1) MOLECULAR MIMICRY AND THE MICROBIOME APPROACH (NOT JUST GUT MICROBIOME, BACTERIA ARE UBIQUITOUS IN THE BODY), SARS-CoV-2 IS A BACTERIOPHAGE:

It appears to be increasingly apparent that metabolism and transcription dysregulation are front and center in COVID-19. It could be
2) that there is a "CO-CONSPIRATOR" in the body of those who suffer from severe disease and death. For example, cross-reactions with H. Pylori alone can trigger idiopathic thrombocytopenic purpura. There may be unidentified bacteria that SARS-CoV-2 is infecting in the body,
causing much of this dysregulation. Please watch the referenced video. It is extremely important.

journals.lww.com/co-rheumatolog…

pubmed.ncbi.nlm.nih.gov/32358202/

ncbi.nlm.nih.gov/pmc/articles/P…

Suppression of LKB1 causes dysbiosis in the gut microbiome.

jimmunol.org/content/200/5/…
AUTOANTIBODY ARRAYS SHOULD BE PERFORMED FOR ALL SPIKE PROTEIN THERAPY RECIPIENTS. IT COULD BE THAT A SIGNIFICANT NUMBER, IF NOT A MAJORITY, HAVE DEVELOPED PATHOGENIC AUTOANTIBODIES. THIS IS NOT A "ONE-AND-DONE" SCENARIO.
And this explains why COVID is so unique to each individual:

Is it not so much pathogenic priming, but rather PRIME YOUR PATHOGENS?

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More from @Parsifaler

6 Jul
1) PLATELET FACTOR 4 AUTOANTIBODIES: THE MOST IMPORTANT RISK FACTOR

I believe I have found the most important risk factor for COVID-19. The frequency of preexisting PF4 antibodies is estimated at 1.4% in normal, 4.5% in elderly, 4.8% in pregnant and 8.6% in diabetic subjects! Image
2) THE DAMAGE DONE BY THE SPIKE PROTEIN TO THE ENDOTHELIUM MIMICS ACUTE CORONARY SYNDROME. THIS ACTIVATES THE IMMUNE RESPONSE TO PF4 AND EXPLAINS WHY HEPARIN MAKES THE CONDITION WORSE!

To explain the preexistence of HIT antibodies, it was proposed that heparin-like molecules
3) (glycosaminoglycans) on injured endothelium bind
with PF4 to form complexes with which the antibodies
react. Neoantigens appeared to cause conformational
change of PF4 to induce the production of heterogenetic antibodies in the Ig subclass in the presence of heparin like
Read 6 tweets
6 Jul
1) There appears to be an intimate associate between the spike protein and clotting. Especially microclotting, which has been obeserved in the alveoli of severe covid. There have been strokes and heart attacks even in asymptomatic cases.

However, what are the mechanisms
2) of this connection? One very important clue is the role of Interstitial Lung Disease. The spike protein has been proven to cause synctia in the lung. Patients showed extensive blood clotting of the lung arteries and veins (thrombosis). Second, several lung cells were
3) abnormally large and had many nuclei, resulting from the fusion of different cells into single large cells. This formation of fused cells (syncytia) is due to the viral spike protein, which the virus uses to enter the cell. When the protein is present on the surface of cells
Read 8 tweets
4 Jul
1) COVID-19: A DISEASE OF TRANSCRIPTIONAL ERROR - EPIGENETICS

COVID-19 is without question a multi-systemic syndrome like no other with vast variance and involvement. I believe we are viewing the disease incorrectly. COVID-19 is unique. Instead of the DISEASE causing PATHOLOGY,
2) the DISEASE dysregulates TRANSCRIPTION causing the HOST to cause PATHOLOGY.

It is the only logical conclusion I can arrive at given the unprecedented panoply of systemic involvement and symptoms, and how UNIQUE it ultimately is, to each host.

Many different diseases and
3) syndromes, including cancer, autoimmunity, neurological disorders, diabetes, cardiovascular disease, and obesity, can be caused by mutations in regulatory sequences and in the transcription factors, cofactors, chromatin regulators, and noncoding RNAs that interact with these
Read 6 tweets
2 Jul
1) LKB1, MASTER COVID SPECTRE: FROM CARCINOGENESIS TO METABOLISM, AM DYSFUNCTION AND SKELETAL MUSCLE HOMEOSTASIS

I believe without question the spike protein is downregulating/"turning off" expression of LKB1. At first glance, the most immediate danger is carcinogenesis
2) as it was found that loss of Lkb1 was sufficient to drive the initial steps of carcinogenesis ex vivo.

Lkb1 plays an important role in regulating glucose homeostasis and energy metabolism. In addition, there is also evidence that has highlighted a prominent role for Lkb1 in
3) the function of macrophages. Lkb1 inhibits the activation and inflammatory function of innate macrophages. It was found that disruption of Lkb1 impaired the self-renewal of AMs, contributing to the reduction of AMs, which led to aggravated symptoms and EXCESSIVE accumulation
Read 9 tweets
2 Jul
1) METABOLICALLY INDUCED IMMUNE DEFICIENCY

Given the mitcochondrial dysfunction obeserved in COVID-19, I have turned my attention towards liver kinase B1 (LKB1). This kinase is intimately involved with both ATP production, T-cell development, peripheral T-cell homeostasis, and
2) T-cell effector function.

I believe SARS-CoV-2 is epigenetically impairing LKB1. LKB1-deficient T cells exhibited defects in cell proliferation and viability and altered glycolytic and lipid metabolism. Interestingly, loss of LKB1 promoted increased T cell activation and
3) inflammatory cytokine production by both CD4+ and CD8+ T cells.

LKB1 was recently found to have prominent roles in hematopoietic stem cell viability and renewal, suggesting a prominent function for LKB1 in hematopoietic cells. These features are also observed in COVID-19.
Read 8 tweets
1 Jul
1) LKB1: THE STAR OF THE SHOW IS STILL WAITING IN THE WINGS: HOW HAVE WE MISSED THIS?

Endothelial Cell-Specific LKB1 Deletion Causes Endothelial Dysfunction and Hypertension in Mice in vivo

The gene, also known as STK11, is involved in controlling blood sugar levels.

LKB1
2) programs the metabolic and functional fitness of Treg cells in the control of immune tolerance and homeostasis. Mice with a Treg-specific deletion of LKB1 developed a fatal inflammatory disease characterized by excessive TH2-type-dominant responses. LKB1 deficiency disrupted
3) Treg cell survival and mitochondrial fitness and metabolism, but also induced aberrant expression of immune regulatory molecules including the negative co-receptor PD-1 and the TNF receptor superfamily proteins GITR and OX40. The results point to functional exhaustion of Treg
Read 9 tweets

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