3.1.3. Potential short-, mid-, and long-term risks of mass COVID-19 inoculation for children
3.1.3.1. Intrinsic inoculant toxicity
Children are unique relative to COVID-19. They have negligible risks of serious effects from the disease, as shown in Fig. 1. Given that the COVID-19 inoculants were only tested for a few months, and mid-or long-term adverse effects are unknown, any mid- or long-term adverse events that emerge could impact children adversely for decades.
We believe that mid-or long-term adverse effects are possible based on the recent emergence of evidence that would support the probability of mid-and long-term adverse effects from the COVID-19 inoculants, such as:
1)
The spike protein itself can be a toxin/pathogenic protein:
2)
S protein alone can damage vascular endothelial cells (ECs) by downregulating ACE2 and consequently inhibiting mitochondrial function [37].
3)
it is concluded that ACE2 and endothelial damage is a central part of SARS-CoV2 pathology and may be induced by the spike protein alone [38].
4)
the spike protein of SARS-CoV-1 (without the rest of the virus) reduces ACE2 expression, increases angiotensin II levels, exacerbates lung injury, and triggers cell signaling events that may promote pulmonary vascular remodeling and Pulmonary Arterial Hypertension (PAH) as well as possibly other cardiovascular complications [39].
5)
the recombinant S protein alone elicits functional alterations in cardiac vascular pericytes (PCs) [40]. This was documented as:
6)
increased migration
7)
reduced ability to support EC network formation on Matrigel

secretion of pro-inflammatory molecules typically involved in the cytokine storm
9)
production of pro-apoptotic factors responsible for EC death. Furthermore, the S protein stimulates the phosphorylation/activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) through the CD147 receptor, but not ACE2, in cardiac PCs, the S protein may elicit vascular cell dysfunction, potentially amplifying, or perpetuating, the damage caused by the whole coronavirus [40].
10)
“even in the absence of the angiotensin-converting enzyme 2 receptors, the S1 subunit from SARS-CoV-2 spike protein binding to neutral phospholipid membranes leads to their mechanical destabilization and permeabilization. A similar cytotoxic effect of the protein was seen in human lung epithelial cells.” [125].
11)
The LNP layer encapsulating the mRNA of the inoculant is highly inflammatory in both intradermal and intranasal inoculation [41] and “Polyethylene glycol (PEG) is a cause of anaphylaxis to the Pfizer/BioNTech mRNA COVID-19 vaccine” [42]. “Humans are likely developing PEG antibodies because of exposure to everyday products containing PEG. Therefore, some of the immediate allergic responses observed with the first shot of mRNA-LNP vaccines might be related to pre-existing PEG antibodies. Since these vaccines often require a booster shot, anti-PEG antibody formation is expected after the first shot. Thus, the allergic events are likely to increase upon re-vaccination” [43].
There is also the possibility that the components of the LNP shell could induce the ASIA Syndrome (autoimmune/inflammatory syndrome induced by adjuvants), as shown by studies on post-inoculation thyroid hyperactivity [44] and post-inoculation subacute thyroiditis [45].
12
The spike protein has been found in the plasma of post-inoculation individuals, implying that it could circulate to, and impact adversely, any part of the body [46].
13
The spike protein of SARS-CoV-2 crosses the blood-brain barrier in mice [47], and “the SARS-CoV-2 spike proteins trigger a pro-inflammatory response on brain endothelial cells that may contribute to an altered state of BBB function” [48].
14
The spike proteins manufactured in vivo by the present COVID-19 inoculations could potentially "precipitate the onset of autoimmunity in susceptible subgroups, and potentially exacerbate autoimmunity in subjects that have pre-existing autoimmune diseases", based on the finding that anti-SARS-CoV-2 protein antibodies cross-reacted with 28 of 55 diverse human tissue antigens [49].
15
“The biodistribution of ChaAdOx1 [Astra Zeneca’s recombinant adenovirus vaccine candidate against SARS-CoV-2] in mice confirmed the delivery of vaccine into the brain tissues [50]. The vaccine may therefore spur the brain cells to produce CoViD spike proteins that may lead to an immune response against brain cells, or it may spark a spike protein-induced thrombosis. This may explain the peculiar incidences of the fatal cerebral venous sinus thrombosis (CVST) observed with viral vector-based CoViD-19 vaccines” [51,52].
A complementary perspective to explain adenovirus-based vaccine-induced thrombocytopenia is that “transcription of wildtype and codon-optimized Spike open reading frames enables alternative splice events that lead to C-terminal truncated, soluble Spike protein variants. These soluble Spike variants may initiate severe side effects when binding to ACE2-expressing endothelial cells in blood vessels.” [100].
16
A Pfizer Confidential study performed in Japan showed that "modRNA encoding luciferase formulated in LNP comparable to BNT162b2″ injected intramuscularly concentrated in many organs/tissues in addition to the injection site [53]. The main organs/sites identified were adrenal glands, liver, spleen, bone marrow, and ovaries. While damage to any of these organs/sites could be serious (if real for humans), adverse effects on the ovaries could be potentially catastrophic for women of childbearing or pre-childbearing age.