1) This is a long one. Please bear with it and read to the end of the thread.
SEVERE COVID, MIS-C, MIS-A, MIS-V, LONG COVID AND AUTOIMMUNITY
MOLECULAR MIMICRY OF THE SARS-CoV-2 SPIKE PROTEIN AS “GRAFT,” ITS ACTIONS IN COVID-19 AND GRAFT VS HOST DISEASE: DISEASES OF TARGET TISSUE
2) DESTRUCTION
In my studies, I keep finding a disease which, like an ostinato, is omnipresent in my research results. Interestingly, a parallel with a game I play to unwind led me to a breakthrough.
I play Hearthstone. It is my “mindless” activity to unwind while being able to
3) use my mind, but not in a mind-bending way. I consider myself to be pretty good at the game. I usually make Legend these days. Another Legend player told me that when you are crafting an original deck, and it is not working, look at the cards that are left in your hand when
4) you lose. Those are the problem cards.
Applying this concept towards research, I have always found Graft vs Host Disease as the “odd man out” that I could not account for in my work. I am always “left” with it. Therefore, I determined it must be the “problem.” Once I began
5) investigating the disease, I realized, it IS COVID. And it is perhaps an explanation for the greatest dangers the virus causes.
You won’t like this. And I certainly don’t. However, the brutal truth is that I believe repeated exposure to the virus and its Spike Protein will
6) inevitably induce “Graft vs Host Disease” (GVHD) in the infected and reinfected.
The story begins with, what else, the Spike Protein of SARS-CoV-2. This monstrous molecule happens to contain TWENTY-SIX peptide sequences which are homologous to human proteins. Some of our
7) cells are Antigen Presenting Cells which “grind up” pathogens and then present “snippets” of them to our adaptive (T and B cells) immune system to create antibodies against them and to “teach” our T Cells to kill them.
Inevitably, when you are dealing with numbers as large as
8) viral proteins and virions, those 26 peptides are going to be “served up” to our immune cells. “Once or twice” may not mean much and our immune system will turn its nose up and move along. However, if you keep shoving those peptides in its face, it will eventually “bite.”
9) PHASE 1 – ACTIVATION OF ANTIGEN PRESENTING CELLS (APCs)
This sets the stage for what is to follow. It is the initial damage stage. It can be caused by many things. Chemotherapy, RADIATION, INFECTION. Severe damage is the key. We know that the Spike Protein causes severe damage
10) to tissues. This releases lots of Danger and Pathogen “molecular patterns” into the extracellular space. Remember, those 26 sequences are among these patterns. There are BILLIONS of them. These are gathered up by the APCs to be given to the T (and B) cells for “action.”
11) PHASE 2 – DONOR T CELL ACTIVATION
This is where things get tricky and interesting. In Phase 2 of GVHD, donor T cell activation, proliferation, differentiation and migration in response to primed APCs occurs during the second phase of acute GVHD. The T cell receptors (TCR) of
12) donor T cells recognize alloantigens on both host and donor type APCs that are present in secondary lymphoid organs. During direct presentation, donor T cells recognize either the peptide bound to host MHC molecules, or the foreign MHC molecules themselves.
13) However, in COVID-19 it is YOUR OWN T cells which are activating, proliferating, differentiating and migrating in response to the primed APCs. The homologies in the Spike Protein are the “alloantigens” – except, they also happen to be yours.
14) PHASE 3 – CELLULAR AND INFLAMMATORY EFFECTOR PHASE
A complex cascade of cellular and inflammatory mediators occurs during the effector phase of acute GVHD and COVID-19. These mediators synergize to amplify local tissue injury and damage target tissues. As such, the effector
15) phase of GVHD and COVID-19 involves aspects of both the innate and adaptive immune response as well as interactions with the proinflammatory cells and cytokines generated during phase 1 and 2.
DESTRUCTION OF TARGET TISSUES. Heart. Lung. Gastrointestinal. Brain. Etc.
16) Followed by – FIBROSIS.
This is Severe COVID. This is Long COVID. This is MIS-C, MIS-A and MIS-V.
Spinning the Wheel of COVID shrinks the number of “prizes” it offers. Every time. Eventually, there is only one “prize” left.
Autoimmunity.
ncbi.nlm.nih.gov/pmc/articles/P…

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More from @Parsifaler

20 Nov
What I have been saying all along.

I take back my self-questioning in a previous post. I am one of the greatest medical geniuses to ever live. I want to help HUMANITY!

