The new paper showing the spike protein is found in armpit lymph nodes at least 60 days after vaccination also shows that immune imprinting from vaccination leads to "original antigenic sin."
Mar 1, 2022·edited Mar 1, 2022Liked by Chris Masterjohn, PhD
Dear Chris, thanks for the great breakdown. I hope you are later able to comment on the new reverse transcription study you were touching on here: https://twitter.com/ChrisMasterjohn/status/1497556655466287106 Igor Chudov did a recent post checking a sequence from that article in BLAST (https://igorchudov.substack.com/p/dna-transcribed-from-pfizer-mrna). The results were nightmarish, to say the least. Really hope we can see your super clear breakdowns on this frightening reverse transcription issue. Keep up the good work!
Your arguments are specious and do not validate the presence of OAS. Your graph does not document OAS. Read: The “original antigenic sin ”and its relevance for SARS-CoV-2 (COVID-19) vaccination, Ger T. Rijkers a , b , ∗ , Frans J. van Overveld a Clinical Immunology Communications 1 (2021) 13–16
Every single study of covid ends with a recommendation for mRNA transfection, regardless of whether the data suggests that. Seems fishy. Anyway, I'll pass on one of these "vaccinations". I took my chances with covid without one of those. Got it, recovered and I'll continue to take my chances without one going forward.
After having just complemented your genome integration analysis, I was afraid I would have to issue a negative review on this one. I'll just say I second Robert Hansen, below. The paper demonstrates that infection resulted in measurable sensitization against Alpha and Delta, leading to a more balanced response. That's not OAS. OAS is not real.
As for as the observed broader baseline cross-affinity, it could be the case that the modRNA is causing a lot more variation in spike expression (as in "mutant" spikes) and/or APC epitope selection vs infection. There may also be more germ centers simultaneously engaged, resulting in less consensus. As for affinity maturation you wouldn't think that would lead to more cross-affinity since it's all measured as vs Wuhan, and I would say it's more likely that long-duration exposure leads to higher dominance of the high affinity clones. And yet that doesn't seem to be happening. So I provisionally lean toward the mutant spike explanation.
Oh, actually I forgot that Cirelli et al. did end up finding more epitope diversity in their slow delivery study (https://www.cell.com/cell/fulltext/S0092-8674(19)30398-8 which is cited by Röltgen et al.) but it is still a stretch to flip this into a paradoxical explanation for higher cross-affinity since absolute values for RBD binding were still higher in Pfizer recipients than the Wuhan-infected cohort.
In reading I've done since writing this, I agree there should be more variation in the spike produced, and that could contribute. However, I don't see any problem with my explanation as also a contributor.
Original antigenic sin is actually mentioned in this paper's discussion, and the results demonstrate it, if one accepts the definition as a bias toward the original strain.
I don't understand your objection to my analysis. The vaccines prior to the variant create a bias toward Wuhan when compared to infection with the variant. That's a key finding of the paper.
You seem to be disputing this on the basis of comparisons to infection with Wuhan. But I acknowledge greater diversity compared to Wuhan infection. The point is that the Wuhan bias is created by the vaccine before the variant infection compared to the variant infection alone.
I like mutant spike as well but I don't consider it mutually exclusive with my explanation.
This paper in Cell reads like the authors are paid cheerleaders for the vaccine without stopping to ponder the significant drawbacks. Madness.
I don't think that a paper can get published unless it *looks*like it is pro-vaccine. As CMj says, the important news is in the data and supplements.
I think the same or similar happened with the Danish mask study, though I'm not positive of that.
Horrible!!!
Dear Chris, thanks for the great breakdown. I hope you are later able to comment on the new reverse transcription study you were touching on here: https://twitter.com/ChrisMasterjohn/status/1497556655466287106 Igor Chudov did a recent post checking a sequence from that article in BLAST (https://igorchudov.substack.com/p/dna-transcribed-from-pfizer-mrna). The results were nightmarish, to say the least. Really hope we can see your super clear breakdowns on this frightening reverse transcription issue. Keep up the good work!
Your arguments are specious and do not validate the presence of OAS. Your graph does not document OAS. Read: The “original antigenic sin ”and its relevance for SARS-CoV-2 (COVID-19) vaccination, Ger T. Rijkers a , b , ∗ , Frans J. van Overveld a Clinical Immunology Communications 1 (2021) 13–16
Could you please summarize the counter-argument?
Every single study of covid ends with a recommendation for mRNA transfection, regardless of whether the data suggests that. Seems fishy. Anyway, I'll pass on one of these "vaccinations". I took my chances with covid without one of those. Got it, recovered and I'll continue to take my chances without one going forward.
After having just complemented your genome integration analysis, I was afraid I would have to issue a negative review on this one. I'll just say I second Robert Hansen, below. The paper demonstrates that infection resulted in measurable sensitization against Alpha and Delta, leading to a more balanced response. That's not OAS. OAS is not real.
As for as the observed broader baseline cross-affinity, it could be the case that the modRNA is causing a lot more variation in spike expression (as in "mutant" spikes) and/or APC epitope selection vs infection. There may also be more germ centers simultaneously engaged, resulting in less consensus. As for affinity maturation you wouldn't think that would lead to more cross-affinity since it's all measured as vs Wuhan, and I would say it's more likely that long-duration exposure leads to higher dominance of the high affinity clones. And yet that doesn't seem to be happening. So I provisionally lean toward the mutant spike explanation.
Oh, actually I forgot that Cirelli et al. did end up finding more epitope diversity in their slow delivery study (https://www.cell.com/cell/fulltext/S0092-8674(19)30398-8 which is cited by Röltgen et al.) but it is still a stretch to flip this into a paradoxical explanation for higher cross-affinity since absolute values for RBD binding were still higher in Pfizer recipients than the Wuhan-infected cohort.
In reading I've done since writing this, I agree there should be more variation in the spike produced, and that could contribute. However, I don't see any problem with my explanation as also a contributor.
Original antigenic sin is actually mentioned in this paper's discussion, and the results demonstrate it, if one accepts the definition as a bias toward the original strain.
I don't understand your objection to my analysis. The vaccines prior to the variant create a bias toward Wuhan when compared to infection with the variant. That's a key finding of the paper.
You seem to be disputing this on the basis of comparisons to infection with Wuhan. But I acknowledge greater diversity compared to Wuhan infection. The point is that the Wuhan bias is created by the vaccine before the variant infection compared to the variant infection alone.
I like mutant spike as well but I don't consider it mutually exclusive with my explanation.