The scientists lied, lol. RNases require Uracil to bind, so these N1-methylpseudouridine zombie mRNAs are impervious to enzyme actions. This was purposeful, of course!
RNA still degrades in water through 2’ base-catalyzed nucleophilic attack, leading to hydrolysis, but the reaction is slow in the cell’s pH. Exosomes of spike are still detectable 4 months after transfection, showing that these zombie mRNAs decay until they are mostly gone after 4 months.
The exosomes piece seems unrelated to the antigen retention in the lymph nodes, though who knows for sure. So it doesn’t necessarily speak for longevity of the RNA - it might or might not. Maybe spike is getting trapped in ECM or biofilms and gradually being released. But if so, weird that it was 100% of subjects in the exosomes study but that Patterson and co. only find it in monocytes for symptomatic PASC. It’s all a big mystery...
I do not know the RNAscope method very well, but I was wondering if there was a chance to explain this prolonged detection of vaccine mRNA by a reverse-transcription in the lymph nodes. As it has been documented in HEK cells https://www.mdpi.com/1467-3045/44/3/73
So the probes would actually detect presumably more stable cDNA and not RNA.
Thank you for this one btw XD:
David “If you time-travelled me back to 1960, I would prescribe my own future mother Thalidomide” Gorski
If the RNA is integrated then it can be subsequently re-expressed / transcribed into new RNA molecules at a later point in time, so that essentially is the non-Unglossed theory for what is going on
Thank you so much for this breakdown. 👍🏽💫 Definitely an important discovery, I wonder what people would say who thought mRNA would be broken down quickly in the muscle. I can't wait to read part two!
Really appreciate the deep dive on this fascinating discovery. I like how Gorski was not only wrong about this topic, but also on whether the mRNA sometimes enters the nucleus, and sometimes reverse transcribes. So far, no evidence it replicates. I guess even he can't be wrong ALL the time.
Something occurred to me while reading:
Why do we see "waning" if the B memory cells are getting programmed?
Given that we now know that some of the mRNA material persists in these centers, is it possible that the "waning" effect actually corresponds to the slow decay of this material, rather than a gradual failure of programmed memory cells?
Humoral B Cells have a half-life while germinal centers are real time. Humoral B Cells also expand if encountering antigen, while germinal centers can persist autonomously for weeks. So, it’s complicated as both elements have different dynamics of acceleration and inertia. Antibody waning can simply be a reflection of clearance of the bigger portion of spike and transfected cells, and the expiration of T-Cell-Independent B Cell antibodies (IgM) depending on the procedures used to measure what’s goin on. Germinal center enrichment can still be ongoing, or novelly initiated by lingering mRNA. So I think there’s a built-in senescence of the earlier B Cell IgG clonal lineages that is poorly understood. It could be that memory B Cells that encounter antigen expire by default, since said encounter should be accompanied by novel germinal centers anyway.
I'm actually surprised that Gorski has as much expertise as he does. Judging by his Twitter feed, I was fairly certain he had no real scientific background whatsoever.
Haha - he is in the same boat as any other science journalist- he has his expertise, but in practice spends 95% of the time trying to report things outside of his wheelhouse and is no more reliable than a lay outsider. Given his choice to focus on the mRNA vaccines that might be more like 70%. And he’s smart. But spiritually bereft, and physically limp, and so hopeless when it comes to conceptualizing biology.
Bulls-eye - the durability of exposed RNA isn’t relevant, just whether body temperature LNP is or is not able to retain the same form as it does in storage.
Both injections replace all instances of the U nucleotide with pseudouridine to reduce innate intracellular immune recognition, but this only comes into play after the mRNA molecule escapes the LNP. And both alter the spelling of amino acids, but the logic on these alterations is basically frat boy “optimization” nonsense and the IRL effect as far as prolonging expression is unknowable (for example, maybe the over-inclusion of G’s results in the RNA knotting up so tightly that it can neither be read nor degraded for several weeks, but it’s not consistent with the normal antibody response so I leave this out of my model).
The scientists lied, lol. RNases require Uracil to bind, so these N1-methylpseudouridine zombie mRNAs are impervious to enzyme actions. This was purposeful, of course!
