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Marc Girardot's avatar

The Yonker report has a major problem.

The myocarditis patients circulating spike samples are much earlier than the ones from the uninjured, but when you compare with ogata et al, it is much more in line.

The circulating spike hypothesis is falsifiable in multiple ways. The most obvious aren't antibodies actually doing the working. If Tcells are primed how can any amount of spike be produced given the speed of Tcell intervention at jab 2 and plus?

But more importantly w

How do spike bypass the vasculaf system's disseminative qualities?

It can't. Circulating spike issued should be in the tissue and in the vein, snd disseminated, ie systemic not in the aorta.

Zn dit would not give rise to Tcell attacks.

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DocKek's avatar

What happens when hypothesis does not match observation?

The observations put forth also surround non-spike related damage due to Cationic LNPs

CD16+ innate antibodies have been shown to induce Long Covid

In addition to the now documented Spike infiltration of CD4+

Spike is immuno-infiltrative within innate and adaptive immune cells

"Immunogenicity" inducing long covid and other auto-immune induced angiogeneis, inflammation, and cytokinemia must take into account clinical reality.

https://www.coffeeandcovid.com/p/jackpot-tuesday-august-8-2023-c-and

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Marc Girardot's avatar

The very mechanism of action of the vaccine is cytotoxic (see "fragmented taeget protein" on MHC-source Pfizer)

https://www.pfizer.com/news/articles/understanding_six_types_of_vaccine_technologies

The LNPs by carrying an antigen or its recipe (mRNA) are cytotoxic. All the observation are consistent with that MoA. Whzt isn't consistent is the location (endothelium) and the extreme concentration (tied to accidental Iv).

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