Everything I have said: GIT2 was originally identified as a keystone protein in aging through latent semantic
Indexing (LSI) in the hypothalamus of aging rats. This involvement of GIT2 in the aging process was further demonstrated by the upregulation in both human and primate hypothalamic tissue and in the presence of hydrogen peroxide. Additionally, it was found that GIT2 was strongly
involved in DNA damage repair, through recruitment of ATM to the sites of damage to start the DNA damage repair process. In this age-controlling paradigm it was demonstrated that GIT2 possessed a NEAR IRREVERSIBLE ASSOCIATION with the senescence regulator p53.
Read 4 tweets
17 Nov
1) COVID-19, ACE2 DEPLETION AND RAMPANT ANG II OVEREXPRESSION: A DISEASE OF LOCAL AND SYSTEMIC RAS
The great puzzle of COVID-19 may finally be solved. The immense number of systems involved, and the vast number of symptoms presented can be explained by the implication of Systemic
2) and Local Renin-Angiotensin Aldosterone (RAS) systems.
The RAS systems (both local (non-Renin dependent) and systemic (Renin-dependent) are primarily responsible for fluid homeostasis, most notably blood pressure regulation. However, the RAS system has evolved over time to
3) be responsible for far, far more than just fluid homeostasis. Everything we are seeing in COVID-19, both acute and in its sequelae, can be explained by the overexpression of a single peptide: Angiotensin II. This peptide, necessary to maintain a healthy blood pressure, is kept
Read 20 tweets
17 Nov
1) LESSONS FROM THE PAST INTENTIONALLY SUPPRESSED: PRE SARS-CoV-2 KNOWLEDGE OF ACE2, ITS FUNCTIONS AND THE SARS-CoV SPIKE PROTEIN
To begin with, please read the following paragraph:
To further clarify whether the intraperitoneally injected Spike-Fc protein directly affected lung
2) pathology in mice, we examined the localization of the injected Spike-Fc protein in lung. Spike-Fc was detected in lung homogenates by western blot using human Fc–specific antibody, whereas injected control-Fc was not detected. In addition, using immunohistochemistry, we found
3) that Spike-Fc protein localized to bronchial epithelial cells, inflammatory exudates and alveolar pneumocytes. Notably, Spike-Fc primarily localized to severe lesions. This localization of Spike-Fc protein is similar to Spike antigen staining in SARS-CoV–infected mice.
Read 17 tweets
16 Nov
1) THE LOSS OF ACE2 RESULTS IN THE ULTRA-RAPID DEVELOPMENT AND PROGRESSION OF ACUTE AND CHRONIC AGE-RELATED DISEASES
If one were to be an enemy of humanity and wished to end the lives of as many people as possible and in the stealthiest way possible and could choose only one
2) protein to remove from the body to accomplish this task – that protein would certainly be ACE2.
The loss of ACE2 causes a massive upregulation of Angiotensin II. This hormone is involved in all the pathologies of aging. Microvascular disease, cancer, neurodegeneration, heart
3) disease, sudden death and immune dysfunction.
GROUND GLASS OPACITIES/LUNG INJURY
As an immediate concern, it is thought that the upregulation of ANG II is responsible for the ventilation-perfusion mismatch seen in COVID-19: We hypothesize that hypoperfusion of apparently
Read 19 tweets
15 Nov
1) IS COVID-19 A DISEASE OF INDUCED DNA AND MASSIVE FREE RADICAL DAMAGE WHEREIN CLINICAL SYMPTOMS ARE ACTUALLY A “POST-VIRAL SYNDROME?” THERE IS NO “ASYMPTOMATIC SPREAD” AS THE MAIN PHASE OF “SYMPTOMATIC COVID-19” OCCURS WITHIN THE TRANSCRIPTOME.
Before COVID-19, the medical
2) community spoke of anosmia, in relation to viruses, as post viral olfactory loss.
If we look at lung radiation damage (not in the context of actual radiation, but in context of the massive amounts of free radicals, which it generates) we see a direct parallel to the lung
3) findings of COVID-19. Ionizing radiation produces reactive oxygen species that induce lesions, and not only is tumor tissue damaged, but overwhelming inflammatory lung damage can occur in the alveolar epithelium and capillary endothelium. Is this not COVID-19?
Read 8 tweets
11 Nov
peptides besides angiotensin I and thereby affects diverse physiological functions, including renal development and male reproduction. In addition, ACE has a role in both innate and adaptive responses by modulating macrophage and neutrophil function — effects that are magnified
when these cells overexpress ACE. Macrophages that overexpress ACE are more effective against tumours and infections. Neutrophils that overexpress ACE have an increased production of superoxide, which increases their ability to kill bacteria. These effects are due to increased
ACE activity but are independent of angiotensin II. ACE also affects the display of major histocompatibility complex (MHC) class I and MHC class II peptides, potentially by enzymatically trimming these peptides. Understanding how ACE expression and activity affect myeloid cells
Read 4 tweets

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