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The Spike Protein Not Only Induces the Production of Deformed Proteins, it Also Induces Cells Themselves To Deform In Vivo
The Surprising Similarity of the Spike Protein’s Cellular Derangement Effects to those of Cocaine: Explains Athletes’ Sudden Deaths
For a discussion of how the Spike Protein induces mistranslated (deformed) proteins, please see my previous posts.
A bombshell paper was published on Saturday which shows that the Spike Protein of SARS-CoV-2 causes platelets to actually DEFORM in vivo upon exposure.
Here, we report the direct observation of the interactions between S protein and platelets. Live imaging shows that the S protein triggers platelets to deform dynamically, in some cases, leading to their irreversible activation. Cellular cryo-electron tomography reveals dense decorations of S protein on the platelet surface, inducing filopodia formation. Hypothesizing that S protein binds to filopodia-inducing integrin receptors, we tested the binding to RGD motif-recognizing platelet integrins and find that S protein recognizes integrin αvβ3. Our results infer that the stochastic activation of platelets is due to weak interactions of S protein with integrin, which can attribute to the pathogenesis of COVID-19 and the occurrence of rare but severe coagulopathies.
This deformation is caused by ACTIN REMODELING via integrin receptor binding.
We hypothesized that the binding of the SARS-CoV-2 is mediated by integrin receptors based on the following reasons; (1) the activation of platelets is governed by filopodia formation, (2) filopodia formation is initiated by integrin receptors, (3) the major receptors on the platelets are integrin receptors and (4) SARS-CoV-2 S protein contains a RGD sequence in the RBD, which is recognized by a subtype of integrin, and therefore we tested the interaction of platelet-expressed integrins with S protein.
Direct Cryo-ET observation of platelet deformation induced by SARS-CoV-2 spike protein
Now, integrin receptors are ubiquitous, and also expressed in the heart. This immediately brought to mind how COCAINE affects the heart. It can REMODEL CELLS IN THE SAME WAY (also related to integrin receptors)!
An earlier study by Welder et al. demonstrated the toxic effects of cocaine in primary cultures of rat cardiac muscle and reported that treatments of 1 x 10-3 M (1000 µM) mediated enhanced vacuolisation, granulation, pseudopodia formation and lactate dehydrogenase release, the latter of which has been shown to represent a clinical signature for cocaine induced cardiotoxicity and apoptotic cell damage.
Cocaine downregulated phosphorylation of cofilin, decreased expression of adhesion modulators (integrin-β3) and increased expression of ezirin within three hours of 1 µg/mL treatments. These functional responses were associated with changes in cellular morphology, including alterations in membrane stability and a stellate-like phenotype with less compaction between cells. Higher dose treatments of cocaine (5–10 µg/mL) were associated with significant cardiomyocyte cell death (p < 0.05) and loss of cellular architecture. These results highlight the importance of cocaine in mediating cardiomyocyte function and cytotoxicity associated with the possible loss of intercellular contacts required to maintain normal cell viability, with implications for cardiotoxicity relating to hypertrophy and fibrogenesis.
Keywords: cocaine; cardiac myocytes; cytoskeleton; actin rearrangement; cardiac toxicity
Furthermore, CHRONIC COCAINE EXPOSURE INDUCES FIBROSIS, via mechanisms parallel to CHRONIC SPIKE PROTEIN EXPOSURE.
A study by Maceira et al. demonstrated focal myocardial fibrosis in chronic cocaine abusers which emphasises the role cardiomyocytes may have in regulating repair and pathology following chronic cocaine exposures.
Cocaine Induces Cytoskeletal Changes in Cardiac Myocytes: Implications for Cardiac Morphology
Therefore, I believe we now need to view the Spike Protein as morphological as well as mutagenic.
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