A Definitive Cause: How the Spike Protein’s Relationship with ACE2 Allows it to Perfectly Mimic Radiation’s Effect in Inducing Systemic Fibrosis

ACE2 and the Endothelium is the key to understanding Post-COVID (Spike Protein) Fibrosis Syndrome.

The primary mechanisms /pathogenesis of radiation-induced lung injury (RILI): direct DNA damage; the generation of ROS; RAAS system activation; the activation of the immune system. ROS, reactive oxygen species; RAAS system, renin-angiotensin-aldosterone system; EMT, epithelial-to-mesenchymal transition. 

I dedicate this post to Dr. Peter McCullough who encouraged me all along to be Bold and Relentless. 

This is by far my most important work to date. To keep in mind: SARS-CoV-2 may have begun its life to treat cancer in a way without radiation. Dual GoF research would naturally lead to its use as a bioweapon, perhaps this bioweapon is what we are now enduring. 

At long last we can now understand how the respiratory effects of SARS-CoV-2 are but a very thin veneer of the damage that can be caused by the virus and its Spike Protein. In fact, the pneumonia observed may be caused by the same mechanism that may induce systemic fibrosis. Please review the above graphic for an overview. 

Radiation Fibrosis Syndrome is caused by radiation treatments for cancer.  

Let us understand how Radiation Fibrosis Syndrome evolves. 

The pathophysiology of RFS generally includes an event comprising the interplay of inflammatory macrophages, differentiation of fibroblasts, and modifications of vascular connective tissues with excessive production and deposition of collagenous and other extracellular matrix proteins. The most prominent player in this complex event is the product of radiation stimulated inflammatory, epithelial, and mesenchymal cells known as transforming growth factor-β (TGF-β) that converts fibroblasts into matrix-synthesizing myofibroblasts. The myofibroblasts on their part secrete excess matrix-forming substances such as collagen, proteoglycans, and fibronectin that result in subsequent and progressive avascularity, thickening, stiffness, scarring, atrophy, and nonfunctionality of the affected tissue. TGF-β reduces the activity of matrix metalloproteinase (MMP)-2 and MMP-9 and therefore results in excess matrix deposits. TGF-β also regulates the production of fibroblast growth factor, tumor necrosis factor, epidermal growth factor, and interleukin-1 that act in various cell lines such as the fibroblasts, smooth muscle cells, and endothelial cells, thus contributing to the process of fibrosis. Various pathophysiological mechanisms have been postulated for RFS including induction of free radical (FR)-mediated DNA damage and subsequent apoptosis as a predisposing event.[6] Pohlers et al. described three histopathological phases of RFS such as (1) prefibrotic phase comprising endothelial cells, (2) fibrotic phase of active fibrosis containing myofibroblasts, and (3) fibroatrophic phase characterized by subsequent loss of parenchymal cells. Radiation-induced accumulation of excess fibrin in the extravascular, intravascular, and perivascular compartments has been described for RFS. Ionizing radiation may directly result in RFS by causing vascular endothelial injury and indirectly by activating the inflammatory, epithelial regeneration, and tissue remodeling pathways and the coagulation cascade. Another important event is the activation of Janus kinase (JAK) and signal transducer and activator of transcription (STAT) proteins along with nuclear factor kappa-light-chain-enhancer of activated B-cell (NF-KB) pathways by radiation resulting in the release of pro-inflammatory cytokines and growth factors. The two mechanisms involved in radiation injury to both tumor and normal cells are the direct and indirect DNA damage through the generation of reactive oxygen species and FRs that destroy protein, lipid, and nucleic acid molecules, thus causing ischemia and thrombosis through the secretion of cytokines and chemokines. 

Radiation Fibrosis Syndrome: the Evergreen Menace of Radiation Therapy 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6518980/ 

The above is how RADIATION causes Radiation Fibrosis Syndrome (RFS).  

Post-COVID (Spike Protein) Fibrosis Syndrome evolves IN PRECISELY THE SAME MANNER. However, it is INDUCED BY A PARALLEL MECHANISM. 

This is where ACE2 becomes ever so critical.  

Radiation is focused energy. It assaults all cells through which it passes, inducing RFS. In particular, it induces it by: 

Ionizing radiation may directly result in RFS by causing vascular endothelial injury and indirectly by activating the inflammatory, epithelial regeneration, and tissue remodeling pathways and the coagulation cascade. 

AND THERE! THERE IT IS! As plain as day. (Quote from above referenced paper.) 

The Spike Protein induces Post-COVID (Spike Protein) Fibrosis Syndrome by causing the VERY SAME DAMGE that induces RFS!!!!! I need not cite papers detailing how the Spike Protein causes the above injury and activation as they are ubiquitous and, at this point, common knowledge. 

The Spike Protein’s binding and interaction with ACE2 allows it to affect the endothelium in PRECISELY THE SAME WAY as RADIATION. This is why so many doctors claimed that the COVID patients they were treating looked like they were suffering from Radiation Sickness. It allows for the full effect of Radiation Damage – without Radiation. 

I will continue to work on discovering therapeutics to treat this. RFS is an incurable, progressive syndrome. Let us hope and pray that Post-COVID (Spike Protein) Fibrosis Syndrome is not.