Thread by @NBoydGibbins

This data is I think one of the most important findings in ME/CFS and ME/CFS-like long Covid research

It shows that the S1 spike protein subunit can cause mitochondrial fragmentation, part of the "mitochondrial pathogen response"

mdpi.com/2073-4409/12/6…

We know that spike can persist long term even in the absence of viral RNA and nucelocaspid, meaning that it may just be very stable in the human body. I think it would be fantastic to make testing for S1 protein routine in LC patients

biorxiv.org/content/10.110…

The key concept for me is that S1 may be enough alone to trigger ME/CFS. If so then that explains why many #vaccineinjured have developed ME/CFS. And given all of the work that was known about spike from SARS1 (some patients are still chronically ill more than 18 years later)

And it also raises the question of why supposed experts thought it was a good strategy to use S1 in the 💉

And also why Peter Daszak spent so much time shutting down all evidence supporting the lab leak origin instead of warning people about the dangers of spike protein

And Peter Daszak even talked candidly about engineering coronaviruses (“recombinant viruses”), testing them in “humanised mice” (expressing human ACE2 in their airways), and that some “don’t respond to MAbs, 💉”