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.
4) Inhibition of mTOR induces immunosuppression in transplant rejections and autoimmune disorders. Furthermore, diminished LKB1 reduced t-cell survival and TCR-induced proliferation; increased metabolism and cytokine production.

Sphingosine-1-phosphate receptor 1 (S1PR1) —
5) a G protein-coupled receptor for the bioactive lipid sphingosine-1-phosphate (S1P) — is a crucial regulator of T cell egress from the thymus and secondary lymphoid organs. G -protein coupled receptors have been implicated in COVID-19.

Upon examination of the above evidence,
6) I believe SARS-CoV-2 is metabolically inducing immune deficiency - both against pathogens and self-tolerance.

journals.physiology.org/doi/full/10.11…

onlinelibrary.wiley.com/doi/abs/10.111…

jimmunol.org/content/187/8/…

nature.com/articles/nri31…
ADDENDUM: This is extremely disturbing. LKB1 is an essential regulator of spermatozoa release during spermiation in the mammalian testis.

europepmc.org/article/PMC/32…
HERE IS THE PROOF

Metformin pharmacodynamically, activates AMP dependent protein kinase (AMPK) via its phosphorylation in the hepatocytes. Metformin causes phosphorylation of AMPK in an LBK1 dependent manner.

neucradhealth.in/language/en/me…

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More from @Parsifaler

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, Image
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 Image
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 Image
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
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
30 Jun
1) ARE REGULATORY T CELLS BEING EXHAUSTED BY EXPOSURE TO THE SPIKE PROTEIN SUPERALLERGEN IN SEVERE COVID?

There has been much discussion of immune dysregulation in COVID-19 disease. One of the most interesting recurring findings is CD8 T-Cell Exhaustion. CD8 T-Cells are
2) regulatory T-cells. What is most curious is that they become MORE exhausted the MORE severe the disease is.

I believe this is due to the increased presence and persistence of SPIKE PROTEINS.

If you look at LKB1, this liver kinase allows access to CHROMATIN (regulates
3) METASTASIS), MITOCHONDRIAL FUNCTION and T-REGS.

Spike Protein sequences interact with WIPI3/WDR45B. which are scaffolds of the LKB1 signalling circuits.

This may offer evidence that prolonged exposure to the spike protein is behind the allergic/superallergen nature of
Read 11 tweets
30 Jun
1) I am looking for the source study, will post once I find. This sounds completely legit:

This analysis by epidemiologist Jessica Rose, PhD, from Canada, indicates that the vax injury syndromes appear to fall into three major categories: neurological, cardiovascular/
2) thromboembolic, and immunological. Because some individuals must get a more substantial distribution and uptake of the mRNA or adenoviral DNA, wherever the density of spike protein generation occurs determines what organ is going to be most prominently injured. To think
3) developers would use genetic platforms coding for NORMAL genes and turn them into delivery vehicles for the code of dangerous SPIKE protein is the most colossal biotech error in the history of medicine. Those working on mRNA had visions of the Nobel prize, while they really
Read 5 tweets
30 Jun
1) 2007 PEPTIDE SHARING STUDY: THE GARROTING OF THE HUMAN IMMUNE SYSTEM

Antibodies against these (spike protein) motifs may contain NEUTRALIZATION activity against SARS-CoV infection OR PARTICIPATE in the immunopathogenesis induced by SARS-CoV.

I believe the massive peptide
2) sharing of the spike protein with human peptides is the elephant in the room - and the one that spike protein therapy developers is, at this point, purposefully ignoring.

In 2007 it was discovered that there was peptide sharing between four pathogenic regions of SARS-CoV
3) S protein which share sequence homology with different human proteins. This was determined to be DOUBLE EDGED. Neutralization OR immunopathogenesis.

Therefore, if immunopathogensis is occurring because of the peptide sharing, then each subsequent exposure of the host to the
Read 5 tweets

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