DPT example tetanus-diphtheria-acellular pertussis vaccine is applicable to COVID vaccine; vaccinating mother for COVID is akin to vaccinating infant in utero or new born; potential risk of vaccine

by Paul Alexander



Pfizer and Moderna never studied this and it was imperative.

The natural innate immune system and especially innate antibodies and natural killer cells will be prevented from binding to the virus (glycosylated pathogen) and as such educating the immune system on how to handle pathogen it is confronted with now and other glycolsylated virus in the future, as well as in the training of the NK cells to educate the immune system in recognizing ‘self’ from ‘non-self’ and as such, mitigating auto-immune disease risk. Natural innate immune system antibodies (first line of defense) (that must bind to virus to educate the immune system on how to handle the viruses) also function to educate the innate immune system’s NK cells and this is a key role. Key in preventing auto-reactivity, auto-immunity.

Key research for you by Orr:

‘Natural killer (NK) cells (that must be trained and educated by the innate immune system) play a key role in the immune response to certain infections and malignancies by direct cytolysis of infected or transformed cells and by secretion of potent immune mediators. NK cells express an array of activating receptors that recognize self-molecules. If not restrained by inhibitory receptors recognizing major histocompatibility complex (MHC) class I proteins on the surface of self cells, NK cells are able to kill normal, healthy cells. Not all NK cells express inhibitory receptors for self-MHC class I; thus, other tolerance mechanisms are necessary to prevent NK cell-mediated autoimmunity. Here we review the major mechanisms of NK cell education and tolerance.’


Natural Killer Cell Education and Tolerance - ScienceDirect

Dr. Geert Vanden Bossche’s teaching here:

Intra-pandemic vaccination of toddlers with non-replicating antibody-based vaccines targeted at ASLVI[1]- or ASLVD[2]-enabling glycosylated viruses prevents education of innate immune effector cells (NK cells).

Key message:

‘Antibody-based vaccines teach the immune system to produce high levels of antibodies that are directed against the surface protein that is responsible for initiation of viral infection. Due to their high specificity and strong binding capacity, these vaccinal antibodies (Abs) outcompete the child’s innate antibodies for binding to the virus[3].  This not only sidelines virus-neutralization by the natural innate immune system but also hampers the ability of innate antibodies to educate the innate immune system’s NK cells (Natural Killer cells) regarding NK cell recognition of (and appropriate response to) molecular self-mimicking patterns that are expressed on virus-infected host cells. This is particularly problematic when mass vaccination campaigns are conducted during a pandemic as those drive natural selection and dominant expansion of more infectious immune escape variants.

Strong immune priming as induced by vaccines elicits long-lived Ab titers. Even in the absence of further booster shots, repeated exposure to more infectious circulating variants will recall these vaccinal antigen (Ag)-specific Abs and thereby sustain high-titer antibody responses. When immature, low-affinity Abs become exposed to the virus, (which may occur when vaccines are administered during a pandemic), these Abs may bind to the virus without neutralizing it. This in its own right could already provoke Ab-dependent enhancement of infection (ADEI) by the target virus. Vaccinated toddlers are particularly at risk of ADEI as their innate immune system has not yet been trained. Consequently, young children who are vaccinated during a pandemic with non-replicating viral vaccines (directed at ASLVI- or ASLVD-enabling glycosylated viruses[1]) are at high risk of developing severe disease.

In addition, boosting of vaccinal Abs as a result of repeated exposure to more infectious immune escape variants will lead to prolonged suspension of NK cell education in these vaccinated toddlers. When, for a prolonged period of time, NK cells are prevented from being sensitized to pathogen-derived self-mimicking peptide patterns that are expressed on infected or otherwise pathologically altered cells, they may end up becoming tolerant to these patterns, which are typically shared among several different glycosylated pathogenic agents (G. Vanden Bossche, former provisional patent application). That is, the NK cells become hyporesponsive or desensitized to these pathogenic agents[2].  This opens the door to recognition by B and T cells of traditional antigens that are naturally expressed later on in the process of infection or pathologic alteration. Recognition by these ‘foreign-centered’ effector cells may enable abrogation but not prevention of infection (i.e., in the case of infectious pathogens) or lead to immune pathology (e.g., in the case of pathologically altered autologous host cells evolving towards expression of foreign proteins).

[1] Examples of glycosylated viruses [other than SARS-CoV-2] causing ASLVI or ASLVDs: seasonal influenza, RSV, dengue virus and viruses responsible for vaccine-preventable infections: measles, mumps, rubella, varicella, rotavirus or other more virulent glycosylated viruses such as zoonotic influenza (e.g., avian influenza virus), parapox virus (e.g., smallpox virus),  Ebola virus, Marburg virus

[2] The biological mechanism for this fine regulation of the NK cell response is due to downregulation of germline encoded “activating receptors” on NK cells, and/or upregulation of “inhibitory receptors” on NK cells, and/or hypo-responsiveness to “activation signaling.” More details on the underlying mechanisms of this fine regulation of NK cells can be found in the literature as , for example, published by Orr, Mark T., and Lewis L. Lanier. "Natural killer cell education and tolerance." Cell 142.6 (2010): 847-856.’


[1] ASLVI: Acute self-limiting viral infection

[2] ASLVD: Acute self-limiting viral disease

[3] For the purpose of this manuscript, ‘virus’ relates to an ASLVI- or ASLVD-enabling glycosylated virus’