The spike proteins that are generated by the mRNA COVID vaccines are said to be identical to those attached to SARS-CoV-2.
[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.
[30] ACE2 receptors are found in cells throughout the human body, and have been shown to have varying effects on different organs. ACE2 receptors have been found to be highly concentrated in cardiac pericytes,
[31] even more so than in the lungs.
[32] But the presence of ACE2 has been observed to have a seemingly paradoxical protective effect in the cardiovascular system, such as preserving ATP production. [33] Spike proteins have been found to down-regulate ACE2.
[34] Human cardiomyocytes have been observed to express the ACE2 receptor, and that is the main portal by which the spike protein of SARS-CoV-2 is observed to attach. In addition to the ACE2 receptor, the CD-147 receptor is also used by the spike protein to enter host cells. [35]
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.”