TLDR:
Frame shifting refers to errors in the protein synthesis process where the ribosome (the molecular machine that reads RNA and builds proteins) slips on the mRNA template and starts reading the sequence at the wrong point, leading to the production of altered proteins. Template switching refers to the RNA polymerase (the enzyme that synthesizes mRNA from DNA) switching templates while transcribing the mRNA, potentially leading to chimeric (mixed origin) mRNA molecules and thus unpredictable protein products.
Kevin and Kory raise concerns about the following:
Purity and Consistency of Protein Production: The vaccine cannot consistently produce the intended spike protein without errors; studies suggest a significant percentage of the proteins might be frame-shifted or otherwise altered.
Genetic Variability Among Individuals: The vast genetic diversity among humans might affect the consistency and efficacy of the dose each individual receives, due to differences in how their cells might interpret and process the mRNA.
Potential for Unexpected Outcomes: The mRNA vaccines may have unintended biological consequences, such as the production of "zombie proteins" or proteins with unknown effects, due to frame shifting and template switching. Concerns about amyloidogenesis (the process leading to the formation of amyloid plaques, which are associated with diseases like Alzheimer's) are mentioned as a potential risk if aberrant proteins are produced.
AI transcript:
And we're also in this world of asking everyone's cells to, you know, Pfizer's outsourcing the manufacturing of their drug to people's cells, right?
This is a pro-drug.
We're giving them an RNA.
We're hoping for it to make a protein, which they've not done a very good job proving that it makes a pure protein.
In fact, Mulroney papers that are out show it makes frame-shifted protein.
So the variability in the human genome is really vast.
So how can you be assured of what dose you're giving every patient, given the genetic complexity of the population?
So Kevin, how serious is the frame shifting issue?
It's very serious.
And I think it's an underestimate of what they have currently.
They showed 8% of the proteins are frame shifted.
I think they're going to find in a year that there's also template switching going on.
Moderna is published on this.
So the process of copying RNA off of DNA uses an enzyme that oftentimes flips back on itself and reads the strand backwards or reads another strand.
And this is why when you look at these RNA integrity plots that many have been critiquing from Pfizer, they're not a perfect peak of one size.
They have the smear of sizes that are smaller and longer than the anticipated peak.
That's all translational or transcriptional fidelity issues from the polymerase they're using to make the RNA off the DNA.
It's not degradation.
Everyone was saying that they're degraded.
That's the enzyme making errors.
And and so I think in a year they'll start to see these these template switching artifacts going on, which would give you chimeric peptides that are even more off target.
and there's risks when you start doing that.
If you look in the Pfizer vaccine, the very end of the vaccine after the stop codons, we're supposed to stop making the message.
There's a human mitochondrial sequence in there that if it ever frame shifts through those stop codons, which those stop codons are published to be notoriously slippery, you'll start making spike mitochondria.
Kevin, why is there stuff after the stop codon?
They put them in there, they claimed to get better expression of the actual RNA and translation of the RNA.
So there's a beta, I think there's a beta globin on the five prime end and a mitosequence on the three prime end.
But there's publications out there from Fernandez that show this N1 methyl pseudouridine makes it so the ribosomes slip, which is giving the frame shifts.
But if you frame shift over the stop codons, you're going to be making proteins that are spike mitoproteins.
And when I talk to a lot of the long vax patients, I hear all these things that remind me of my time in the mitochondrial disease sequencing space.
They've got POTS, they've got dysautonomia, they've got...
And I'm like all right what if the immune system somehow getting you know targeted against the mito that would be a disaster so hold on let me let me stop there so I mean what you're saying is that the frame you know these vaccines were supposed to just make spike protein right make spike protein that's the antigen you form antibodies but now with the frame shifting
We're understanding that you can have zombie proteins, just weird proteins being made and who knows what their effects are.
But you just said because of those mitochondrial sequences after the stop codon, if there's frame shifting, some of those could be explaining the disease that we see, which is these chronically ill patients with this vast majority of this really wide diversity of symptoms that are related to the mitochondria.
Yeah, we published this or tried to publish this in 2021 with Peter McCullough.
Two reviewers signed off on it and then the editor stepped in and torpedoed the paper.
And this is so the frame shifting stuff we predicted in October of like 2021.
And then, you know,
Fast Forward a Few Years and They Find It.
And, you know, I'm just waiting for them to do this on the template switching artifacts because Moderna published a really clever paper where they mutated the enzyme, this T7 polymerase that makes the RNA off the DNA.
They mutated it because they were having template switching problems.
And if you look at that paper, like the template switching going on that paper is crazy.
It's this N1 methyl pseudouridine I think is exacerbating that template switching.
But that paper published in 2023, so they didn't have this mutated polymerase that cleans up the template switching for the batches that are out in the public right now.
So odds are there's a fair amount of template switched RNA out there that is causing more than just- Kevin, what's the difference between frame shifting and template shifting?
So the template switching is when the polymerase travels on one strand.
There's two flavors of it.
There's cis template switching and trans.
Trans is when the molecule partially extends on making the spike protein.
And then due to just the thermodynamics of these things in solution, it then hops over to another strand.
And because there's maybe six or seven bases of homology, it takes off on that one.
So it makes a chimeric molecule.
Sys template switching is when the molecule gets extended, and then it makes a hairpin onto itself and starts reading your strand backwards the other direction.
That's a sys event because you're on the same template, but you just did a hairpin and ran backwards the other direction.
So you're saying it's basically reading the messenger RNA backwards?
Yes.
And that's the big problem in Pfizer because the reverse strand in Pfizer has no stop codons for 1,252 amino acids.
It's all open reading frame.
So that is very bizarre, actually, from anyone who's done codon optimization.
This is like writing a chapter of the Bible and having it read sensibly forward and reverse.
It's more than the Beatles album.
I mean, it's very hard to make that happen.
Usually in nature, you only get about 50 to 100 amino acids that ever overlap in the genome that are coding because it's just hard to make things make sense both directions on a strand of DNA.
But Pfizer somehow pulled it off.
And the entire sequence there in the spike is amyloidogenic on both strands.
So if we start making aberrant peptides, we've got to pay close attention to amyloid and amyloidogenesis because that's an event that also is a a self-amplifying event.
Well, that's the thing, Kevin.
Can you explain to our audience why amyloid is such a four-letter word when you have an amyloidogenic protein?
It's because of the fact that it chain reacts.
So it's an amplifiable.
It's an exponential, if you will.
When you start making amyloidogenic peptides, they force other proteins to misfold and pass on that behavior.
It's this chain reaction of misfolding.
It's like an infectious disease.
It's contagious.
In the body, you're now disturbing lots of proteins being made into toxic proteins.
Yes, ones that are very difficult to degrade usually.
That's one of the key characteristics of them.
And when that happens, you get, you know, mad cow disease, bovines, you know, you get all these encephalitis types of behavior from spongiform encephalitis comes from a prion like this.
A prion is another term for these amyloids.
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