Antibodies as Dual Weapons: Against the Virus – and Against the Host

July 16, 2022

I believe I have discovered what unites the observed Autoimmunity, Immune Deficiency, Neurodegeneration and Fibrosis. It also explains COVID, PASC, and especially Severe Covid.


Let us first address Severe COVID and the now infamous, lethal Cytokine Storm.

To begin, it must be understood that those who have severe COVID have much higher levels of circulating antibodies to the Spike Protein. Compared with those in moderate patients, neutralizing antibody and IgG-S antibody titers in severe patients were significantly higher.


Different Profiles of Antibodies and Cytokines Were Found Between Severe and Moderate COVID-19 Patients

But, what does this have to do with the induction of a fatal cytokine storm? The answer resides with both TLR2 and Fc receptors. It is the unique synergy between these two that hyperaccelerate the Cytokine Storm, and why we have not observed anything quite like it in all of medicine.

Notably, upon recognition of S protein, TLR2 dimerizes with TLR1 or TLR6 to activate the NF-κB pathway. Taken together, these data reveal a mechanism for the cytokine storm during SARS-CoV-2 infection and suggest that TLR2 could be a potential therapeutic target for COVID-19.

SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway

Being the most abundant in Severe COVID, it must then be assumed that it is the Spike Protein antibody bound interaction with the Fc receptor which is causing the increased severity of symptoms, and ultimately, the Cytokine Storm.

Multiple betacoronaviruses including SARS-CoV-2 and SARS-CoV-1 expand cellular tropism by infecting some phagocytic cells (immature macrophages and dendritic cells) via antibody bound Fc receptor uptake of virus. Antibody-dependent enhancement (ADE) may be involved in the clinical observation of increased severity of symptoms associated with early high levels of SARS-CoV-2 antibodies in patients. Infants with multisystem inflammatory syndrome in children (MIS-C) associated with COVID-19 may also have ADE caused by maternally acquired SARS-CoV-2 antibodies bound to mast cells.

SARS-CoV-2 antibodies bound to Fc receptors on macrophages and mast cells may represent two different mechanisms for ADE in patients. These two different ADE risks have possible implications for SARS-CoV-2 B-cell vaccines for subsets of populations based on age, cross-reactive antibodies, variabilities in antibody levels over time, and pregnancy.

Two Different Antibody-Dependent Enhancement (ADE) Risks for SARS-CoV-2 Antibodies


What is most revelatory, and concerning, is that it is the CO-ENGAGEMENT of these two (TLR2-FvyR) that can profoundly increase the IL-6 and Cytokine Response.

Consistent with this report, our work suggests that remodeling of MØ lipid rafts using either methyl-β cyclodextrin (MβCD) or filipin profoundly changes (that is, increases or decreases, respectively) the MØ interleukin-6 (IL-6) cytokine response to TLR2–FcγR co-engagement (D. Hunt and J.R. Drake, unpublished data).

Molecular mechanisms of macrophage Toll-like receptor–Fc receptor synergy


I believe it is the Spike Protein immune complexes which are causing the massive amounts of Autoimmune Disease and Conditions which are now appearing. I believe the mechanism of this prompted by the Spike Protein’s interaction with FcγRIIB, inhibiting its protective function.


FcγRIIB is one of the pivotal elements for controlling the activation of autoreactive B cells — which are often present even in normal individuals — and is important for maintaining peripheral tolerance. Its functional impairment leads directly to IC-induced autoimmune diseases. In relation to this, the extent of downregulation of expression of FcγRIIb in germinal-centre B cells was shown to be inversely related to the upregulation of IgG antibody responses and to correlate well with susceptibility to autoimmune diseases in several mouse strains, which indicates that maintaining the expression level of FcγRIIB, especially in germinal-centre B cells, is important for suppressing the unwanted expansion of autoreactive B-cell populations.

So, FcγRIIB deletion, which leads to marked augmentation of autoantibody production, due to loss of the negative-feedback loop of B-cell regulation, and enhanced effector-cell responses, is sufficient for the onset of induced or spontaneous autoimmune disease, at least in mice.

Roles of Fc receptors in autoimmunity

The results of a study from March, 2022 underscore the concern. It is the discussed interaction which impairs the protective function of FcγRIIB.

Together, our results identified a novel ADE mechanism of SARS-CoV-2 pseudovirus in vitro, FcγRIIB-mediated uptake of SARS-CoV-2/mAb complex with bivalent interaction.

Antibody-dependent enhancement (ADE) of SARS-CoV-2 pseudoviral infection requires FcγRIIB and virus-antibody complex with bivalent interaction


IMMUNE COMPLEXES in Systemic Sclerosis (SSc) stimulate endosomal TLRs after Fc-mediated internalization by plasmacytoid dendritic cells (pDCs). IFNs block the effects of TGF-β on fibrosis, suggesting that they might actually ameliorate this aspect of SSc pathogenesis. However, the use of IFNs in clinical trials has not shown any significant inhibition of collagen synthesis and instead suggested that IFN treatment aggravated disease activity in some SSc patients [100], indicating that impairment of IFNs might promote progression of the disease. Furthermore, as TLR activation of dendritic cells and macrophages also stimulates IL-1β, TNFα and IL-6 production, these or other undefined mediators might be more important in driving fibrosis in SSc.

New Insights into the Mechanisms of Innate Immune Receptor Signalling in Fibrosis

I believe the above is (perhaps one of several) the very mechanism by which the Spike Protein is inducing systemic fibrosis.


The mechanism described here may also be the driving mechanism behind the aged being more susceptible to experiencing Severe COVID.

Increasing evidence is emerging that FcγR expression on CNS resident cells, including microglia and neurons, is increased during aging and functionally involved in the pathogenesis of age-related neurodegenerative diseases. Therefore, we propose that increased expression and ligation of FcγR in the CNS, either by endogenous IgG or therapeutic antibodies, has the potential to induce vascular damage and exacerbate neurodegeneration.

New roles for Fc receptors in neurodegeneration-the impact on Immunotherapy for Alzheimer's Disease

The very same mechanism that drives the cytokine storm, is the engine here as well. It is the IMMUNE COMPLEXES of the Spike Protein interacting with FcyR receptors, that I believe is inducing Amyloidosis and the observed Neurodegenerative conditions appearing ubiquitously.


This is one of the most disturbing findings. What you are about to read is from the year 2014. That’s right. 2014.

Antibodies against a viral protein named Spike that enables the severe acute respiratory syndrome coronavirus to enter into and to infect epithelial cells can prevent these cells from being infected. Antispike antibodies, however, were recently found to enhance the infection of human immune cells through their interaction with FcγR.

Fc Receptors in Immune Responses

Yet, how does this cause Immune Deficiency?

The following paper discusses, among other issues, the Spike Protein immune complex interactions with the FcRn receptor.

Endocytosis and Transcytosis of SARS-CoV-2 Across the Intestinal Epithelium and Other Tissue Barriers

If this, as I believe it does, does indeed impair the function of FcRn, then it will perform PRECISELY the same task that FcRn inhibitors do. This, I believe, explains why we are observing a reduction in antibodies to other diseases.

Targeting FcRn for immunomodulation: Benefits, risks, and practical considerations

Study shows reduced respiratory syncytial virus antibody levels in women of childbearing age and infants during the COVID-19 pandemic

I believe I have demonstrated the concern that a “Robust Immune Response” to SARS-CoV-2 is almost certainly double-edged. It is Janus. And it is very dangerous.