ACE2 (in mouse chimera) which then bind the Spikes and affect the titration curves???
Just one link more, for everybody to know, that the SYNTHETIC coronavirus was by then, already mostly ready, progress can be seen in Baric’s CurriculumVitae: https://sph.unc.edu/wp-content/uploads/sites/112/2016/09/CV_Ralph_Baric.pdf
That docking of the viral surface of the 1273 aa large Spike on the viral surface to the ~800 aa large ACE2 MEMBRANE bound receptor happens via the RBD domain, according to NIH data base, which spans residues from a Region 319..541, with a single letter code for all amino acids:
301 ctlksftvek giyqtsnf>>>rv qptesivrfp nitnlcpfge vfnatrfasv yawnrkrisn
361 cvadysvlyn sasfstfkcy gvsptklndl cftnvyadsf virgdevrqi apgqtgkiad
421 ynyklpddft gcviawnsnn ldskvggnyn ylyrlfrksn lkpferdist eiyqagstpc
481 ngvegfncyf plqsygfqpt ngvgyqpyrv vvlsfellha patvcgpkks tnlvknkcvn
541 f<<<nfngltgtg vltesnkkfl pfqqfgrdia dttdavrdpq tleilditpc sfggvsvitp
Spike original data: https://www.ncbi.nlm.nih.gov/nuccore/NC_045512 (YP_009724390.1 protein in it)
this gives at least 222 Spike residues, which can mutate.. How many choices that gives? 222!=1.120507558E+426, which is basically infinity, infinity of tests, lockdowns, injections targeting the immune response to every single of these variants.
Again, the ACE2 surface does NOT mutate, it is a FIXED entity, binding to its small ligands and performing PROTEOLYTIC enzymatic actions at fixed positions, outside of cells expressing it, participating in pathways of many essential short peptides:
Angiotensin I DRVYIHPFH→L P
Angiotensin 1–9 DRVYIHPFH N
Angiotensin II DRVYIHP→F C
Angiotensin 1–7 DRVYIHP N
Angiotensin 1–5 DRVYI. N
Apelin-13 QRPRLSHKGPMP→F C
Apelin-36 (C terminus shown) . . .QRPRLSHKGPMP→F C
Bradykinin RPPGFSPFR N
des-Arg9 -bradykinin RPPGFSP->F C
Lys-des-Arg 9 -bradykinin KRPPGFSP→F P
Bradykinin fragment 1–7 RPPGFSP N
beta-Casomorphin YPFVEP->I C
Neocasomorphin YPVEP→I C
Dynorphin A 1–13 YGGFLRRIRPKL→K C
Ghrelin (C terminus shown) . . .ESKKPPAKLQP→R P
Neurotensin 1–8 pE-LYENKP→R P
i.e. all what ACE2 does, as defined by uniprot data (https://www.uniprot.org/uniprotkb/Q9BYF1/entry), it is producing:
angiotensin II + H2O = angiotensin-(1-7) + L-phenylalanine
vasoconstriction peptide hormone and precursors for neurotransmitters^3, discussed in 2022 post:
Just few thoughts about how to fit specific facts, like the viral transmission issue and have to digest… If you think otherwise and have 100% proof of the issue in question, please let me know in comments. Last but no least, imagine a huge hole in cell membranes letting in ‘just’ the 1273 Spike amino acids, at once, in the same time where the same membrane regulates every single water molecule…
Thank you for getting that far! This post will be edited, or corrected, like all many other posts, to reflect feedback about new coming FACTS.
The most important: NEVER FORGET, NEVER GIVE UP, ALWAYS FIGHT FOR YOUR RIGHTS TO STAY HUMAN, NEVER EVER ALLOW TO INJECT YOURSELF with FOREIGN, SYNTHETIC GENETIC MATERIAL produced by those who want to change us via genetic engineering!!!
