LOOK AT 27, 28, 29 AGAIN
“27] The spike protein in SARS-CoV-2 is a trimeric, or three-part protein, composed of two functional S1 subunits, as well as a structural S2 subunit. Each of those three units are, incidentally, bound and inactivated by the drug ivermectin.
[28] In the absence of ivermectin or hydroxychloroquine, the two drugs most thoroughly studied and most widely used in early and late cases of COVID-19,
[29] the spike protein remains in a conformation that enables it to attach to the ACE2 receptor on human cells, and to enter by that portal. Conversely, either of those drugs are able to change the conformation of the spike protein in such a way that prevents entry to the human cell.”
Spike protein was found to enter cardiomyocytes in vitro, and cytotoxicity was detected at 24 hours post exposure, and “profound cytopathogenic effects” were visible at 96 hours in cardiomyocytes. [36]
The spike protein alone of SARS-CoV-2 has been found to have damaging effects on endothelial function. [37] In fact, the spike protein alone was found to produce pro-apoptotic factors that were determined by researchers to be responsible for endothelial cell death. [38] Endothelial cells that were treated with the spike protein showed mitochondrial fragmentation and dysmorphic changes, as well as reduced mitochondrial respiration with redox stress, but increased glycolysis, and it was shown that the S protein alone damaged endothelial cells by this mechanism. [39] Interestingly, in those in vitro studies, cell function was found to be restored by adding N-acetyl-L-cysteine, which is a reactive oxygen species inhibitor.
The spike protein has been found, without other viral elements, to stimulate cell signaling in human cardiac pericytes that has been associated with cardiac cell dysfunction. Some of this dysfunction includes findings of increased amounts of the following pro-inflammatory cytokines (those involved in cytokine storms) in cardiac pericytes on in vitro exposure to S protein: MCP1, IL-6, IL-1B and TNF-alpha. [40] TNF-alpha is specifically associated with heart failure and myocarditis. [41]
Caspase-3 is associated with apoptosis. When coronary artery endothelial cells were exposed to spike protein, they were found to have increased Caspase 3/7 activity, which was correlated with pro-apoptotic effect. Some of the above activity was through the ACE-2 receptor, but more data showed involvement of the CD-147 receptor on those cells, [42] and we have seen above that both pathways are used by spike proteins for cell entry. The cell death experienced in myocarditis seems likely to be at least partly due to this activity.
Electrocardiogram (EKG) abnormalities have also been found following COVID vaccine administration. This includes diffuse ST elevation and an inverted T-wave in lead III, as well as sinus tachycardia. [43]
What the hell?
Trump knew early on or suspected it. And the Fauci/Birx FDA, NIH traitors buried him in scientific haze and shiny...look over here vaccine legacy chatter.
Well we know the virus causes all kinds of damage for some people. But there is a good chance they knowingly failed to disclose this side-effect to anyone until it was too late. And they continue to deny the American public drugs that can protect them from severe damage by the virus.
I wonder what other truths are out there. They were telling people not to take certain OTC before the jabs. Why? Because they interfered with the efficacy or the jab? No, they told people it would interfere or cause worse side-effect.