IS THE SPIKE PROTEIN BINDING METALS IN OUR CELLS? IS THE SPIKE “CHELATING” THE BODY OF ESSENTIAL BIOMETALS? IS THIS WHY PRION DISEASE IS RAPIDLY PROLIFERATING?

I believe that, apart from the deleterious effects the Spike Protein has on the Endothelium, it is having another extremely sinister effect on the body. It is REMOVING ESSENTIAL METALS from the body, inducing the observed ROS-generated hyperinflammation. This “chelation” of metals from the body is also, I believe, why we are observing a dramatic increase in neurodegenerative diseases, in particular, the exponential rise of Prion diseases.

A paper from March of this year I find to be particularly important.

Of particular concern is that metal ions that bind to viral proteins play a key role in the pathogenesis of the virus. In particular, trace metal ions such as copper influence the course of a viral infection and its consequences. The spike protein of SARS-CoV-2 triggers inflammation and during inflammation, the concentration of Cu(II) ions rises significantly. The possibility of metal ions binding to the spike protein and resulting in Cu(II) complexes might be involved in cell damage.

It is well established that the lungs are strongly affected by SARS-CoV-2 [103]. K18-hACE2 transgenic mice injected with the S1 subunit of the spike protein showed histological evidence of lung injury. A high concentration of Cu(II) is observed in lungs when they are infected with a pathogen. Studies in mice have shown that these easily accessible Cu(II) ions can bind to the spike protein and initiate ROS formation in lungs. This leads to oxidative stress, cell death (through apoptosis), and subsequent inflammatory reactions. The latter causes pulmonary lesions. Therefore, it is likely that the spike protein fragments after metal ion chelation may be involved in the Fenton reaction and the induction of oxidative stress. In turn, the oxidative stress can lead to lung damage in COVID-19.

The Bright and Dark Sides of Reactive Oxygen Species Generated by Copper–Peptide Complexes
https://www.mdpi.com/2297-8739/9/3/73/htm

My point is the following: THE SPIKE PROTEIN IS BINDING THE COPPER THAT THE PRION PROTEIN “USES” TO PROMOTE IS NATURAL STATE OF ANTIOXIDANT DEFENSE.

In vitro metal ion occupancy experiments showed that when Mn2+ replaced the Cu2+ ion in the prion protein, PrPC altered its structure and took on a more PrPSc-like conformation [20]. The prion protein also lost its SOD-like function.

A striking elevation of Mn2+ and to a lesser extent Zn2+ accompanied by a significant reduction in Cu2+ binding to purified PrP were found in subtypes of sporadic Creutzfeldt-Jakob disease (sCJD), the most common type of human prion disease.

Neurodegeneration and oxidative stress: prion disease results from loss of antioxidant defence
https://www.termedia.pl/ORGINAL-ARTICLE-Neurodegeneration-and-oxidative-stress-prion-disease-results-from-loss-of-antioxidant-defence,20,5367,1,1.html

I am certain that this mechanism is involved in much of COVID and Spike Protein pathology and will be researching and posting more findings.