October 19, 2021
THE LUNG AND ORGAN DAMAGE CAUSED BY THE SPIKE PROTEIN IS PARALLEL TO DAMAGE CAUSED BY ASBESTOS: RESISTANCE TO DIGESTION
It has been observed that the S1 unit of the Spike Protein of SARS-CoV-2 has been found in monocytes up to 15 months past infection. The reason for this is almost certainly that the S1 unit is resistant to digestion. Asbestos shares this “quality” and is the basis for its pathology.
In fact, I believe the Spike Protein causes an “accelerated asbestosis.” I have substituted Spike Protein for Asbestos in the following:
When Spike Proteins reach the alveoli in the lung, where oxygen is transferred into the blood, the foreign bodies (Spike Proteins) cause the activation of the lung’s local immune system and provoke an inflammatory reaction. This inflammatory reaction can be described as chronic rather than acute, slow ongoing activation of the immune system in an attempt to eliminate the Spike Proteins. Macrophages phagocytose the Spike Proteins and stimulate fibroblasts to deposit connective tissue. Due to the natural resistance of Spike Proteins to digestion, the macrophage dies off, releasing cytokines and attracting further lung macrophages and fibroblastic cells to lay down fibrous tissue, which eventually forms a fibrous mass. The result is interstitial fibrosis. The fibrotic scar tissue causes alveolar walls to thicken, which reduces elasticity and gas diffusion, reducing oxygen transfer to blood as well as the removing of carbon dioxide.
This is PRECISELY what happens in Severe COVID-19. It is an accelerated asbestosis.
What follows is Long COVID. Once again, I substitute Long COVID for silicosis and Spike Protein for asbestos:
Furthermore, the complications in Long COVID and in people who have been exposed to Spike Proteins are also different. Patients with Long COVID often present with complications involving autoimmune diseases such as rheumatoid arthritis (known as Caplan’s syndrome), systemic sclerosis, systemic lupus erythematosus, and antineutrophil cytoplasmic antibody (ANCA)-related vasculitis/nephritis.
We observe in COVID-19 the EXACT SAME REDUCTION IN CXCR3 Expression and IFN-y as well as UPREGULATION OF IL-6. One of the interesting molecular changes in asbestosis regarding tumor immunity is the reduction of CXCR3 expression and IFN-γ production. In COVID-19 patients displayed a lower percentage of cells expressing CCR6 or CXCR3.
The pulmonary fibrosis being observed post COVID, I believe, is due to the indigestible nature of the Spike Protein. Again, referring to Asbestosis:
Release of silica particles and asbestos fibers from alveolar macrophages and the repetition of similar cellular reactions described above by newly recognized nearby macrophages. Transfer of silica particles and (partially cleaved) asbestos fibers to regional lymph nodes. As these cellular and molecular reactions are continuously repeated, pulmonary fibrosis will appear gradually and progressively.
HOWEVER, there is one ENORMOUS difference between Asbestosis and Spike Proteins. The Spike Proteins are almost certainly causing this in every organ/tissue it interacts with. Given the recent finding that the spike travels incognito via endosomes, humans may be turning into, not crocodiles, as Mr. Bolsonaro would have us believe, but “living” mounds of cartilage.
Asbestos-Induced Cellular and Molecular Alteration of Immunocompetent Cells and Their Relationship with Chronic Inflammation and Carcinogenesis
Marked T cell activation, senescence, exhaustion and skewing towards TH17 in patients with COVID-19 pneumonia
Persistence of SARS CoV-2 S1 Protein in CD16+ Monocytes in Post Acute Sequelae of COVID-19 (PASC) Up to 15 Months Post-Infection