resist degradation, and also to produce spike protein at a much greater rate than the original virus version does. Although this was unexpected, it has recently been demonstrated that spike protein can be detected in the blood of people vaccinated with an mRNA vaccine as early as one day after their first administered dose, and that it remains detectable for up to two weeks.
It had been known as early as 2005 that the original SARS-coronavirus binds to ACE2 receptors as a step towards gaining entry into cells, and that it is specifically the spike protein, which makes up the majority of its protein coat, that binds to the receptors. These same authors also showed that the spike protein by itself worsened acute lung failure in infected mice. They proposed that spike binding to the ACE2 receptors disabled their normal function in the renin-angiotensin pathway, resulting in damage due to an acute inflammatory response.
Like SARS-CoV, SARS-CoV-2, the virus responsible for COVID-19, also binds the ACE2 receptors, except that its binding affinity is ten to twenty-fold higher than that of its predecessor, and its binding to the receptor also disables the normal function of ACE2. Maruhashi and Higashi argued in a peer-reviewed paper that decreased ACE2 expres- sion in endothelial cells could be pivotal in the observed cardiovascular sequelae in patients suffering from COVID-19.
A study by Nuovo et al. demonstrated that, if the S1 subunit of the spike protein by itself was injected into the tail of mice, it induced endothelial cell damage in their blood vessels. These authors wrote: “It is concluded that ACE2 plus endothelial damage is a central part of SARS-CoV2 pathology and may be induced by the spike protein alone.” Endothelial dysfunction and endothelial damage are well established predictors of congestive heart failure.
Ominously, the version of the spike protein coded for by the vaccines is different from the one produced by the virus in a highly significant way: it has been engineered to be disabled in its ability to change its shape following attachment to the ACE2 receptors, a necessary step to allow it to fuse with the plasma membrane and gain entry into the cell. This was achieved by changing the code for a pair of adjacent amino acids in the fusion domain of the spike protein to two proline residues.
Their logic in doing this was that it would allow this important part of the protein to be highly exposed to the immune cells to afford easier production of antibodies, the only goal of the vaccination procedure.
However, this would also mean that the spike protein would remain attached to the ACE2 receptors. It has been shown that a complex consisting of the S1 component of the spike protein attached to ACE2 receptors gets detached from the membrane by enzymatic action, and this of course completely disables ACE2’s function in the membrane.
There is no compelling need for a vaccine to protect children from COVID-19, as the death rate among children is vanishingly small.
However, children do rarely experience a serious condition such as multisystem inflammatory syndrome from COVID-19 infection, where the child may develop generalized organ inflammation. This is treatable, however with well-established safe medications.
For example, there is excellent data showing how ivermectin (an antiparasitic drug made from a bacterium Streptomyces avermitilis) can dock in the region of two of the amino acids (leucine and histidine) of the ACE2 receptor and interfere with the attachment of the spike protein to the human cell membrane.
Many other studies have shown that this drug has been used successfully in the prevention and treatment of SARS CoV-2 infections.
There has been an exclusion and obfuscation of the various therapeutics available to be used against this viral infection. The suppression of information about the prevention and treatment with other modalities including pharmacologics that are safe for children and natural supplements is an equally criminal issue to be discussed at a future date.