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 |  Subject: The Spike Protein As a Pore-Forming Toxin  Sat Mar 19, 2022 5:24 pm | |
| The spike protein pokes holes in cell membranes at concentrations much lower than those achieved with vaccination, contributing to COVID-like illness and mitochondrial damage. But is the J&J immune?
The spike protein from the COVID vaccines is found in humans for at least four months after injection.
It is a direct toxin that pokes holes in cell membranes. It causes mitochondrial damage in cells and COVID-like illness in mice.
But is it found in humans at concentrations that will create these problems? And are the modifications made to the vaccine spike proteins likely to reduce this toxicity?
This is the first in a series of posts in which I will outline the potential mechanisms of spike protein toxicity and vaccine side effects and brainstorm actionable steps vaccinees can take to protect against these effects or heal from them.
In this first post in the series, we look at the spike protein as a pore-forming toxin.
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The Spike Protein is a “Pore-Forming Toxin” that Pokes Holes in Cell Membranes
The free S1 subunit of the spike protein is a toxin that destabilizes and disrupts lipid membranes without the need to interact with any receptors or other proteins. This is shown by making synthetic lipid bilayers permeable to charged ions. This suggests that it pokes holes in lipid membranes, making it a “pore-forming toxin.”
The membrane is the principal form of cellular organization and its integrity is central to the cell’s ability to produce energy, survive, and thrive. As such, it is difficult to understate how all-encompassing this type of toxicity is. For more background on the importance of membrane integrity, see the footnote.2
With well characterized pore-forming toxins we know details of exactly how the pores form, how big they are, and what size substances they do and do not let through. We do not have these details for the spike protein. We only know that its subunits make membranes permeable to charged ions they would otherwise not let through.
This effect occurs in synthetic lipid membranes at concentrations at least as low as 40 nanomolar (nM, a measure of the concentration of molecules).
Within human lung cancer cells, the concentration required to kill cells starts somewhere between 1 and 2 micromolar (μM), which is 1000-2000 nM, and 25-50 times greater than 40 nM. 24-hour exposure to 2 μM kills off 30% of the cells.
In in vitro models of the blood-brain barrier (BBB) using human cells, both S1 and S2 disrupt the integrity of the barrier in concentrations as low as 0.1 nM.
This BBB paper also showed several other things:
50 nM S1 causes a loss of proteins that form the junctions between the cells.
10 nM S1, S2, or RBD cause the cells to make ICAM-1 and VCAM-1, which are two “adhesion molecules.” The production of adhesion molecules can be seen as the cells crying out to the immune system that they need help. That is, these are molecules that will cause immune cells to migrate to the BBB.
Consistent with these cries for help, the same treatments cause increases in inflammatory cytokines and inflammatory zinc-dependent enzymes known as MMPs that break down tissues.
The authors of the BBB paper argued that the breach of barrier integrity was due to the inflammatory response attacking the proteins at the cell junctions.
However, they showed this breach of integrity starting at 100 times lower concentration (0.1 nM) than they used to show a pro-inflammatory response (10 nM), and at 500 times lower concentration than they used to cause loss of proteins at cell junctions (50 nM).
This paper showed a “breach” in the barrier function of the BBB by showing that it became permeable to small, charged molecules. This is very similar to what the first paper had shown in synthetic lipid membranes. Yet those synthetic membranes did not have any ability to initiate an inflammatory response and did not have any proteins forming junctions. There were no immune cells involved. Thus, the findings of the BBB paper are at least as attributable to the spike protein acting as a direct, pore-forming toxin, poking holes in the cell membrane, as they are to the inflammatory response destroying the junctions between the cells.
The findings of these papers are consistent with a minor finding in a subsection of a mouse paper discussed below, where S1 at concentrations at least as low as 10 nM disrupted the barrier formed between primary human lung microvascular endothelial cells. These are the cells that make up the lining of the small blood vessels of the lungs, which are part of the gas exchange machinery.
Taken together, these papers suggest the following:
S1 and S2 probably both act as direct, pore-forming toxins at concentrations as low as 0.1 nM.
Concentrations at least as low as 10 nM elicit an inflammatory response.
The inflammatory response creates a second layer of destruction that compromises the junctions between cells.
Most likely the inflammatory response is “intended” to get the immune system to come remove the source of the problem. However, immune cells need to infiltrate tissues, which requires making those tissues more permeable so the immune cells can get through, and this might be why the initial inflammatory response actually worsens the problem by disrupting cellular junctions.
The pore-forming toxin effect would likely create all sorts of cellular destruction everywhere, since no cell can function at all without healthy membranes.
Cellular junctions are important everywhere, but their disruption would be particularly damaging to tissues that form important barriers. These would especially include the skin, blood vessels, blood-brain barrier, and the mucous membranes of the eyes, nose, mouth, throat, respiratory tract, and gut. It would also disrupt the function of fibers that rely on such connections to act in unison, such as the contractile units of the heart responsible for its rhythm.
.https://chrismasterjohnphd.substack.com/p/the-spike-protein-as-a-pore-forming?s=r
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| | Subject: Re: The Spike Protein As a Pore-Forming Toxin Sat Mar 19, 2022 6:45 pm | |
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