If the innate immune system is able to quickly clear a pathogen, then an adaptive immune response is not needed to combat the infection. Therefore no antibodies are employed against the pathogen. However, adaptive immunity is triggered when an infection eludes the innate defense mechanisms and generates a THRESHOLD DOSE OF ANTIGEN. This antigen then initiates an adaptive immune response, which becomes effective only after several days, the time required for antigen- specific T cells and B cells to locate their specific foreign antigen, to proliferate, and to differentiate into armed effector cells.

I believe it is this very activation of the adaptive immune system which is causing severe COVID, fatal COVID and Long COVID. This is also why a vast majority of those infected have little to no symptoms. Their innate immune system clears the virus and the adaptive immune system does not become involved.

Yet, it appears that the Spike Protein itself “wants” to ensure that the adaptive immune response is employed. The protein suppresses ACE2 and Type I Interferon expression. Furthermore, there has been evidence presented that vaccination induces a profound impairment in type I interferon signaling.

Do you understand the implications? If the innate immune system is impaired and cannot clear the virus, then the adaptive immune system is activated, setting in motion the potential creation of autoantibodies.

If we look at the autoimmune conditions appearing, including MIS-C and MIS-A we must note the following from Characterization of autoantibodies to endothelial cells in systemic sclerosis (SSc): association with pulmonary fibrosis.

AECA (anti-endothelial cell antibodies) were also detected in Kawasaki disease, systemic vasculitis, multiple sclerosis, Wegener's granulomatosis, and Takayasu arteritis.

I am not the only one to raise these concerns. A Letter to the Editor from May of last year was titled Anti-Endothelial Cell Antibodies are not frequently elevated in hospitalized patients with COVID-19.

In it, the authors express their concerns over the title’s implications, questioning them.

While  the  presence  of  AECA  may represent an epiphenomenon of endothelial dam-age, there is a possibility that pathogenic AECA could be driving the vasculopathy in COVID-19.

The conclusion is very telling:

In  conclusion,  AECA  identification  was  a  relatively  infrequent  finding  in  COVID-19  patients  on  admission,  and  their  presence,  albeit  in  only  2/33  patients,  was  not  associated  with  disease  severity.  However,  as  the  autoantibodies  were  only  measured at  admission,  we  cannot  exclude  the  possibility  of  pathogenic  AECA  developing  later  in  the  course  of  disease.

I don’t need to tell you where I stand on that possibility.

So, ultimately, what are we looking at? I refer you to yesterday’s post for the mechanism of these autoantibodies appearance. We must also consider Molecular Mimicry contributing to the development of the autoantibodies.

SUDDEN DEATHS

I would like to conclude this post with the suggestion that, indeed, the autoantibodies generated by the presence of the Spike Protein may indeed be responsible for the deluge of sudden deaths appearing globally.

Over the last decade, a potential involvement of autoantibodies against cardiac proteins in the pathogenic processes that either cause or accelerate SCD has been studied.

I highly advise all to read the referenced paper:

Autoantibodies for Cardiac Channels and Sudden Cardiac Death and its Relationship to Autoimmune Disorders
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6367693/

Referenced/Related Papers

Autoantibodies for Cardiac Channels and Sudden Cardiac Death and its Relationship to Autoimmune Disorders
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6367693/

The course of the adaptive response to infection
https://www.ncbi.nlm.nih.gov/books/NBK27125/

Characterization of autoantibodies to endothelial cells in systemic sclerosis (SSc): association with pulmonary fibrosis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1905540/

Autoantibodies Against Human Epithelial Cells and Endothelial Cells After Severe Acute Respiratory Syndrome (SARS)-Associated Coronavirus Infection https://onlinelibrary.wiley.com/doi/epdf/10.1002/jmv.20407

Anti-Endothelial Cell Antibodies are not frequently elevated in hospitalized patients with COVID-19
https://www.mattioli1885journals.com/index.php/actabiomedica/article/view/10799/10548

Mechanisms of Immune Dysregulation in COVID-19 Are Different From SARS and MERS: A Perspective in Context of Kawasaki Disease and MIS-C
https://www.frontiersin.org/articles/10.3389/fped.2022.790273/full

SARS-CoV-2 Spike Protein Suppresses ACE2 and Type I Interferon Expression in Primary Cells From Macaque Lung Bronchoalveolar Lavage
https://www.frontiersin.org/articles/10.3389/fimmu.2021.658428/full

Innate immune suppression by SARS-CoV-2 mRNA vaccinations: The role of G-quadruplexes, exosomes, and MicroRNAs
https://www.sciencedirect.com/science/article/pii/S027869152200206X