COVID-19, REDRUM AND MURDER
REDRUM: THE ENTIRE RESPONSE TO THE COVID-19 PANDEMIC HAS BEEN INTENTIONALLY BACKWARDS – NURSING HOMES ARE NOT AT THE VANGUARD OF OUTBREAKS - H1N1 BEGAN APRIL 2009, FIRST NURSING HOME OUTBREAK WAS OCTOBER 2009.
MURDER: Prion weapons can be used not only by governments but also by terrorists. Furthermore, hypothetically, if Prions were used as a biochemical weapon, they could damage not only humans and animals, but the worldwide economies; therefore, even if Prions do not kill instantly a target, they can be a very persuasive object for those who have access to it.
What must be understood here is that, to have the same (I believe greater) effect on morbidity and mortality, the Prion itself is actually a rather second-rate pathogen. The Prion-like mechanism of amyloid fibrillogenesis is far more dangerous as it can systemically affect all organs.
In non-prion diseases, a host-derived protein is misfolded and persists in an aggregated form that may damage nearby cells [β-amyloid (Aβ) in AD, α-synuclein (α-syn) in PD, and tau-protein (τ) in tauopathies and AD . Although prions and amyloids related to non-prion diseases share structural properties and their conformation, only a small handful of non-prion amyloids display the main prion behavior, i.e., the capacity to spread the self-propagating misfolded proteins from neuron to neuron throughout the brain. In recent years, evidence for prion-like mechanisms in neurodegenerative diseases has come to light. Thus, proteins such as τ, α-syn, Aβ, huntingtin, SOD1 or TDP-43 have been shown to undergo seeding aggregation in cell cultures, and some of them even exhibit trans-cellular propagation and the induced spread of pathology in vivo.
Amyloid fibrillogenesis is a nucleation-dependent process which depends on protein concentration and can be promoted or triggered by homologous preformed amyloids that act as templates in a mechanism known as seeding. The simplified nucleation–elongation model is divided into three phases: (1) the lag phase, when the soluble and monomeric species cluster to form nuclei; (2) the elongation phase, when monomeric species are exponentially added to previously formed nuclei, entailing the formation of transient species such as protofilaments and protofibrils; and (3) the maturation phase, when the transient species as well as oligomers are grouped together, leading to fibril maturation. Moreover and very interestingly, the possibility of a direct relationship between the concentration of nuclei and the amount of oligomeric material, via “nucleation growth”, has been proposed.
THE POINT: This very activity, a SELF-PROPOGATING PATHOGENIC PROTEIN (in this case an AMYLOID COMPLEX (THE SPIKE FORMS COMPLEXES WITH ALL AMYLOID PROTEINS) as opposed to an ACTUAL PRION) invading all organs, I believe, is almost certainly occurring. Indeed, the Spike Protein induces nucleation.
A team of researchers discovered seven synthetic (amyloidogenic) peptides which were 20 amino acids in length within the S protein and found that six of them were in beta-sheet conformation as observed in the cryo-EM structure of SARS-CoV-2 S protein in its closed state. It was noted that these peptides in isolation could aggregate as fibrils at 37°C during incubation. Of these seven peptides, three peptides were found to meet the criteria of amyloid fibrils: sigmoid ThT kinetics, congophilicity, and ultrastructural fibrillar morphology. These peptides were Spike191, Spike532, and Spike1165, which are named according to the starting position of the S-protein.
Further, the researchers analyzed the fibril formation with these seven peptides as a mixture resulting in sigmoidal ThT kinetics based on a NUCLEATION-DEPENDENT mechanism and noticed that the fibril morphology was similar to that of Spike191 indicating that this peptide was dominant in the mixture.
How could we have been so blind and foolish to actually believe a pandemic BEGINS in nursing homes?
Why are we refusing to accept the reasons China, correctly, views the virus as an existential threat?
All exposure to the SARS-CoV-2 Spike Protein must be avoided. We must find treatments for amyloidosis, or much life (not just human) is in great peril.