I thought the mRNA vaccines encoded the prefusion spike that was locked in place and stable against cleavage? It was shocking to see that high levels of S1 were reported. If I'm not mistaken, S1 is much more pathogenic than full spike.
I have been mulling over what the puzzle piece means, hence not making a post on it.
Rather than a difference in cleavage, I think the question is why spike would be circulating instead of bound to the membrane of transfected cells. So it may just be that the spike is released when transfected myocardiocytes are blown up by the immune system.
Not satisfied, is why that would be specific to myocarditis. You would think there would be a tolerated level of cellular destruction and whole spike release in all recipients. Especially given that the spike-positive case kids were sampled days after symptom onset which would suggest spike isn't transient.
All I come up with is that suggests serious disparities in "bolus," though not necessarily due to IM as opposed to product variability. I would say both are likely at play. So the lack of circulating spike in the control group reflects that they had much less dosage and dispersion so the cell-killing-released spike is at trace levels. Meanwhile you can still have myocarditis without a huge dose/dispersion, since there's variability in dispersion. So "bolus" isn't everything.
I thought the mRNA vaccines encoded the prefusion spike that was locked in place and stable against cleavage? It was shocking to see that high levels of S1 were reported. If I'm not mistaken, S1 is much more pathogenic than full spike.
With every passing day I am more and more thankful that I didn't inject my kids.
I have been mulling over what the puzzle piece means, hence not making a post on it.
Rather than a difference in cleavage, I think the question is why spike would be circulating instead of bound to the membrane of transfected cells. So it may just be that the spike is released when transfected myocardiocytes are blown up by the immune system.
Not satisfied, is why that would be specific to myocarditis. You would think there would be a tolerated level of cellular destruction and whole spike release in all recipients. Especially given that the spike-positive case kids were sampled days after symptom onset which would suggest spike isn't transient.
All I come up with is that suggests serious disparities in "bolus," though not necessarily due to IM as opposed to product variability. I would say both are likely at play. So the lack of circulating spike in the control group reflects that they had much less dosage and dispersion so the cell-killing-released spike is at trace levels. Meanwhile you can still have myocarditis without a huge dose/dispersion, since there's variability in dispersion. So "bolus" isn't everything.