Comment // Coronavirus

Covid Vaccination and Cancer

I’ve written on potential cancer-causing mechanisms from Covid vaccination over the last four years.

And, of course, key to protecting the body from cancer is the immune system. What we don’t want is for it to become dysregulated and dysfunctional.

Immune Dysregulation

The immune system is highly regulated with interconnected paths that immunologists are still discovering, and by changing one part you affect another. If SARS-CoV-2 vaccination is changing something in our immune system, be it via changes in vaccine mRNA code and negatively affecting toll-like receptors or by other means, what else does it change in our immunity?

Lynn et al. describe the importance of toll-like receptors in Impact of Polymer-TLR-7/8 Agonist (Adjuvant)Morphology on the Potency and Mechanism of CD8 T Cell Induction: ‘Small molecule Toll-like receptor-7 and -8agonists (TLR-7/8a) can be used as vaccine adjuvants to induce CD8 T cell immunity’. [Emphasis added]

InvivoGen, summarising Craft et al. (2005) and Reece et al. (2005), support that finding: ‘The ability of TLR7-8 agonists to activate DCs and thus elicit Th1 and CD8+ T cells responses can be exploited to enhance the efficacy of vaccination’. [Emphasis added]

From those authors, we see an important connection between toll-like receptors, dendritic cells (DC) and T cells, specifically CD8 T cells. Toll-like receptors activate dendritic cells, eliciting a response from CD8 T cells. CD8 T cells are established as a vital part of the immune system’s defence against infection but also cancer. Fu and Jiang, in Dendritic Cells and CD8 T Cell Immunity in Tumor Microenvironment, explore the complex interplay further and reveal the importance of dendritic cells in the role CD8 T cells play in fighting cancer: ‘While direct presentation of tumor antigens onto their MHCI by tumor cells play an important role in effector function of CD8 T cells, cross-presentation by professional antigen presenting cells in particular DCs are required for prime naive CD8 T cells and sustaining the cytotoxic immune responses’ [Emphasis added].

If, as the authors state, that toll-like receptors are required to activate dendritic cells, and dendritic cells sustain T cell cytotoxic killing against cancerous tumours, then what happens if those toll-like receptors are not working so well? An uptick in cancer? And infection?

The toll-like receptors 7 and 8 are described in the literature as important in eliciting the vital CD8 T cell response. With that in mind, let us remind ourselves what Drs Weissman and Kariko wrote in Suppression of RNA recognition by Toll-like receptors: the impact of nucleoside modification and the evolutionary origin of RNA (2005): ‘We show that RNA signals through human TLR3, TLR7, and TLR8, but incorporation of modified nucleosides m5C, m6A, m5U, s2U, or pseudouridine ablates activity’. 

That very technology is being used in SARS-CoV-2 vaccines; it switches off TLR 7 & 8 signalling  that the immune system needs to fight infection and cancer.

Also, repeated Covid vaccinations, as Uversky et al. described, can lead to an increase in IgG4 antibodies with negative outcomes:

However, emerging evidence suggests that the reported increase in IgG4 levels detected after repeated vaccination with the mRNA vaccines may not be a protective mechanism; rather, it constitutes an immune tolerance mechanism to the spike protein that could promote unopposed SARS-CoV2 infection and replication by suppressing natural antiviral responses. Increased IgG4 synthesis due to repeated mRNA vaccination with high antigen concentrations may also cause autoimmune diseases, and promote cancer growth and autoimmune myocarditis in susceptible individuals. [Emphasis added]

The Latest Study

The latest study to raise concerns was just published, titled Proteomic and serologic assessments of responses to mRNA-1273 and BNT162b2 vaccines in human recipient sera. There are several points to consider with this research.Their analysis demonstrated an upregulation of Glutathione-specific gamma-glutamylcyclotransferase 1 (CHAC1). The raised glutathione enzyme CHAC1 acts on Glutathione, and Glutathione plays a major role in health. Kennedy et al. described its role:

Glutathione (GSH) is the most abundant non-protein thiol present at millimolar concentrations in mammalian tissues. As an important intracellular antioxidant, it acts as a regulator of cellular redox state protecting cells from damage caused by lipid peroxides, reactive oxygen and nitrogen species, and xenobiotics. Recent studies have highlighted the importance of GSH in key signal transduction reactions as a controller of cell differentiation, proliferation, apoptosis, ferroptosis and immune function. Molecular changes in the GSH antioxidant system and disturbances in GSH homeostasis have been implicated in tumor initiation, progression, and treatment response.

Also for consideration is the role of CHAC 1 and Glutathione Unfolded protein response. If UPR is not functioning properly then that may lead to fatal pathology involving mis-folded proteins, like dementia.

[CHAC1 catalyzes] the cleavage of glutathione into 5-oxo-L-proline and a Cys-Gly dipeptide. Acts specifically on glutathione, but not on other gamma-glutamyl peptides (PubMed:27913623). Glutathione depletion is an important factor for apoptosis initiation and execution. Acts as a pro-apoptotic component of the unfolded protein response pathway by mediating the pro-apoptotic effects of the ATF4-ATF3-DDIT3/CHOP cascade (PubMed:19109178).

The authors of Proteomic and serologic assessments of responses to mRNA-1273 and BNT162b2 vaccines in human recipient sera Hickey et al. also note:

Overexpression of the enzyme results in glutathione depletion, which adversely impacts the regulation of the cellular oxidative balance between reactive oxygen species and antioxidant defences.

Keeping Glutathione in balance is therefore important, and any abnormal upregulation of enzymes affecting how much Glutathione is available may indicate a significant problem; both too little and too much can lead to fatal pathology, including cancer.

Hickey et al. also demonstrated an upregulation of the Cancer/testis antigen 1 (CTAG1A|CTAG1B) in sera from BNT162b2 (Pfizer Covid vaccine) recipients, and they noted:

Cancer-testis antigen are antigens identified in a variety of malignant tumors and are normally only expressed in testis tissues.

In light of previous research findings and the latest sera results, the concern that these vaccines may contribute to or cause a significant, even fatal disease like cancer is now very high.

Of course, we wait to see that the latest sera study can be repeated and confirmed but nonetheless, the risk to reward for these vaccines is, in my opinion, firmly on the risk side.