CODED TO KILL: A SHORT-RANGE, MID-RANGE AND LONG-RANGE CELLULAR WEAPON
A CAVALCADE OF CASCADES
The Spike Protein of SARS-CoV-2 is able to induce several fatal cascades
Even I am astounded. I was walking today after discovering the coagulation and fibrotic cascade, when it hit me. I stopped in my tracks. The Spike Protein is not only able to induce this cascade, which can prove fatal, it can also induce several others, equally devastating.
SHORT-RANGE: THE CYTOKINE STORM
The most direct and fastest way the Spike Protein can kill is via induction of the now infamous Cytokine Storm. The pathogenesis of COVID-19 is associated with a hyperinflammatory response; however, the precise mechanism of SARS-CoV-2-induced inflammation is poorly understood. Here, we investigated direct inflammatory functions of major structural proteins of SARS-CoV-2. We observed that spike (S) protein potently induced inflammatory cytokines and chemokines, including IL-6, IL-1β, TNFα, CXCL1, CXCL2, and CCL2, but not IFNs in human and mouse macrophages. No such inflammatory response was observed in response to membrane (M), envelope (E), and nucleocapsid (N) proteins.
SHORT-RANGE AND MID-RANGE: THE COAGULATION/FIBROSIS CASCADE
Please see my previous post for the details about this mechanism.
MID-RANGE AND LONG-RANGE: ONCOGENIC AND NEURODEGENERATIVE CASCADES
The Spike Protein dysregulates RAS. This is how, if it does not kill you with a Cytokine Storm, it can then induce cancer, via its dysregulation of RAS. If you review the graphic, the RAS feedback loop initiated by the Spike Protein is shown with orange arrows. SARS-CoV-2, which acts on ACE2 through the binding of its spike protein, is indicated in magenta.
This brings us back to the birthplace of cancer biology, how one of the first discovered oncogenes, RAS, drives cancers in new and unexpected ways. As our understanding of oncogenic signaling has evolved, it is clear that RAS signaling is not homogenous, but activates distinct downstream effectors in different cancer types and grades. RAS signaling is tightly controlled through a series of post-transcriptional mechanisms, which are frequently distorted in the context of cancer, and establish key metabolic and immunologic states that support cancer growth, migration, survival, metastasis, and plasticity.
In yet another cascade, the Spike Protein is able to induce neurodegeneration via its ability to AGGREGATE AMYLOID PROTEINS. SARS-CoV-2 S1 RBD binds to a number of aggregation-prone, heparin binding proteins including Aβ, α-synuclein, tau, prion, and TDP-43 RRM. These interactions suggests that the heparin-binding site on the S1 protein might assist the binding of amyloid proteins to the viral surface and thus could initiate aggregation of these proteins and finally leads to neurodegeneration in brain.
These sudden realizations bring to life the “Swiss Army Knife of Death” analogy to the SARS-CoV-2 Spike Protein. The implications should be obvious. Please pause all Spike Protein Accelerants immediately.