March 21, 2022

I read a paper from a group in Hong Kong that had injected a Spike Protein Accelerant into mice. With the surprising result that within two days THE HEART WAS SIGNIFICANTLY CALCIFIED. So, I decided to look into this a little deeper.

It turns out that Cellular Senescence, Decreased Autophagy and most importantly EXTRACELLULAR VESICLES contribute to Vascular Calcification in Aging. These are exactly the mechanisms that the Spike Protein uses and/or induces.

This may be the underlying mechanism to all the Post COVID and Post Spike Protein pathologies, including Long COVID. The vasculature may be aged fifty years by the Spike Protein.

More disturbingly, in a recent study, it was found that the CaMKII-like domains of the S protein mediated the fusion of virus and infected cells, and it involved calcium ions in this process. In membrane fusion, calcium ions near the interface between S protein and cell membrane quickly accumulated, which produced abnormal calcium ion currents. Besides that, abnormal flow of calcium ions caused depolarization of cells near the infected cell, prompting many calcium ions to flush into nearby cells. Finally, the calcium ion demand in serum accelerated in a short time, thus facilitating the release of calcium in the body. If the SARS-CoV-2 virus infection area was large, it encouraged the abnormality of serum calcium levels and disrupted the body’s calcium homeostasis.

Concluding that membrane fusion is increasing the risk of coagulation and VASCULAR CALCIFICATION.

On top of all of this, results of seven autopsies were as follows:  Seven deceased COVID-19 patients underwent MIA with brain MR and CT images, six of them with tissue sampling. Imaging findings included infarcts, punctate brain hemorrhagic foci, subarachnoid hemorrhage and signal abnormalities in the splenium, basal ganglia, white matter, hippocampi and posterior cortico-subcortical. Punctate brain hemorrhage was the most common finding (three out of seven cases). Brain histological analysis revealed reactive gliosis, congestion, cortical neuron eosinophilic degeneration and axonal disruption in all six cases. Other findings included edema (5 cases), discrete perivascular hemorrhages (5), cerebral small vessel disease (3), PERIVASCULAR HEMOSIDERIN DEPOSITS (3), Alzheimer type II glia (3), abundant corpora amylacea (3), ischemic foci (1), periventricular encephalitis foci (1), periventricular vascular ectasia (1) and fibrin thrombi (1). SARS-CoV-2 RNA was detected with RT-PCR in 5 out of 5 and IHC in 6 out 6 patients (100%).

In a patient that survived, a repeat MRI of the brain without contrast agent enhancement showed residual T2 hyperintensities and hemosiderin deposition in the medial thalami; T2 hyperintensities significantly improved and HEMOSIDERIN DEPOSITION REMAINED UNCHANGED.

This would indicate that subsequent exposures to the Spike Protein would incrementally increase the amount of iron deposited into the vasculature. And how do we know it is Spike? The following is very telling: SARS-CoV-2 spike protein was also detected in cytoplasm of cutaneous dermal vessels and eccrine cells on immune-histochemistry (IHC) of a 35-years-old man presenting with acral purpuric macules although his RT-PCR was negative. As the lesions evolve, the color changes to copper red and violaceous due to associated red cell extravasation and then orange-brown as a result of HEMOSIDERIN DEPOSITION.

This Perivascular Hemosiderin Deposition also occurs in MS! Where it causes a VASCULITIS! Hemosiderin deposition was common in the substantia nigra and other pigmented nuclei in all cases. It is concluded that the cerebral vein wall in multiple sclerosis is subject to chronic inflammatory damage, which promotes haemorrhage and increased permeability, and constitutes a form of vasculitis.

And the white clots? Calcium!

This may be the answer to them as well. The dimeric FXIII-A2, a pro-transglutaminase is the catalytic part of the heterotetrameric coagulation FXIII-A2B2 complex that upon activation by calcium binding/thrombin cleavage covalently cross-links preformed fibrin clots protecting them from premature fibrinolysis. Note, that in COVID, a comparison between healthy plasma and acute COVID-19 solubilized clots also showed a significant increase in coagulation factor XIII A chain, VWF Complement component C7 and CRP.

Yes, it is this bad. Please stop all the “all fear, no solutions” mantras against me. We cannot even begin to find solutions until we know what it is actually doing. Eventually we have to reach the bottom of this pit. Let’s just hope that isn’t the discovery that infection or transfection with the Spike Protein of SARS-CoV-2 ultimately results in 100% mortality. Believe me. I do not want to find that.

You MUST remember. HIV starts with a “mild flu-like illness.” Stop calling COVD a damn cold. And we ABSOLUTELY MUST stop forcing Spike Protein Accelerants on the Known Universe!

Referenced/Related Papers
SARS-CoV-2 spike protein S1 induces fibrin(ogen) resistant to fibrinolysis: implications for microclot formation in COVID-19

Perivascular iron deposition and other vascular damage in multiple sclerosis

COVID-19: the CaMKII-like system of S protein drives membrane fusion and induces syncytial multinucleated giant cells

Clinical Course of a Patient with Radiographically Described Acute Necrotizing Encephalopathy

Idiopathic perniosis presenting as acral purpuric lesions: Clustering of cases before COVID-19 pandemic and their comparison with chilblain like lesions reported in the literature

Postmortem brain 7T MRI with minimally invasive pathological correlation in deceased COVID-19 subjects

Extracellular vesicles carry SARS-CoV-2 spike protein and serve as decoys for neutralizing antibodies

Multifaceted Mechanisms of Vascular Calcification in Aging