THE SPIKE PROTEIN IS A FOLDAMER AND A SELF-REPLICATOR: THE INDUCTION OF MULTIPLE LETHAL PROTEINOPATHIES
March 30, 2022
The more I go down the proteinopathy rabbit hole, the more trouble I see that we are in. Even I am in shock and awe, and I have been often, recently. I keep thinking I have found the worst that the Spike Protein can do, but I keep looking one move deeper. And what I see is utterly terrifying and without an effective therapeutic will, in a very few number of years, most likely spell the end of humanity.
Most people hear the word “Prion” and think Mad Cow Disease. While this is true, it doesn’t really explain what HAPPENS during the course of Mad Cow Disease. Remember, Mad Cow Disease is just ONE WAY that AGGREGATED PROTEINS can cause fatal disease. They are TOXIC.
This occurs via the conformation/oligomerization hypothesis, which proposes an intermediate view, with conformational changes leading to the formation of an unstable amyloidogenic OLIGOMER, which will eventually grow to produce the solid aggregate. Following the latter hypothesis, the misfolding of low complexity domains (LCDs) into β-strands produces the active monomer, which appears to be the initial stage in the paths towards toxicity.
THE SPIKE PROTEIN IS AN OLIGOMER!
The key to all of this?
LIKE THE PRION THE S2 SUBUNIT OF THE SPIKE PROTEIN IS RESISTANT TO DEGREDATION! THIS IS ITS MOST “PRION-LIKE” QUALITY!
Back in 2018. 2018!!!!!!!!!!!!!
It was discovered that limited proteolysis experiments showed that neither receptor binding nor trypsin cleavage expose the S2′ cleavage site for proteolysis within the stabilized spike ectodomains. Additionally, in January of this year (2022) it was determined that some sub-genomic RNA may be resistant to degradation since these pieces of RNA are tightly packed in with membranes and proteins.
So, efficient autophagy is required to remove protein aggregates and prevent neurodegeneration.
And this is the point. The spike, by its ability to form a complex with all amyloidogenic proteins PROTECTS THEM from degradation. This is how it exponentially accelerates all diseases associated with amyloids.
This most likely explains the hypertrophic cardiomyopathy being observed. It is a proteinopathy. The process of decompensation, which is characterized by dramatic cardiac remodeling, a transition from hypertrophy to dilation as a result of significant cardiomyocyte cell death, necessarily involves an imbalance between protein synthesis and degradation and modulation of autophagy during these processes has been attempted.
WHY IT IS HAPPENING TO ATHLETES FIRST
Although changes in cardiomyocyte size can be beneficial, such as occurs in an athlete’s heart, sustained, increased load due to conditions such as hypertension, results in a transition from a compensated hypertrophy to decompensated heart failure, with cardiomyocyte hypertrophy a hallmark of the process.
THEIR HEARTS HAVE ALREADY BEGUN THE PROCESS OF HYPERTROPHY!
The Spike Protein must be avoided at all costs, and effective treatments to degrade it must be found, or we will certainly all perish.
Proteotoxicity: An Underappreciated Pathology in Cardiac Disease
The Diverse World of Foldamers: Endless Possibilities of Self-Assembly
Two Sides of the Same Coin: Emergence of Foldamers and Self-Replicators from Dynamic Combinatorial Libraries
Highly efficient intercellular spreading of protein misfolding mediated by viral ligand-receptor interactions
SARS-CoV-2 spike protein interactions with amyloidogenic proteins: Potential clues to neurodegeneration
Viral Infection May Enhance Misfolded Protein Spread, Accelerate Neurodegeneration
Synthesis and Characterization of a Native, Oligomeric Form of Recombinant Severe Acute Respiratory Syndrome Coronavirus Spike Glycoprotein
Are Proteinopathy and Oxidative Stress Two Sides of the Same Coin?
SARS-CoV-2 spike promotes inflammation and apoptosis through autophagy by ROS-suppressed PI3K/AKT/mTOR signaling
Protein Aggregation Landscape in Neurodegenerative Diseases: Clinical Relevance and Future Applications
Persistence of SARS CoV-2 S1 Protein in CD16+ Monocytes in Post-Acute Sequelae of COVID-19 (PASC) up to 15 Months Post-Infection