COVID-19: AN IMMUNE MEDIATED DISEASE OF PROGRESSIVE SYSTEMIC FIBROSIS INDUCED BY THE SPIKE PROTEIN AND ITS IMMUNE COMPLEXES
THE PRESENCE OF SPIKE PROTEIN WITH SPIKE ANTIBODIES IS EXTREMELY DANGEROUS; INCREASED TROPISM GIVING THE SPIKE A HUMAN Fc RECEPTOR!
This is an urgent warning to all clinicians and public health professionals. We have been lied to and led astray as to the true nature of SARS-CoV-2 and the Spike Protein.
It is established that those with increased NON-NEUTRALIZING afucosylated immunoglobulin G (IgG) antibodies are associated with severe disease. However, in those without severe disease, these antibodies, I believe, are inducing a systemic fibrosis, which may be progressive and ultimately fatal.
When administered immune complexes formed by spike protein and antibodies from patients with severe or mild COVID-19, as well as vaccine-elicited antibodies, to the lungs of mice expressing human Fc receptors, finding were that antibodies from individuals with severe COVID-19 drove inflammatory cytokine production and immune cell infiltration into the lung.
But, what about those who do not experience severe disease? The results may be, ultimately, as serious.
First, we have been wrong about WHY those with comorbidities are affected. Those severely affected are those who ALREADY HAVE fibrosis underway, to some degree. What are FIBROGENIC TRIGGERS? fibrogenic triggers that initiate and maintain fibrotic pulmonary remodeling remain controversial, but probably include infections, cigarette smoke, radiotherapy, chemotherapy, environmental and occupational pollutants, obesity, diabetes mellitus, gastroesophageal reflux, pulmonary hypertension, obstructive sleep apnea, chronic graft-versus-host disease, and connective tissue diseases/autoimmune disorders, such as rheumatoid arthritis, scleroderma, and Sjögren's syndrome.
So, not only does the Spike Protein damage the endothelium and induce fibrosis, its IMMUNE COMPLEXES do as well, and may indeed AMPLIFY this effect as they can attach to MORE CELLS (increased tropism) due to the Spike Protein now having a HUMAN Fc RECEPTOR!
Fibrosis has been induced in a parallel way before. Intraperitoneal administration of HSA to make rat immune complex induced liver fibrosis model is convenient with high liver fibrosis formation rate and long fibrosis lasting time. The model may be used to evaluate the therapeutic effect of antifibrotic drugs.
But what of evidence for Spike Protein Accelerants participating in this macabre game? It is emerging. A case report relates the first description of immune complex vasculitis after COVID-19 vaccination with BNT162b2.
We can understand what is happening by looking at Cystic Fibrosis. Circulating immune complexes were detected in serum and sputum of patients with cystic fibrosis (C.F.). There were extensive deposits of immunoglobulins and complement immune complexes in several of the C.F. organs, especially the respiratory and gastrointestinal tracts, but not in the kidneys. Significant concentrations of IgG and of complement complexes could be eluted from the lungs of the C.F. patients but not from those of controls.
IT IS ABSOLUTELY IMPERATIVE THAT THE WORLD PAUSE ALL SPIKE PROTEIN ACCELERANTS IMMEDIATELY!
Walter, you are talking about fibrosis, rather than fibrinogen - is that correct? They are different things, generally? I am pulling a few papers on fibrosis, stumbled over this one wrt hearts: https://pubmed.ncbi.nlm.nih.gov/31284728/
So all those monoclonal antibodies not a good idea in the longer run I suspect. Front line doctors using them reporting mixed results, sometimes finding people do worse. There were warnings early on too about their potential for contributing to autoimmunity.