Respiratory mucosal layer & mucosal immunity (Sucharit Bhakdi MD, Karina Reiss PhD, and Michael Palmer MD): "Gene-based vaccination–quo vadis? Immunity to respiratory viruses: systemic versus mucosal"

SOURCE:

https://doctors4covidethics.org/gene-based-vaccination-quo-vadis/

This passage is critical and I will let it speak for itself. It really explains how out of the box, the COVID gene injection vaccine could not work. It is not only that it is driving variants today, but shockingly, it just could not work day one! Intramuscular vaccines inducing serum antibodies (IgG and circulating IgA) and not secretory IgA (in the mucus cells of the respiratory tract) cannot protect the upper airways (respiratory mucosal layer) where the virus lands. This entire COVID gene injection was a lie, all aspects of it.

“A key aspect of this functional separation between mucosal and systemic immunity concerns the nature of antibodies produced by plasma cells located directly beneath the mucous membranes. These antibodies—secretory immunoglobulin A (sIgA)—are secreted across the mucous membranes to their surface. They are thus on site to meet airborne viruses, and they may be able to prevent them from binding and infecting the cells within those mucous membranes. The same mode of protection pertains to the digestive tract as well.

In contrast, IgG and circulating IgA are the main antibodies found in the bloodstream. They cannot prevent the entry of viruses into the cells that line the airways or the gut, and they may at best counteract their spread if they gain entry to the circulation. Crucially, vaccines that are injected into the muscle—i.e., the interior of the body—will only induce IgG and circulating IgA, but not secretory IgA. The antibodies induced by such vaccines therefore cannot and will not effectively protect the cells of the respiratory tract against infection by airborne viruses [1,2]. This realization is neither contentious nor new. As long as 30 years ago, McGhee et al. [2] concluded:

It is surprising that despite our current level of understanding of the common mucosal immune system, almost all current vaccines are given to humans by the parenteral route [i.e. by injection]. Systemic immunization is essentially ineffective for induction of mucosal immune responses. Since the majority of infectious microorganisms are encountered through mucosal surface areas, it is logical to consider the induction of protective antibodies and T cell responses in mucosal tissues.

The failure of intramuscular injection to induce secretory IgA has been confirmed in a study on Middle East Respiratory Syndrome (MERS) [3]. Like COVID-19, this disease is caused by a coronavirus, and the experimental vaccine used in the study was gene-based, like all of the major vaccines currently deployed against COVID-19. More recently, another study has shown that the mRNA COVID-vaccines also do not stimulate substantive production of secretory IgA [4]. For this simple reason, one cannot expect that vaccination will inhibit airway infection. Indeed, the utter failure of the vaccines to prevent SARS-CoV-2 infection is today solidly documented [5,6].

It is general knowledge that secretory IgA antibodies (sIgA) are produced in response to naturally occurring airway infections. The mucous membranes of healthy individuals are consequently coated with antibodies directed against common respiratory viruses. However, the capacity of these antibodies to prevent infections is limited. The outcome of an encounter with a virus is not “black or white”—numbers are all-important. A wall of protective antibodies may ward off a small-scale attack, but it will be breached at higher viral loads. This is why infections with airborne viruses occur repeatedly throughout life, a fact that will not even be altered by the use of intranasal vaccines in order to stimulate sIgA-production, even though intranasal vaccine application does induce stronger mucosal immune responses than does intramuscular injection [3,7].

The subordinate role of secretory IgA in combating systemic viral infections is highlighted by the fact that individuals with a very common genetic defect—selective sIgA deficiency—who are unable to produce sIgA do not suffer from dramatically increased susceptibility toward severe respiratory infections. This observation can be understood from the following two principles: firstly, immunological protection against respiratory viruses rests mainly on T-cells; and secondly, in those with preexisting immunity, levels of bloodstream antibodies (circulating IgG and IgA) are generally sufficient to prevent severe disease through viral spread within the body.”