February 7, 2022

You need to think like a pool player and a chess player to understand the Spike Protein. It is not only what it stakes claim to, but also what it removes. I can’t think of anything more obviously and occultly carcinogenic than the Spike Protein of SARS-CoV-2 and its effect on ACE2 and RAS.


Think of the Spike Protein as a cue ball that sets off a cascade to CREATE A TUMOR MICROENVIRONMENT while SIMULTANEOUSLY inducing the EPIGENETIC MODULATIONS to COMMENCE A TUMOR.

JUST LIKE A SEED, the Spike Protein (tumor) not only can “grow” itself (once it takes hold), it can also FEED ITSELF by CREATING IT’S OWN IDEAL ENVIRONMENT.

After all, is what follows not exactly what the Spike Protein does?

Local RAS works synergistically and independently of systemic RAS in a paracrine fashion. Ang II mediates effects that reduce tumor perfusion and oxygenation, resulting in hypoxia and subsequent acidosis within the tumor stroma. For example, local Ang II, predominantly exists in hypoxic regions of nasopharyngeal carcinoma and breast cancer cells, where it is autocrinely produced by chymase-dependant rather than ACE dependent mechanism. In which case the action of ACEi will not be effective to inhibit tumor growth. Tumor hypoxia and acidosis trigger a cascade of up-regulation of transcription factors, growth factors and cytokines, including hypoxia inducible factor (HIF), VEGF and Transforming growth factor beta (TGF-β) that together promote immunosuppression within the TME. An immunosuppressive microenvironment includes impaired function of T cells, dendritic cells the accumulation of M2-like macrophages and MDSC, but also increased expression of immune check point molecules such as PD-L1 / PD-1 on tumour / stromal cells and the immune cells.

And is the following not exactly what we see during the course of COVID? Unlike ANY OTHER pathogen yet seen?

The TME is bound to the dynamic between malignant and non-transformed cells. Non-malignant cells are reprogrammed to accomplish tumor-promoting functions during all stages of carcinogenesis [66]. Intercellular interactions modulate the chemical and physical properties of any tissue through a diverse pool of secreted cytokines, chemokines, growth factors, and inflammatory or matrix remodeling enzymes. TGF-β suppresses the differentiation and function of T helper (TH), CD8+ cells, Natural Killer (NK) cells, and tumor-associated neutrophils (TANs), tumor associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs). Tumor supporting cytokines are released from tumor and stromal cells upon AT1R activation via Ang II including, TGF-β Interleukins (IL-1a, IL-1B, IL-6, IL-8) and MCP-1: (monocyte chemoattractant protein 1), macrophage colony-stimulating factor (M-CSF), cyclooxygenase 2(COX-2), C- reactive protein (CRP). Immunomodulatory cytokines may up-regulate immunosuppressive pathways, i.e. COX-2 via prostaglandin E2 synthesis, and impair dendritic cell (DC) function by reducing their migration. Ang II/AT1R signaling induces reactive oxygen species (ROS) generation and related proteins such as inducible nitric oxide synthase in the tumor cells and stroma cell. Exposure to ROS in the TME can impair T cell function while enhancing T regs and TAMs, as has been previously reported in prostate cancer. Treatment with the ARB candesartan diminishes ROS generation.

Again, the Spike Protein is curiously the antithesis of oncogenic therapy:

Targeting RAS conventional axis (Ang II/AT1R), KKS and enhancing RAS alternative axis (ACE2/Ang-(1-7)/MasR) seem to be promising strategies to effectively influence TME toward an immunostimulatory milieu, and subsequently improve immunotherapy outcome for a larger population of cancer patients.

Referenced/Related Paper

Renin-angiotensin inhibitors reprogram tumor immune microenvironment: A comprehensive view of the influences on anti-tumor immunity