TLR4 and MyD88. These have been discussed at
length in my threads dealing with the CYTOTOXIC nature of the SPIKE PROTEIN.
There is a parallel scenario which
involves these very same proteins and genes. TLR2 or TLR4 deficiency alone or
Myd88 deficiency restricted to either donor or host was not sufficient to
prevent rejection.
Cell damage or death associated with the
transplantation procedure releases a large variety of ‘danger’ molecules that potentiate rejection.
What is interesting is that drugs against HLA
antibodies, such as Rituximab and Bortezomib, post transplantation ENHANCE
coronavirus disease in mice and COVID-19 in humans. Whilst drugs against
alloimmunty, such as Alemtuzumab, are highly effective.
The immense peptide sharing of the spike protein
may mimic injection of self-peptides, which has proven fatal in mice.
Is this why the virus MIMICS ALLERGY?
DOES THE SPIKE PROTEIN MAKE US ALLERGIC TO OURSELVES?
Referenced/Related Papers
Anti-peptide autoantibodies and fatal anaphylaxis in NOD mice in response to insulin self-peptides B:9-23 and B:13-23
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC151146/
The Proteasome Inhibitor Velcade Enhances rather than Reduces Disease in Mouse Hepatitis Coronavirus-Infected Mice
https://journals.asm.org/doi/10.1128/JVI.00486-10
Cases of COVID-19 in Alemtuzumab-Treated Patients With MS: Pharmacovigilance Report (2059)
https://n.neurology.org/content/96/15_Supplement/2059
The Innate Immune System in Transplantation
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3535269/