The Spike Protein Alone Activates All Major Pathways Involved in Chronic Disease

This is in addition to its ability to induce all Nine Hallmarks of Aging. We can age faster; we can get sick faster – and stay sick.

SARS-CoV-2 spike protein induces reactive oxygen species (ROS), and DNA double-strand breaks (measured by H2AX) in human lung cells. Single-cell suspension of freshly explanted normal human lung cells (A-B) were seeded at 104 cells per well into 96-well plates. Half of the culture wells were incubated with the antioxidant MMS350 (400 μM) one hour before addition of spike protein (0.50 μg/ml), 5 Gy irradiation or both spike protein plus 5 Gy. One hour later, cells were assayed for ROS (A) and DNA double-strand breaks (B). For the statistical analysis, analysis of variance followed by a Student’s t-test were used. ROS increased in human lung cells under all conditions and was reduced when cells were incubated in MMS350. DNA double-strand breaks in human lung samples (n=4) were increased under all treatments but were reduced when the cells were treated with MMS350. Significantly different at p<0.05 vs. *0 Gy, # MMS350.

Perhaps the singular most important reason for the recent emergence of what I shall call catastrophic chronic diseases, is the introduction of the Spike Protein into the human body. By catastrophic, I mean the sudden onset of turbocancers, T2D and other aggressive autoimmune/chronic diseases.

Years ago, I demonstrated that the Spike Protein of SARS_CoV-2 could, on its own, induce the canonical Nine Hallmarks of Aging.

Those, of course, make us age faster. It has now also occurred to me that, in tandem with this acceleration in aging, there is also an acceleration in inducing diseases associated with aging. This is accomplished by the Spike Protein, on its own, as well. How? By activating all the major pathways associated with chronic disease; the diseases of aging.

First, let us take a look at the major pathways involved in chronic disease.

Chronic diseases are frequently linked to the activation and dysregulation of various cellular pathways, particularly those involved in inflammation.

Here are some key pathways and their involvement in chronic diseases:

NF-κB pathway: This protein complex regulates DNA transcription, cytokine production, and cell survival, playing a significant role in inflammatory and immune responses. Its dysregulation is linked to inflammatory, autoimmune, and metabolic diseases, as well as cancers.

MAPK pathways: Mitogen-activated protein kinases are involved in cellular responses to stimuli like inflammatory cytokines and stress. They regulate processes like proliferation, differentiation, and cell survival. Abnormal signaling in these pathways is implicated in inflammatory, autoimmune, and metabolic disorders, along with cancer.

JAK-STAT pathway: This pathway controls gene expression in response to extracellular factors like cytokines and growth factors. Dysregulation is associated with inflammatory, autoimmune, metabolic diseases, and various cancers.

Oxidative stress pathways: An imbalance between reactive oxygen species production and detoxification leads to oxidative stress. This can activate transcription factors, increasing the expression of genes promoting inflammation. Oxidative stress is linked to cardiovascular disease, cancer, diabetes, and aging.

Google AI, July 13, 2025

Inflammation is a biological response of the immune system that can be triggered by a variety of factors, including pathogens, damaged cells and toxic compounds. These factors may induce acute and/or chronic inflammatory responses in the heart, pancreas, liver, kidney, lung, brain, intestinal tract and reproductive system, potentially leading to tissue damage or disease. Both infectious and non-infectious agents and cell damage activate inflammatory cells and trigger inflammatory signaling pathways, most commonly the NF-κB, MAPK, and JAK-STAT pathways.

Inflammatory responses and inflammation-associated diseases in organs
https://pmc.ncbi.nlm.nih.gov/articles/PMC5805548/

One-by-one, we see that the Spike Protein, alone, activates these pathways.

NF-kB

When stimulated with extracellular S protein, human and mouse lung epithelial cells also produced inflammatory cytokines and chemokines. Interestingly, epithelial cells expressing S protein intracellularly were non-inflammatory, but elicited an inflammatory response in macrophages when co-cultured. Biochemical studies revealed that S protein triggers inflammation via activation of the NF-κB pathway in a MyD88-dependent manner.

SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway
https://pmc.ncbi.nlm.nih.gov/articles/PMC8709575/

MAPK

Please also note the activation of monocytes and microglia, which I have previously discussed.

A growing number of studies (in multiple cell types) demonstrated that treatment of cells with the S1 spike protein changes cell signaling, especially the activation of MAPK ERK1/2, and promotes pro-inflammatory cytokine production [18,19,43,61]. These largely lung cell types also include direct activation of monocytes and microglia by S1 spike [62,63].

The SARS-CoV-2 S1 Spike Protein Promotes MAPK and NF-kB Activation in Human Lung Cells and Inflammatory Cytokine Production in Human Lung and Intestinal Epithelial Cells
https://pmc.ncbi.nlm.nih.gov/articles/PMC9607240/

JAK-STAT

To investigate the mechanism underlying the synergistic effect of IL-2 and spike protein in inducing CRS, transcriptomic analysis was conducted on PBMCs treated with PBS, spike protein, IL-2, or a combination of spike protein and IL-2. Our analysis revealed that stimulation with spike protein activated multiple signaling pathways, including NF-κB, TNF, and Janus kinase-signal transducer and activator of transcription (JAK-STAT) in PBMCs (Supplementary Figures S4A–C).

SARS-CoV-2 spike protein induces the cytokine release syndrome by stimulating T cells to produce more IL-2
https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1444643/full

OXIDATIVE STRESS

Also, please note the observed similarities between Spike Protein exposure and radiation. A finding I predicted years ago. Please see wmcresearch.org for the post.

SARS-CoV-2 spike protein induced reactive oxygen species, DNA double-strand breaks, transforming growth factor-β signaling pathways, and senescence, which were exacerbated by prior or subsequent ionizing irradiation. The water-soluble radiation countermeasure, MMS350, reduced spike protein-induced changes. Conclusion: In both the SARS-Co-2 and the irradiation mouse models, similar responses were seen indicating that irradiation or exposure to SARS-CoV-2 virus may lead to similar lung diseases such as pulmonary fibrosis.

SARS-CoV-2 Spike Protein Induces Oxidative Stress and Senescence in Mouse and Human Lung
https://iv.iiarjournals.org/content/38/4/1546.long

So, what we have here is a pathogenic protein which not only accelerates aging but also induces an environment in which the diseases of aging can much more easily take root and rapidly accelerate themselves. It is almost like a conveyer belt. Wherever you are on the spectrum of biological age, the Spike Protein hurries the body’s trajectory along that belt towards the inevitable decline into the maladies of old age. It also makes it far more likely that one of the fatal diseases of old age will develop – and kill far more quickly. I simply find it difficult to believe that such a protein occurred naturally.

Fortunately, these pathways of chronic disease can be attenuated, and biological age can be slowed down. The more we understand, the more we can heal. I will continue to battle on both fronts. Thank you, as always, for your readership, dialogue and support. I am extremely grateful that another individual made a generous direct donation over the weekend, and we gained another paid subscriber. You keep me going. Please have a blessed week.