innate immune suppression
First posted online: 17 April 2022
These COVID-19 “vaccines” threaten children’s vital(!) innate immune system when deployed in pandemic conditions at an age when their innate immune system is still under training. Their immature innate antibodies need a chance to train through pathogen exposure.
Innate IgM antibodies (Abs):
guard against inflammation and autoimmune diseases by recognising “self” antigens
suppress allergic responses
efficiently destroy dying cells
are polyreactive, binding to a broad range of antigens with low affinity
Once bound to a virally-infected cell, IgM Abs can trigger the classical complement pathway via bonding protein C1q, an effector function known as complement-dependent cytotoxicity (CDC).
The COVID-19 “leaky vaccines” cannot prevent transmission, so increasingly infectious variants propagate and dominate, as per previous studies on Marek’s disease in poultry. Highly infectious strains guarantee reexposure, reboosting vaccinal high-affinity anti-S Abs.
Even the Lancet recognises children have an inherent “immune preparedness” to novel pathogens including SARS-CoV-2, likely driven by their innate IgM Abs, which contain the virus for up to 2 weeks of infectivity, long enough to produce antigen-specific Abs if needed.
As innate Abs with high avidity (overall binding strength) but low affinity (binding strength at a given binding site), IgM can broadly cross-react to different antigens. They are broad, which is good. But they are susceptible to being outcompeted, which is a concern.
Dr Geert Vanden Bossche is very concerned non-neutralising highly specific anti-S vaccinal Abs will outcompete innate IgM due to their higher affinity. Thus, vaccinal Abs will coat the virus in a way that does not prevent cellular infection but will also block IgM Abs.
IgM Abs may sadly be outcompeted by vaccinal anti-S Abs constantly elicited through exposure to Omicron. Recent evidence indicates IgM is trainable, with IgM memory B cells broadly cross-reacting against distinct bacterial antigens in the murine model.
In response to influenza infection, broad acting, polyreactive (non-antigen specific) IgM is secreted by B-1a cells. Critically, such innate Abs against SARS-CoV-2 would not be liable to lose their functionality due to changes in S, RBD amino acid or O-glycosite mutations.
It is reckless to experiment untried “vaccines” on children with such naïve innate antibodies. Substituting training up functional polyreactive IgM for non-neutralising anti-S vaccinal Abs, at the cost of exposure to a systemically spread toxin (Spike), is unthinkable.
Innate IgM act broadly with non-specificity: binding with low affinity, high avidity
IgM can trigger cytotoxicity via C1q bonding protein
Carsetti et al, Lancet Child Adolesc Health. The immune system of children: the key to understanding SARS-CoV-2 susceptibility
Muthana et al. Competition between Serum IgG, IgM, and IgA Anti-Glycan Antibodies
Weill and Reynahud, IgM memory B cells: specific effectors of innate-like and adaptive responses
Patel and Kearney, Immunological Outcomes of Antibody Binding to Glycans Shared Between Microorganisms and Mammals