I didn’t expect to write this today. You may also use the search function in my Substack page, search for Th17, and get a lot of articles to read if you wish. For a shorter and more direct context to this article.
For the best part of 3 years, I was among the first to keep research, reverse engineering, doing meta-analysis into the highly complex immune response to SARS (both 1 and 2), and warning, over and over again its highly curious and substantial Th17 response.
Most of the earlier work and “de-construction” of the viral and vaccine pathways were based on the observation of this dominant immune response, while among the first, I wasn’t exactly THE first. Two scientists saw it first. Peter Hotez published a paper warning about it in 2020, and the other person was none other than Ralph Baric, also very early in 2020.
“There is the potential for ADE, but the bigger problem is probably Th2 immunopathology,” says Ralph Baric, an epidemiologist and expert in coronaviruses—named for the crown-shaped spike they use to enter human cells—at the University of North Carolina at Chapel Hill. In previous studies of SARS, aged mice were found to have particularly high risks of life-threatening Th2 immunopathology
The title of the paper says it all, let’s quickly break it down. FYI they are NOT using mRNA, just Spike Protein + Alum and CpG ODN… this one will be important in about 5 minutes.
Let us get down to brass tacks. The only possible way this paper would get ever published even on a pre-print server is by painting the vaccine as they did, so they could bring up potential issues. Upon exposure to the virus twice, while reduced viral loads were observed, something else was also observed.
Even though the survival rate of vaccinated mice was high, all vaccinated animals who suffered breakthrough infection had both significant levels of interstitial pneumonia, and the same had high levels of perivascular and peribronchial inflammation compared to unvaccinated + infected mice. The authors also found the following:
Flow cytometric analyses of cells recovered from the lungs further revealed significant accumulation of eosinophils and IgE-bound basophils/mast cells in the vaccinated mice with breakthrough infections
For the layperson, this is a textbook Type 2 immune response, in simple terms a dominant allergic response, something I brought up over, and over again that breakthrough infections were causing, and leading to a dominant Th17 response. They followed with investigating which type of lymphocytes got recruited into the lung. While they found NK, NKT invariant, and CD8+ T cells in significant levels, they found an abundant level of CD4+ T cells in breakthrough infections.
I will now leave snippets of the next two sections, they speak for themselves.
Th2 and Th17-associated pulmonary inflammatory cytokine responses following Spike vaccination and breakthrough infection
Vaccination showed an inhibitory effect on virus-associated induction of the expression of Il10 and Csf2. To our surprise, the expression of Il17a was significantly higher in the vaccinated and infected animals, as compared to any other groups, suggesting that a Th17-associated inflammatory response was likely involved in the development of the VAERD observed in the Spike-vaccinated mice that suffer a breakthrough infection
A systemic Th17 inflammatory response following Spike vaccination and breakthrough infection
Our results suggested that the COVID-19 VAERD observed in the ACE2-humanized mouse model is associated with enhanced local Th1, Th2 and Th17 inflammatory responses, as well as systemic Th17-associated inflammation.
The authors finish the paper by raising the point that it is not merely the adjuvant that causes these immune responses, but intrinsically it most likely is the nature of the viral Spike Protein itself to induces it, highlighting a specific section of the spike and alluding that other sections may induce it (the RBD does, the FCS does, both via over 6 different mechanisms).
The best part of all of this ? Pfizer announced a few months ago a promising new drug which the primary mechanism is *check notes
Modulating Th1 and Th17 immune responses. It is nothing personal, just good business.
Vaccine injury, vaccine damage, and vaccine long-term injury in all its forms, all stem from a Th2, Th17 immune response, that stacks over time. Endotoxins induce a Th17 response. As Omicron finds itself right now, it is mostly a long-term problem as I wrote multiple times this year, but if the vaccinated do not take extensive care of their immune responses after their multiple breakthrough infections, immune damage piles up, and diseases soon follow.
Do you want to know can act as a very potent CpG adjuvant, being able to induce a potent Th17 immune response, even without the addition of the Spike Protein, among many other nasty biological effects ?
Double-stranded DNA. dsDNA. By now everyone must be aware it is a large contaminant of the mRNA vaccines. Opsie. Oh almost forgot. dsDNA can also induce HERV-W and HERV-K expression. And their byproducts will also induce or further incentivize a Th17 response.
All roads lead to Rome. And Rome has a retroviral problem.
I wish everyone a great weekend. If you choose to support my work, I am grateful to you.
The next piece will be about Misfolded Proteins and their "secrets", and another one unrelated to science, but to Language. Both will take a few days, so I am already thanking people for their patience.
And I take no pleasure anymore of being "right" everytime, and no sense of vindication. I am numb to being right on such depressing matters.
Thank you SO much for your time and the diligence you exhibit. Truly valuable!