January 14, 2022
TGF-β DRIVEN IMMUNITY, SEVERE COVID-19 OR PROLONGED SPIKE PROTEIN EXPOSURE RESULTS IN AUTOIMMUNE/FIBROTIC DISEASE (VASCULITIS)
A very interesting paper from March of 2021 made a startling observation which was concluded with the foreboding statement: Whether or not the antibodies generated in the continued immune reactions of COVID-19 patients in the ICU are harmless, or whether they may even cause detrimental immunopathology remains to be shown.
Why is this of interest now? We have been searching for a satisfactory explanation for the observed myocarditis, autoimmune issues and vasculitis which are appearing ever increasingly.
What the paper demonstrated was that they analyzed samples from six patients within the first week after ICU admission, ALL EXCEPT FROM ONE (patient #11, day 7) being SERONEGATIVE FOR THE SPIKE (S) PROTEIN OF SARS-CoV-2.
Now, let’s move forward a week. All patients who had been in the ICU for MORE THAN 7 DAYS HAD in their serum SARS-CoV-2 SPIKE (S) PROTEIN-specific IgM, and IgG ANTIBODIES.
What we must bear in mind is that PROTRACTED VIRAL SHEDDING AND VIRAL LOAD ARE ASSOCIATED WITH ICU MORTALITY IN COVID-19.
Therefore, those patients who end up in intensive care and/or dead have a far LONGER period of and amount of EXPOSURE to the Spike Protein. This may explain why so many people with mild/asymptomatic disease test negative for Spike Protein antibodies.
But this isn’t the end of the tale. What happens next is something most extraordinary. The adaptive response to the Spike Protein results in plasmablasts (stem cells which are precursors of B Cells and secrete antibodies) which DO NOT TARGET SARS-CoV-2!
Even MORE bizarre is that these plasmablasts were not even prevalent in the lungs of those that died! The immune responseof these plasmablasts is also driven by TGF-β, which is the engine of fibrosis.
COVID-19 patients which required prolonged ICU care (or, I believe, prolonged/high volume exposure to the Spike Protein) show a continued immune reaction reflected by egress of plasmablasts into the blood. This immune reaction is initially controlled by IFNs, IL-21, and TGF-β, which target antibody class switching to IgG1 and IgA1. At later time points IFN is no longer involved, and the immune reactions are controlled by IL-21 and TGF-β, which in the end drives cells to switch to the terminal antibody class IgA2. Such cells do not relocate to the lung and they contribute little to humoral immunity to SARS-CoV-2. The specificities of the antibodies generated remain to be identified, but most of them are not specific for the spike protein, its receptor-binding domain (RBD) or NP. Whether or not the antibodies generated in the continued immune reactions of COVID-19 patients in the ICU are harmless, or whether they may even cause detrimental immunopathology remains to be shown. Therapeutic targeting of TGF-β may be a way to ameliorate severe COVID-19, especially, when considering the fibrosis-inducing capacity of TGF-β.
At this moment, I believe we can safely say, those antibodies are real, and very pathogenic.
The Spike Protein therapies must come to a full stop. Immediately. While this is investigated.
Protracted viral shedding and viral load are associated with ICU mortality in Covid-19 patients with acute respiratory failure
SARS-CoV-2 in severe COVID-19 induces a TGF-β-dominated chronic immune response that does not target itself