Spike Protein-Induced Mistranslation as Cause for Observed Emerging Excess Autoimmune and Neurodegenerative Diseases

A Mechanism Inducing Autoimmunity and the Formation of INSOLUBLE PROTEIN AGGREGATES (AMYLOIDS)

For a discussion of the mechanisms involved regarding Spike Protein and Mistranslation, please see my previous posts.

I would like to bring to everyone’s attention a remarkable paper I discovered. The paper discusses how mammalian cells are extremely sensitive to errors in translation. In fact, the entire organism can be impacted by introducing global changes in protein sequences.

The observed sensitivity of mammalian cells to errors in translation raises the broader question of the mechanistic basis. Through many routes, cell and whole-organism physiology can be impacted by introduction of global changes in primary protein sequence. These routes include disruption of protein folding pathways, creation of altered proteins with newly acquired interactions, or induction of autoimmune-type responses (above). During the folding process, proteins collapse into their globular native states in a manner determined by their primary amino acid sequence. Thus, small changes in amino acid sequence have the potential to create unfolded polypeptides or misfolded protein aggregates. The appearance of misfolded and/or aggregated proteins in the endoplasmic reticulum (ER) of eukaryotic cells activates a signaling cascade (the unfolded protein response [UPR]) that, when overwhelmed, can lead to cell death via apoptosis. In this scenario, the formation of statistical proteins leads to the initiation of the UPR and induction of an apoptotic response. The accumulation of insoluble protein aggregates is linked to many etiologically unrelated neurodegenerative disorders, pointing to what could be a potential disease-related connection.

At the organism level, amino acid misincorporation could plausibly trigger an autoimmune-like response. By chemically altering tyrosine residues on the surface of the native form of thyroglobulin by using arsenillic or sulfanillic acid, Weigle and coworkers demonstrated that, upon injection of the conjugated proteins into rabbits, antibodies formed over time and developed crossreactivity with their own native thyroglobulin. Prolonged exposure to these self-antibodies resulted in thyroiditis. In principle, this phenomenon can occur when altered proteins are generated by amino acid misincorporation, that is, an immune response provoked in response to altered proteins formed through translational errors could result in the targeting of native proteins and the onset of an autoimmune-like condition.

Global Effects of Mistranslation from an Editing Defect in Mammalian Cells
https://www.sciencedirect.com/science/article/pii/S107455210600305X#fig6

As you may observe, mistranslation not only induces autoimmunity, but also INSOLUBLE PROTEIN AGGREGATES. This, I am almost certain, is the Amyloidosis that has been appearing under many (in additional to traditional) new and unusual circumstances.

I also believe this demonstrates that ANY exposure to the Spike Protein greatly increases the chances of inducing autoimmune disease and developing systemic amyloidosis. I have, from the very beginning, likened the repeated assault of the Spike Protein to Grond in LOTR.

I will continue working to further clarify how Mistranslation can explain the pathologies of COVID, Long COVID and Spike Protein Progeria Disease (SPPD). I will also continue to work towards discovering therapeutics to address these pathologies.