RNA still degrades in water through 2’ base-catalyzed nucleophilic attack, leading to hydrolysis, but the reaction is slow in the cell’s pH. Exosomes of spike are still detectable 4 months after transfection, showing that these zombie mRNAs decay until they are mostly gone after 4 months.
The exosomes piece seems unrelated to the antigen retention in the lymph nodes, though who knows for sure. So it doesn’t necessarily speak for longevity of the RNA - it might or might not. Maybe spike is getting trapped in ECM or biofilms and gradually being released. But if so, weird that it was 100% of subjects in the exosomes study but that Patterson and co. only find it in monocytes for symptomatic PASC. It’s all a big mystery...
Yeah, a study from Pfizer or Moderna on the half-life of these zombie mRNAs would have been nice.
Also, the timeline of spike production 4 months after injection is consistent with the data from autopsies of gene therapy deaths:
https://www.transcend.org/tms/2022/03/covid-vaccine-injuries-the-german-pathologists-findings/
I do not know the RNAscope method very well, but I was wondering if there was a chance to explain this prolonged detection of vaccine mRNA by a reverse-transcription in the lymph nodes. As it has been documented in HEK cells https://www.mdpi.com/1467-3045/44/3/73
So the probes would actually detect presumably more stable cDNA and not RNA.
Thank you for this one btw XD:
David “If you time-travelled me back to 1960, I would prescribe my own future mother Thalidomide” Gorski
If the RNA is integrated then it can be subsequently re-expressed / transcribed into new RNA molecules at a later point in time, so that essentially is the non-Unglossed theory for what is going on
Glad the nickname was enjoyed, haha
Thank you so much for this breakdown. 👍🏽💫 Definitely an important discovery, I wonder what people would say who thought mRNA would be broken down quickly in the muscle. I can't wait to read part two!
Well done. Even this old retired chiropractor can understand this.
Really appreciate the deep dive on this fascinating discovery. I like how Gorski was not only wrong about this topic, but also on whether the mRNA sometimes enters the nucleus, and sometimes reverse transcribes. So far, no evidence it replicates. I guess even he can't be wrong ALL the time.
Something occurred to me while reading:
Why do we see "waning" if the B memory cells are getting programmed?
Given that we now know that some of the mRNA material persists in these centers, is it possible that the "waning" effect actually corresponds to the slow decay of this material, rather than a gradual failure of programmed memory cells?
Humoral B Cells have a half-life while germinal centers are real time. Humoral B Cells also expand if encountering antigen, while germinal centers can persist autonomously for weeks. So, it’s complicated as both elements have different dynamics of acceleration and inertia. Antibody waning can simply be a reflection of clearance of the bigger portion of spike and transfected cells, and the expiration of T-Cell-Independent B Cell antibodies (IgM) depending on the procedures used to measure what’s goin on. Germinal center enrichment can still be ongoing, or novelly initiated by lingering mRNA. So I think there’s a built-in senescence of the earlier B Cell IgG clonal lineages that is poorly understood. It could be that memory B Cells that encounter antigen expire by default, since said encounter should be accompanied by novel germinal centers anyway.
I'm actually surprised that Gorski has as much expertise as he does. Judging by his Twitter feed, I was fairly certain he had no real scientific background whatsoever.
Haha - he is in the same boat as any other science journalist- he has his expertise, but in practice spends 95% of the time trying to report things outside of his wheelhouse and is no more reliable than a lay outsider. Given his choice to focus on the mRNA vaccines that might be more like 70%. And he’s smart. But spiritually bereft, and physically limp, and so hopeless when it comes to conceptualizing biology.
Bulls-eye - the durability of exposed RNA isn’t relevant, just whether body temperature LNP is or is not able to retain the same form as it does in storage.
Both injections replace all instances of the U nucleotide with pseudouridine to reduce innate intracellular immune recognition, but this only comes into play after the mRNA molecule escapes the LNP. And both alter the spelling of amino acids, but the logic on these alterations is basically frat boy “optimization” nonsense and the IRL effect as far as prolonging expression is unknowable (for example, maybe the over-inclusion of G’s results in the RNA knotting up so tightly that it can neither be read nor degraded for several weeks, but it’s not consistent with the normal antibody response so I leave this out of my model).