Scientists found a mystery gene sequence in a Pfzer COVID π lot. What could this do in the body? π§΅
Geneticist @Kevin_Mckernan explains in his sstack Nepetalactone Newsletter:
The protein expressed is similar to the protein profile for silk protein, and to bacterial collagen and fibroin.
The "uncharacterized protein" is from Oscillibacter,
which is a butyrate producing bacteria. >
Oscillibacter is a bacteria found in the gut microbiome. It is involved in insulin homeostasis. Recall that Dr. Sabine Hazan found that the COVID π can wipe out the good gut bacteria. Is this protein (or the others) related to her finding, or is loss from something else? >
Human cells cannot make a spider's silk protein, but they can make a similar amyloid (misfolded) protein. >
Spider silk can self-assemble into nano fibrils. >
Spiker silk is the strongest fiber found in nature. Scientists use bacteria to try to reproduce synthetic spiker silks. >
These proteins are studied for the fibrillar structures. >
Given the amyloid clotting properties of the SARS2 spike protein, well documented in several papers (see #TeamClots Pretorius and Kell) these additional mystery proteins might give a gain of function effect of amplifying the spike's amyloidosis. >
Here Jessica explains the amyloidosis.
The spike protein has a prion genesis site on it so it is already highly efficient at misfolding proteins.
The SARS S1 subunit can activate the complement system (ITR) even without the presence of the virus.
The #ITR #InflammoThromboticResponse is described here by Dr. Flemming. This response attacks and destroys cells of the endothelium (lining of vessels and organs) as they express spike protein. This causes a release of collagen and cell debris. >
If the mystery proteins produced are also a form of collagen, then this would add to the amount of collagen released when the tunica layers are destroyed. In the presence of PEG, this would aid in the possible formation of a hydrogel like substance. >
Multiple factors implicated in clotting from the π: the lipid nanoparticles. see @_HeartofGrace_, and the free spike see @lasikeyecenter1 #StringTheory
The mystery proteins might aid in stabilizing the clots formed by the spike protein, perhaps giving durability and redundancy.
Here is Christie Grace's explanation of how Zeta potential (charge on an LNP) causes clots to be produced in the body by the LNPs.
This effect ALONE can explain the #CalimarClots. >
Now imagine if billions of charged LNPs are introduced into the bloodstream (not the deltoid) >
If billions of LNPs increase clotting by 1000xs and we add that ability to the spike protein's ability to form amyloid micro clots, then the use of a LNP casing for an mRNA expressing a spike protein is a GAIN OF FUNCTION, increasing its amyloid clotting formation. >
This is a similar #BaitAndSwitch the drug makers of the 1976 Swine Flu vaxx used which caused thousands of cases of Guillane Barre Syndrome. >
Manufacturers would have known about this effect from the clinical trials and a simple blood analysis. And Pfzer knew from their leaked biodistribution study. #TheyKnew >
This is why Speicher and McKernan's study is so important. More bacterial contamination = more adverse events.
Correlation, not causation indicates this contamination is having some effect, perhaps causing clotting? >
Does PEG play a role in the #CalimariClots and to what effect?
Less PEG = clotting OR more PEG = more clotting?
We need reproducible studies on this. >
>
Great research, thanks @_HeartofGrace_! >
Between Christie's research and Greg's research showing metals in the body act as catalysts for clotting and Dr. Lee's showing free spike binds many more antibodies into chains, there are many redundant explanations explaining post π aberrant clot formation. #CalimariClots
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How the SARS-CoV-2 spike protein chimera persists in the body chronically and activates a dual mTOR response, and remodels the immune system.
Including Annelise Bocquetβs Janus mTOR theory, my SAPIR model and published papers given to Grok. π§΅
π₯ Toxic Phoenix Hypothesis π₯
The spike protein of SARS-CoV-2
(whether from π¦ or mRNA π) behaves like a
"Toxic Phoenix"
a mythic creature of self-consuming π₯ and regenerative venom.
It ignites a destructive π₯ in the host
(acute hyper-mTOR activation, cytokine storm, oxidative inferno),
it appears to π or be cleared, only to rise renewed and more toxic from its own ashes through persistent immune sanctuaries, microbiome reprogramming, and self-amplifying loops.
Each rebirth is more insidious than the last, turning the hostβs own biological pathways into fuel for chronic pathologies. >
π₯
The TP theory is an extension of my #ItsAlive theory on the π§ Frankenstein nature of SARS2, positing that short gene sequence analogs in the lab-created spike protein can cause similar pathologies in C0VID infected patients as the original organisms do.
I.e. when you put an an abby normal π§ of a murderer into the backbone of several corpses, you shouldnβt be surprised when it goes berserk and starts killing the townsfolk after you revive it.
Because these gene analogs come from diverse progenitors:
HIV, SEB, venoms,
they cause heterogeneous symptoms and pathological mechanisms in the body.
This is why C0VID and the C0VID π have different symptoms/adverse events in different people and different persistent sequelae. > x.com/janiesaysyay/sβ¦
Self-Amplifying Cardiac Inflammation After mRNA π
Updated π§΅ (published research + autopsies + Grok)
The C0VID mRNA-LNP platforms (BNT162b2 & mRNA-1273) were deliberately engineered with specific modifications to maximize antigen expression, evade innate immunity, and produce a stable immunogen.
These exact choices create extraordinary durability for both the mRNA cargo and the synthetic spike protein β and they are the root of the platformβs π« vulnerability.
π
2 proline substitutions (K986P + V987P = S-2P) act as a molecular π
They sit in the S2 subunit and create rigid kinks that block the natural pre-to-post-fusion refolding.
This keeps the spike in its prefusion shape for better antibodies β but also makes the synthetic spike far more resistant to degradation and unfolding. >
π
Every uridine is replaced with N1-methylpseudouridine (m1Ξ¨) β the single most powerful durability factor.
m1Ξ¨ fools TLR7/8 and RIG-I/MDA5 sensors, suppresses inflammation, boosts translation efficiency, stabilizes mRNA structure, and resists RNase enzymes.
What was meant to solve short half-life now lets mRNA persist for weeks to years. π‘οΈ >
Together these aggregate to form #WhiteClotSyndrome #CalimariClots #CalamariClots which have a tougher tensile strength, like EPDM rubber.
(@Greg21143362)
Ultimate Spike Detox canβt thoroughly remove the clots.
>
The carcinogenic potential of the SARS2 spike protein
in the π« due to fibrosis and inflammation via
upregulation of TYMP - STAT 3.
π§΅
Covid causes lung fibrosis, fibrosis is a precursor for cancer in the lungs.
Looking at this preprint and other published research with Grok, on SARS-CoV-2 and the platelet endothelial growth factor enzyme, Thymidine Phosphorylase, TYMP a mechanism for lung cancer post C0VID develops. >
They are π because of the disastrous pandemic response directed by Fauci.
Fauci gave conflicting medical advice and censored
life-saving early πs in order to shield DoD bi0weapons programs from scrutiny and enable a novel warp speed mRNA π >