COVID-19, REDRUM AND MURDER
1
May 12, 2022

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.

https://www.cdc.gov/mmwr/preview/mmwrhtml/mm5903a3.htm

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.

https://www.scielo.br/j/cta/a/d4vQCh4VrtsMv84Hp8FSVRc/?lang=en

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.

https://www.frontiersin.org/articles/10.3389/fnmol.2016.00029/full

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.

https://www.news-medical.net/news/20211221/Understanding-SARS-CoV-2-induced-systemic-amyloidosis.aspx

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.