Spike at the center of the vaccine-related clots?
And are scientists checking for any seeding agents in these clots and plaques being described?
Several months back Brian Mowrey provided a video interview between Alzheimer’s researcher Dr. Rudy Tanzi and Dr. Amy Proal.
I didn’t view the video at the time that Brian Mowrey reported on it, and only viewed it a few weeks prior when looking at Parkinson’s in relation to SARS-COV2 and the vaccines.
I found the discussion so fascinating, especially when Tanzi noted that these plaque formations in the brain can be seeded by pathogens. As Tanzi’s team has argued, these amyloid plaques are possibly part of a larger group of antimicrobial peptides, which also includes proteins such as alpha-synuclein which are responsible for Lewy body formation.
That is, the neuroprotective effects of these plaques are derived from their coalescence around an invasive agent, which helps traps said agents, possibly for later disposal.
But even more fascinating is the fact that researchers have been able to scour plaques to search for what would otherwise be considered seeding agents, which include virions, viral proteins, and even genetic material that form the center of these protein aggregates and initiate the plaque formation.
Interestingly, the compound nacre utilized by mollusks may themselves act as antimicrobial agents, trapping foreign agents into a pearl sac which we then utilize as jewelry. It’s proposed that pearl formation is likely driven by this antimicrobial process and suggests an extremely old evolutionary defense mechanism (skip to 4:10 for comments relating to an antimicrobial factor):
In a similar fashion that oysters form pearls and that snow crystals form, something has to serve as the agent in which structures are built upon, thus seeding the plaque, pearl, or snow crystal formation.
Within the context of amyloid formation and blood clotting there’s been a general argument that the spike protein can lead to protein aggregation, relying on in vitro studies of mixing spike with other proteins or cells to determine aggregate formation, which is then used to argue that such phenomenon may be occurring in those who were either infected with SARS-COV2 or received COVID vaccines.
This is an interesting hypothesis which may explain much of what we are seeing. Unfortunately the hypothesis may predict these possibilities of protein aggregation, but they can’t confirm them.
Consider the fact that the documentary Died Suddenly proposes all of these protein structures and blood clots within the body of deceased individuals, and yet we as viewers are left to assume a correlation with the vaccine even though the characterization and identification of these clots were not provided.
Hence, this is why I found Tanzi’s remarks extremely interesting- if we are to argue that various proteins or invasive agents are the seeds of protein aggregation, then surely a search for these seeding agents would provide something fruitful.
Essentially, this is an examination in reverse which would corroborate the initial hypothesis of spike-derived protein aggregation. If one were to check these amyloid plaques or clots for spike protein (and even possibly spike mRNA), then there would be even further evidence that spike protein may be the seeding agent.
To that, I came across this report from August 20221 in which pathologists did just that- they looked at the blood clots of those who suffered from ischemic strokes and myocardial infarctions related to COVID-19.
Note that these are not related to the vaccines, especially given the timeframe of sample collection.
Here, the intent was to see if spike protein and other viral proteins could be detected within the blood clots of these patients via immunohistochemical staining for spike protein, nucleocapsid protein, as well as PCR for genetic material. Patients included were those who admitted to Policlinico Umberto I Hospital, University of Rome La Sapienza from March 2020 - April 2021.
These patients had large vessel occlusion (LVO)-related AIS (acute ischemic stroke) and/or AMI (acute myocardial infarction) concurrent with a SARS-COV2 infection as determined by nasopharyngeal PCR test. Although sequencing was not conducted, it was assumed that the timing of the infection would relate to the Wuhan strain of the virus.
Thrombi from LVO-related AIS patients not infected with SARS-COV2 were used as negative controls.
When examining the thrombi pathologists detected some spike without any indication of either nucleocapsid protein or SARS-COV2 RNA (emphasis mine):
The relative amount of platelets and fibrin/red blood cells did not significantly differ from COVID-19 thrombi and controls. COVID-19 thrombi retrieved from cerebral arteries showed mild positivity for SP, whereas SP immunostaining was more marked in the COVID-19 thrombus retrieved from anterior descending coronary artery (Fig. 1, Panel 1 A, C). Interestingly, in the clot of the AMI patient, immunostaining for CD61 was patchy, yet substantially overlapped with SP (Additional file 1: Fig. S1). Neither cerebral nor coronary artery thrombi showed cells positive for NP (Fig. 1, Panel 1 B, D). As for comparison, Fig. 1 Panel 2 reports representative immunohistochemical staining for SP and NP which was positive for both (E and F, respectively) in the lung of a patient affected by COVID-19 (positive control) and negative (G and H, respectively) in a thrombus retrieved from the middle cerebral artery of a patient not affected by COVID-19 (negative control).
Here, the results corroborate prior hypotheses in spike-derived clot formation:
The main limitation of this study was the very limited sample size which prevented us from drawing definite conclusions. However, in our opinion, the present data could support the hypothesis that free SP, besides the whole virus, may be the trigger of platelet [1, 2] and endothelial [6] activation, and clot formation in COVID-19. This event could precede or run in parallel with the recently hypothesized spike-specific immune-complex (IC)-mediated platelet activation in COVID-19 critically ill patients [9, 10].
It’s important to remember that the presence of spike does not directly implicate it as inducing clot formation. However, given the prior in vitro evidence these results does provide some validation of this model.
And it’s generally a lack of validation of hypotheses or models that tend to be lacking. Let’s suppose that we have various ideas circulating with respect to amyloid formation cuased by spike proteins as well as the clots found in Died Suddenly.
And yet, not only were the proteins found never characterized, but the cause of the blood clots were never verified, in the same ways that hypotheses over amyloid formation has never sourced amyloid plaques in the brains of individuals for spike seeds (so to speak).
Keep in mind that one hypothesis relating to the adenoviral vectors and thrombosis suggest an immunological response to a PF4-viral vector complex. Not much appears to have come from this speculation, but once again if we are to argue that this PF4-viral vector complex is what is causing the thrombosis wouldn’t it be within the interest of the public to search for these complexes?
So far, histology reports are limited. Several reports which have looked at thrombosis relating to vaccination have not conducted staining for spike or other vaccine-related agents, leaving serious holes in the evidence. It’s possible that not many would consider to look for spike and instead look biomarkers which indicate a thrombotic event.
Thus, in order to unravel what is happening with these vaccines it may be worth unraveling what agents are seeding these protein aggregates.
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De Michele, M., d’Amati, G., Leopizzi, M. et al. Evidence of SARS-CoV-2 spike protein on retrieved thrombi from COVID-19 patients. J Hematol Oncol 15, 108 (2022). https://doi.org/10.1186/s13045-022-01329-w