Doctors 4 Covid Ethics: why intramuscular COVID-19 vaccination must fail

Many countries are currently experiencing a wave of COVID-19 “breakthrough cases” in spite of high vaccination rates. In this paper, we explain the fundamental reason why such cases had to be expected: the antibodies induced by intramuscular vaccination will only circulate in the bloodstream, but they will not reach the surface of the mucous membranes in the upper airways. We also briefly discuss possible mechanisms of vaccine-induced immunopathology.

1. Introduction: All antibodies are not created equal

There are different types of antibodies utilized by the human immune system. The major ones are IgM, IgG and IgA [1]; there are two other classes, IgD and IgE, but there is no need to discuss them here.

IgM is generated in the early stages of an adaptive immune response and is then gradually replaced with IgG antibodies. Both IgM and IgG circulate mainly in the bloodstream. IgG is the most abundant antibody in the blood. On the other hand, while some IgA is found in the bloodstream as well, most IgA is secreted across the mucous membranes of the respiratory tract and the gut, which it then covers and protects.

When our immune system is confronted with an invading pathogenic microbe, the predominant type of antibody it produces depends on the location of that pathogen. If the pathogen is encountered in the bloodstream or inside of tissues within the body, e.g. the muscle, then the immune system will produce mainly IgG antibodies, which will accumulate in the bloodstream. On the other hand, if the pathogen is introduced through the respiratory tract (e.g. the nostrils), then the immune system will produce mainly IgA antibodies—to be more specific, secretory IgA, or sIgA.

While sIgA dominates in the upper airways, some IgG is found along with IgA in the lower airways, that is, the bronchi and lung alveoli. In addition to sIgA, an immune response triggered by a respiratory tract infection will also generate both IgG and IgA within the bloodstream, which provides a safeguard in case the barriers of the respiratory tract are breached and the pathogens enter the tissues. In short, sIgA is the main antibody the immune system relies on in the upper respiratory tract (URT), and it forms the first line of defense against respiratory pathogens.

2. Why is sIgA antibody important?

The key reason why an sIgA-based antibody response is desired against respiratory pathogens is that sIgA does not promote inflammation. Binding of sIgA antibodies to the antigens (such as viruses or bacteria) leads to “quiet” expulsion of these pathogens from the body, but it does not elicit any additional damaging immune responses. In contrast, an IgG-based response is followed by an inflammatory immune reaction. This reaction is triggered by a change in the molecular shape of the Fc region (the tail end) of IgG antibodies, which causes them to activate inflammatory cells as well as the serum complement system.

Since our respiratory tract constantly encounters viruses and bacteria within the air we inhale, IgA-based immune responses help avoid unnecessary and repeated inflammations in our airways. sIgA in the mucous membranes of the respiratory tract can subdue the infection and stop the transmission of these germs safely.

Considering these well-established scientific facts, it is beyond perplexing that people only talk about antibodies (mainly IgG antibodies) in the bloodstream after COVID vaccination. If a vaccine should protect us from respiratory viruses and from transmitting them to others, it should elicit an IgA-based immunity in our respiratory tract, especially in the upper airways.

3. What is really damaging our body: viruses, or our own immune system?

Respiratory viruses rarely cause direct damage to our body. It is typically the overreaction of our immune system against those viruses that does the damage [2,3]. With respect to COVID-19, a recent paper on the causation of clinically severe disease sums it up as follows [4]:

[Severity of COVID-19] is suggested not to be a direct effect of viral infection but instead to be caused by the over-activation of the immune system in response to infection, because worsening of disease coincides with the activation of adaptive immunity. This excessive immune response is frequently described as a “cytokine storm” … Together, high pro-inflammatory cytokines, known to induce collateral damage to tissues, and muted anti-viral responses suggest that an unfavorable immune response may be driving disease in patients with severe cases of COVID-19. CONTINUE READING