9/13: Analysis of the publication at https://onlinelibrary.wiley.com/doi/10.1002/jmv.27927 titled “Omicron (BA.1) and sub-variants (BA.1.1, BA.2, and BA.3) of SARS-CoV-2 spike infectivity and pathogenicity: A comparative sequence and structural-based computational assessment“ by Suresh Kumar et al. in Jun 2022. Now check it for yourself. At https://www.rcsb.org/fasta/entry/7T9L/display is the sequence of the Spike and ACE2 used in this publication to predict the PHYSIOLOGICAL parameters, which will set people in quarantaines!!! Take ACE2 first and compare the sequence with NATURAL human ACE2 at https://www.uniprot.org/uniprotkb/Q9BYF1/entry. For ACE2:
missing the entire N-terminal portion ‘MSSSSWLLLSLVAVTAA’ in the model
the residue 616Q in natural ACE2 was changed to CHARGED His! but this was NOT enough!
the ENTIRE C-terminal in MODELLED ACE2 is MISSING: SIKVRISLKSALGDKAYEWNDNEMYLFRSSVAYAMRQYFLKVKNQMILFGEEDVRVANLKPRISFNFFVTAPKNVSDIIPRTEVEKAIRMSRSRINDAFRLNDNSLEFLGIQPTLGPPNQPPVSIWLIVFGVVMGVIVVGIVILIFTGIRDRKKKNKARSGENPYASIDISKGENNPGFQNTDDVQTSF ==»> ONE HUNDRED EIGHTY NINE residiues were ERAZED and instead s.c. Histidine tag attached: HHHHHHH
For the ‘mutated’ Spike VARIANT:
the entire C-terminal section of the wild type SPike is NOT there in the ‘model’ YIKWPWYIWLGFIAGLIAIVMVTIMLCCMTSCCSCLKGCCSCGSCCKFDEDD SEPVLKGVKLHYT
the furin site is MISSING, BLAST comparison of the model with the natural Spike:
Query 655 NSYECDIPIGAGICASYQTQTKSHGSASSVASQS VARIANT MODEL NSYECDIPIGAGICASYQTQT S A SVASQS Sbjct 658 NSYECDIPIGAGICASYQTQTNSPRRARSVASQS Natural Spike
the model has 1285 residues, the ‘natural’ 2020 PATENTED Spike only 1273 residues=> the VARIANTS are GROWING and loosing entire sections of their sequences???!!!! And now read the PUBLISHED abstract in THE MOST PRESTIDIOUS JOURNAL of all times ((2022) Science 375: 760-764), for that 3 dimensional VARIANT analysis at https://www.rcsb.org/structure/7t9l , quote:
“The newly reported Omicron variant is poised to replace Delta as the most prevalent SARS-CoV-2 variant across the world. Cryo-EM structural analysis of the Omicron variant spike protein in complex with human ACE2 reveals new salt bridges and hydrogen bonds formed by mutated residues R493, S496 and R498 in the RBD with ACE2. These interactions appear to compensate for other Omicron mutations such as K417N known to reduce ACE2 binding affinity, resulting in similar biochemical ACE2 binding affinities for Delta and Omicron variants. Neutralization assays show that pseudoviruses displaying the Omicron spike protein exhibit increased antibody evasion. The increase in antibody evasion, together with retention of strong interactions at the ACE2 interface, thus represent important molecular features that likely contribute to the rapid spread of the Omicron variant.“
Every single process here is a COMPUTER SIMULATION resulting in The Table 1. Its title: “The predicted effect of Spike protein single mutations of Omicron variants on pathogenicity by using PredictSNP tool.”
Table 2 titled “Docking analysis of single-point mutation of Wuhan-RBM (receptor-binding motif), Omicron (BA.1)-RBD, and sub-variants (BA1.1, BA.2, and BA.3)-RBD residues with ACE2 using HEX software.” lists docking energies WITHOUT units…
Table 3 is interesting, salt bridge formation and hydrogen bond formation between ACE2-RBD predicted for Omicron and sub-variants using PDBePISA (PISA) web-based tool.
