Conversation so far

1. 1 Discuss the implications of 250x fold elevations of spike protein detectable in a patient's exosomes, with zero spike detectable in plasma or immune cells + a private exchange
2. 2 Maugeri et al 2019 note that transcytosis is consistent with their findings on mRNA-LNP delivery. Is this transfection, rather than transcytosis? + a private exchange
3. 3 How do later studies explain mRNA-LNP crossing the BBB? + a private exchange
4. 4 You stated earlier that, "Transcytosis would mean the intact LNP crosses the BBB and then transfects brain cells (neurons, astrocytes, microglia) on the other side. Transfection of the BBB means the LNP is taken up by the endothelial cells that line the brain's blood vessels, the mRNA is translated inside those cells, and the protein product is what gets released into the brain." Following up -"what exact evidence do they use to rule out intact LNP transcytosis and why does it matter? + a private exchange
5. 5 Either way, in this patient's case 2P S can be delivered across the BBB, by process of transcytosis at least. Explain the likely effects of such a process + a private exchange
6. 6 Tell me about the likely implications for disease-injury processes once 2P spike has been transcytosed across the BBB. + a private exchange
7. 7 Which specific injury mechanisms are most likely after BBB crossing? + a private exchange
8. 8 to what extent are these pathways consistent with neuro-inflammation and, in effect, autoimmune encephalitic processes? + a private exchange
9. 9 How do these mechanisms differ between infection-related encephalitis and autoimmune? + a private exchange
10. 10 Please share more about The 2025 PANS/PANDAS review - with references - that shows autoantibodies to striatal cholinergic interneurons, Th17-driven BBB disruption, and microglial activation. What were the symptoms specificially associated with such striatal cholinergic interneurons + a private exchange
11. 11 How do infection-related encephalitis mechanisms compare to BBB/Th17 autoimmunity? + a private exchange
12. 12 To what extent can these Th17-autoantibody mechanisms be characterised as T and B cell mediated humoral autoimmunity + a private exchange
13. 13 What evidence would distinguish humoral autoimmunity from innate Th17? + a private exchange
14. 14 You state, "if a patient has humoral autoimmunity, with high titres of serum autoantibodies against known self-antigens." Such as what? + a private exchange
15. 15 Hmm. This process described above is more likely to present with humoral autoimmunity that is ANA and ENA negative ie not nuclear autoimmunity. + a private exchange
16. 16 But, as established before, such patients have no N in exosomes. It is not WT, but 2P spike in play. + a private exchange
17. 17 What studies compare 2P spike vs wild-type spike in exosome loading? + a private exchange
18. 18 iF the evidence does show is that spike protein from natural infection is actively packaged into exosomes, how long can it persist given the relative fragility of the molecule compared with the 2P mutated version? + a private exchange
19. 19 You say, "For spike to still be in circulating exosomes five years later, either the protein must be continuously produced from a persistent mRNA reservoir, or it must be recycled through cells repeatedly." Recycled by transcytosis. My point entirely. + a private exchange
20. 20 the mechanism would require continuous production or near-total recycling failure. Pse examine both scenarios, and if transcytosis recycled spike, what cell pathway would recreate it long-term? + a private exchange
21. 21 With respect, Bansal et al 2021 demonstrated exosome titres that were not zero after 4 months. No follow ups on trial subjects beyond 4 months. Absence of evidence.......etc + a private exchange
22. 22 Perhaps such as study should be conducted as a matter of urgency.