1) NOT JUST ACE-2: THE CLEAVED S1 UNIT OF THE SPIKE PROTEIN BINDS TO DECTIN-1. THIS CAN EXPLAIN THE INCIDENCE OF MYOCARDITIS AND DE NOVO ONSET OF DIABETES POST SPIKE PROTEIN THERAPY

The Spike Protein of SARS-CoV-2 has been found to bind to several additional receptors other than
2) ACE-2. Dectin-1 is one of those additional receptors that the S1 unit of the Spike Protein binds to.

I believe that the S1 unit is being cleaved in Spike Protein experimental therapies and binding to Dectin-1 (among other receptors). This binding to Dectin-1 downregulates
3) the expression of Dectin-1 which is implicated in the pathogenesis of Myocarditis and Diabetes.

It is also possible that this binding is causing toxification of Dectin-1 and autoantibodies may develop. This could explain the incidences of Mucormycosis, as Dectin-1 is a
4) primary antifungal signaling protein.

Note that monocytes from T2D patients with poor glycemic control (HbA1c>8%) showed a diminished percentage of Dectin-1(+)/TLR2(+) cells. Negative correlations between the percent of Dectin-1(+)/TLR2(+) cells and fasting plasma glucose
5) levels (FPG) and HbA1c levels were found.

Please note that the referenced Myocarditis article refers to Myocarditis as a "devastating heart disease." No such thing as a "mild case of Myocarditis." Yet another lie.

jimmunol.org/content/181/12…

jian-zhang.lab.uiowa.edu/4-regulation-a…

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More from @Parsifaler

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 Image
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 Image
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
29 Jun
1) SPIKE PROTEIN DISPLAYED ON CELL MEMBRANE THEN CLEAVED: PRIONS, FERROPORTIN, THE BLOOD BRAIN BARRIER AND HEPCIDIN

Concerning iron dysmetabolism in COVID-19, Ehsani has highlighted a remarkable similarity between the distant amino acid sequence of SARS-CoV-2 spike glycoprotein Image
2) cytoplasmic tail and the hepcidin protein.
Coronaviruses recognize host receptors using their spike proteins, facilitating conformation transition, so to bind cell membrane and enter host cytoplasm; by using host furins and proteases, coronaviruses may cleave their spike Image
3) polypeptides, thus favoring the cell entry. The found hepcidin mimicry by the virus would take place through this complex mechanism.

Perhaps the reason we are seeing strokes, blindness and other neurodegenerative activity post spike protein therapies is that that ferroportin
Read 5 tweets
28 Jun
1) THE POTENTIAL IMMENSE DANGER OF THE S2 SUBUNIT SPIKE PROTEIN THERAPIES (FYEZER, MOETERNA, KNOFAFAX)

In short, the vaccines cause the full spike to be displayed on the cell surface, yet the therapy targets S2. I believe that S1 is being CLEAVED and is circulating freely.
2) Evidence for this comes in a very interesting form. A paper was published on Friday that showed a statistically significant number of non-classical monocytes contained SARS-CoV-2 S1 protein in both severe (P=0.004) and PASC patients (P=0.02) out to 15 months post infection.
3) Why is important? Because non-classical and intermediate monocytes are PROFESSIONAL ANTIGEN PRESENTING CELLS. They scour the ENDOTHELIUM looking for pathogens and grind them up to present to adaptive immune cells. However, the S1 subunit is like "grist" that cannot be "chewed"
Read 5 tweets
26 Jun
Due to tournaments and parties Chris and I only get one dinner together this weekend. We decided to make it count!

1st Course:

OG Mesclun. OG Cucumber. OG Olives. OG Feta. OG Oregano Vinaigrette.

La Cle de la Femme Champagne. Image
2nd Course:

OG Coq au Vin. OG Basmati Rice

2011 Chateau Montelena Estate Cabernet Sauvignon. Image
Fromage

Young Farmdahl Cheese Image
Read 5 tweets
25 Jun
URGENT!

1) A paper published on June 16, 2021 proves my hypothesis that the spike protein therapies are sensitizing recipients to the Spike Protein super-allergen of the SARS-CoV-2 virus.

The SARS-CoV-2 S-protein, a surface exposed viral receptor binding protein and important Image
2) as vaccine antigen triggers NLRP3 inflammasome activation and cytokine secretion selectively in COVID-19 patient-derived macrophages. SARS-CoV-2 infection leads to reprogramming of human macrophages providing an intracellular landscape that allows for rapid inflammasome
3) assembly.

The findings reveal that SARS-CoV-2 infection causes profound and long-lived reprogramming of macrophages resulting in augmented immunogenicity of the SARS-CoV-2 S-protein, a major vaccine antigen and potent driver of adaptive and innate immune signaling.

The
Read 5 tweets
24 Jun
1) OVEREXPRESSION OF PRPc CHELATES COPPER, AFFECTS T-CELL DEVELOPMENT AND CAUSES ACERULOPLASMINEMIA: THE SPIKE PROTEIN (ESPECIALLY IN mRNA) MIMICS PRPc, LEADING TO OVEREXPRESSION OF PRPc: HYPERFERRITEMIA IS A HALLMARK OF ACERULOPLASMINEMIA

A paper from 2006 revealed a very
2) interesting (and for us, now, fortuitous) phenomenon. If the prion protein is overexpressed, it chelates copper. It is known that the Spike Protein of SARS-CoV-2 mimics the human prion protein. It is highly likely that the body perceives this as an overexpression of the prion
3) protein.

Overexpression of PrPC induces strong alterations at different steps of T cell maturation. On TgA20 mice, we observed that these alterations are cell autonomous and lead to a decrease of αβ T cells and a concomitant increase of γδ T cell numbers. PrPC has been shown
Read 7 tweets

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