Salt bridge formation(ACE2‐RBD) Hydrogen bondformation (ACE2‐RBD)
WTa ASP 30-Lys417 Gln24-Asn487 (PDB ID: 6MOJ) Asp30-Lys417
BA.1.1 GLU 57-LYS 478 LYS 31-TYR 450
GLU 35-ARG 490 LYS 68-TYR 470
GLU 35-ARG 493 GLN 42-ALA 481
ASP 38-ARG 490 GLN 42-CYS 485
ASP 30-ARG 495 THR 27-THR 497
ASP 30-ARG 498 ASP 30-TYR 446
BA.2 ASP 30-ARG 490 ARG 559-ALA 472
ASP 30-ARG 490 GLN 388-ASN 484
GLU 35-ARG 495 LYS 68-THR 497
ASP 38-HIS 502 ASP 30-ARG 490
ASP 38-ARG 400 GLU 35-ARG 495
As you can see there are basically FOUR NEGATIVELY charged amino acids on the ACE2 interface, Asp30, Asp38, Glu34, Glu57, to which the positively charged residues of the Spike mutants attach with the strongest electrostatic forces caused by their total charge of -4. No matter how many positively charged Spike residues are around, that binding will take place if there is no steric hindrance to it. And now the CUT off of the first N-terminal residues in the ACE2 molecule, even if uncharged, will leave ‘lot of space’ for possible ‘new variants’… The official interpretation of the VARIANTS is using AFFINITY of the Spike to the ACE2 receptor, ‘binding strength’ if you will, but since that BINDING was ‘improved by design’ illustrated in the countless patents over decades, one can assume, once The spike binds, it binds, and it DOES NOT MATTER whether it is strong or weak, just my opinion as non-chemist..
The above listed positively charged ACE2 residues, attacked by the Spikes, on a micro-level, can be very easily handled, by adding SINGLE positively charged AMINO ACIDS, L-Lys, L-Arg, L-His to your diet, which will help to neutralize and shield of the ‘however mutated’ spikes… There are some studies confirming exactly that:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8264737/ →supplementation with zinc and zinc ionophores; vitamins C, D3 and E; and l-lysine during covis19
https://pubmed.ncbi.nlm.nih.gov/34372507/ →lysine supplementation
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8619186/ →arginine supplementation
I can only add one, to this CRIMINAL SCAM, the published conclusion, quote:
“In this study, Omicron (BA.1) and sub-variants (BA.1.1, BA.2, and BA.3) are compared and investigated with WT using various computational tools. There are 11 shared common mutations G339D, S373P, S375F, K417N, N440K, S477N, T478K, E484A, Q493R, Q498R, and N501Y in RBD Omicron and sub-variants that may contribute significantly to changing the host spectrum of SARS-CoV-2 in immune evasion and potential transmission. The Omicron sub-variants (BA.1.1, BA.2 and BA.3) are likely more transmissible than omicron (BA.1) and Delta.“
puts a HUGE QUESTION MARK to it all, even without the s.c. COOT, a 3D visualization tool for macromolecules, which became unavailable with windows 10… How strange, Gates knew what he was doing years back!!!
Literature.
Please open BLAST at https://blast.ncbi.nlm.nih.gov/Blast.cgi and search for patented sequences similar to YP_009724390.1. You will get: Altimmune Inc.; DEFENCE THERAPEUTICS INC.; NOVAVAX, INC.; Janssen Pharmaceuticals, Inc. and Beth Israel Deaconess Medical Center, Inc.; CUREVAC AG (german company with the highest numbers of patents of Spike); Regeneron Pharmaceuticals, Inc.; Suzhou Abogen Biosciences Co.; University of Pittsburgh now patented the spike inserted into Measles virus vaccine(US 11103576-B1),and many more. Something happened to the NIH data base of the patented sequences, because right now among thousands of entries, you will NOT find Pfizer, Mod-E-RNA patents ANY MORE..
2005 [YEAR:20-4-2005]Li,W., Zhang,C. et al. Receptor and viral determinants of SARS-coronavirus adaptation to human ACE2. EMBO J (20-4-2005) 24, 1634-1643.
John D Fernstrom 1 , Madelyn H Fernstrom “Tyrosine, phenylalanine, and catecholamine synthesis and function in the brain“ J Nutr. 2007 Jun;137(6 Suppl 1):1539S-1547S. https://pubmed.ncbi.nlm.nih.gov/17513421/
Thank you for all your hours of research and hard work !! You are always looking at the bigger picture, connecting the dots.....
mejbcart, this is definitely off topic, but would love to hear, as a scientist, your thoughts. Also, Jeff Wexler, who I know is one of your respected followers, was involved in passing along questions. Thank you!
Dr Ana's toxic errors
https://covidandvaxfaqs.substack.com/p/dr-mihalceas-toxic-errors?utm_source=cross-post&publication_id=1011006&post_id=136995192&utm_campaign=667911&isFreemail=true&r=xiwhi&utm_medium=email
Plus, the video
https://rokfin.com/stream/38860
Start at 57 minutes
EDTA, methylene blue, and quercetin.