1) THE. AUTOIMMUNE. MECHANISM.
THE SPIKE WILL NOT BE FOUND IN THE BLOOD. IT IS TRAVELLING “INCOGNITO” INTRACELLULARLY.
WE KNEW IT ENTERED CELLS VIA ENDOCYTOSIS IN 2008!
Yesterday I observed that every cell the Spike Protein invades seems to cause the body to develop autoimmunity
2) against it. I believe I have discovered the mechanism.
It is a very brief and straightforward mechanism.
Most likely many spikes do NOT stay on the cell surface, once they are expressed via spike protein therapied. The Spike is proven to be brought into the cell by
3) Endocytosis. The spike protein is internalized into cells rapidly and is detected in cells within 5 mi, a hallmark of endocytosis. The amount of spike protein in cells continues to increase for up to 30 min. Thus, SARS-CoV-2 spike protein enters cells via endocytosis.
Once it
4) is in the cell, its signaling damages mitochondria. The team then replicated this process in the lab, exposing healthy endothelial cells (which line arteries) to the spike protein. They showed that the spike protein damaged the cells by binding ACE2. This binding disrupted
5) ACE2’s molecular signaling to mitochondria (organelles that generate energy for cells), causing the mitochondria to become damaged and fragmented.
Once the mitochondria are damages, this then activates the autoimmune response of the body. The accumulation of defective
6) mitochondria led to overproduction of an inflammatory protein called type 1 interferon. The findings suggest that failed quality control of mitochondria may cause Sjogren’s, lupus, and other autoimmune diseases through production of interferon.
The Spike Protein then proceeds
7) to travel from cell to cell via EXTRACELLULAR VESICLES. This means, of course, they will NOT BE FOUND IN THE BLOOD. We would not have been aware all this time. As the S1 unit has been found in monocytes 15 months post infection, it may be traveling intracellularly, executing a
8) “Sherman’s March Through Georgia” on the mitochondria, resulting in multisystemic autoimmunity.
Again, we have known the spike enters cells via endocytosis since 2008.
jbc.org/article/S0021-…
salk.edu/news-release/t…
factor.niehs.nih.gov/2021/3/papers/…
biorxiv.org/content/10.110…

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More from @Parsifaler

18 Sep
1) THE SPIKE PROTEIN AND ITS ANTIBODIES: PARTNERS IN CRIME
A SIGNALING PARALLEL BETWEEN SARS-CoV-2 SPIKE PROTEIN ANTIBODIES AND α-SYN FIBRILS: THE INDUCTION OF MULTIPLE SYSTEM ATROPHY AND AN EXPLANATION FOR THE DEMYLENATION SYMPTOMS OBSERVED IN COVID AND LONG COVID
A mechanism Image
2) for the induction of Multiple System Atrophy may have been discovered. The molecular mimicry of spike protein antibodies is alarming (see image). Among the tissues that the spike protein antibodies interact with is Alpha Myelin. They also interact with FcγRIIB receptors. These Image
3) receptors are what dampen, and in some cases completely turn off, the interferon response to SARS-CoV-2. It is thought this may be one of the main mechanisms of severe disease.
Interaction with FcγRIIB receptors may also be the mechanism for induction of Multiple System Image
Read 7 tweets
15 Sep
1) THE SPIKE PROTEIN: ANTIHERO OF THERAPEUTICS
What if a strong immune response IS A SIDE EFFECT OF INDUCING AUTOIMMUNE DISEASE?
Biologics are a class of drug that is made inside a cell. They must be kept cold. You can have an immune reaction to them. Not every
2) biologic medication is associated with the same chance of creating antibodies. In one small study comparing three popular biologic medications, it was found that anti-drug antibodies were present in 42% of those receiving Remicade (infliximab), 33% of those receiving Humira
3) (adalimumab), and in none of those patients receiving Enbrel (etanercept).
A review of 443 studies was done to find out how often antibodies were present in patients who had rheumatoid arthritis and were treated with biologics. This review showed that antibodies were found in
Read 9 tweets
14 Sep
1) WAIT! Are we all dogs trying to chase our own tails? ENOUGH! I will cut this Gordian's Knot! THE SPIKE PROTEIN INDUCES AUTOANTIBODIES IN EVERY TYPE OF CELL IT ENTERS/INTERACTS WITH!!!

Autoantibodies against ACE2 and angiotensin type-1 receptors increase severity of COVID-19
2) Autoantibodies against AT1 Receptor Contribute to Vascular Aging and Endothelial Cell Senescence - At COVID diagnosis, AT1 receptor and ACE2 autoantibodies were higher than in controls.

Let us review the mechanisms of autoantibodies. COVID checks every box. It gets an A+.
3) 1. Mimic hormone stimulation of receptor: thyroid-stimulating autoantibodies (TSAb) in Graves’ disease.

2. Blockade of neural transmission by receptor blockade or alteration of the synaptic structures: antibodies against muscle nicotinic acetylcholine receptors (AChRs) in
Read 10 tweets
14 Sep
1) THE SPIKE PROTEIN, TRANSDIFFERENTIATION AND MOYAMOYA SYNDROME: COVID-19 VASCULOPATHY

A collateral circulation developing to compensate for the vascular thickening caused by the transdifferentiation actions of the Spike Protein may be behind the vasculopathy of COVID-19. This
2) is manifest in almost precisely the same way as in MOYAMOYA DISEASE. Interestingly, those with DOWN SYNDROME are extremely susceptible to this. I believe the spike protein is transdifferentiating endothelial to mesenchymal cells. SARS-CoV-2 is also dedifferentiating at least
3) multiciliated cells and monocytes. The virus is erasing/changing cellular identities.
Unlike the flu or SARS-1 which left NO vascular thickening, SARS-CoV-2 is leaving its victims with vascular thickening of 15.4μm. Let us compare that to those that died of flu, which was
Read 13 tweets
13 Sep
SUBCLINICAL MYOCARDITIS IN CHILDREN

We may be aware of only the tip of an iceberg. Subclinical myocarditis resulting in hospitilization and death is far more common in children than most are aware of. We need serial workups of children given spike protein therapies ASAP.
A study suggests that the prevalence of "silent" myocarditis may be higher in the pediatric population than is generally suspected and may contribute to a significant number of sudden and unexpected deaths in children, particularly those older than one year of age.

In both
children and adults, most cases are subclinical; thus, the true incidence of myocarditis in children is unknown.

Children who have had COVID are advised to be screened for sports to determine the presence of myocarditis. If the spike is responsible, as I believe it is, we must
Read 4 tweets
13 Sep
1) A NOVEL NEURODEGENERATIVE DISEASE MOST CLOSELY RESEMBLING MULTIPLE SYSTEM ATROPHY MAY BE THE RESULT OF INFECTION WITH THE SARS-CoV-2 VIRUS
We have been overwhelmed with hypotheses trying to determine exactly what COVID-19 is. I, myself, am certainly a generous contributor to
2) this tsunami of conjecture as to what exactly is happening pathologically in a SARS-CoV-2 infection. This is understandable as the disease manifests itself with such a wide variety of symptoms.
And this is the point. It is a MULTI-SYSTEMIC DISEASE. As with all other
3) multi-systemic diseases, there is no concrete order for the appearance of symptoms as everyone will have symptoms present in accordance with their respective genetics. The end results will be the same, the roads traveled to reach those results will be unique.
If we look at the
Read 20 tweets

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