Can the Recent Surge in Cancers Be Considered a Possible Complication of Persistent SARS-CoV-2 Infection/Viral Proteins?

It is time to seriously investigate whether SARS-CoV-2 infection can induce a long-term inflammatory and microvascular disease state — both clinical (Long COVID) and subclinical.

Comparison of means by histological grade. Error bars indicate standard errors of the mean (sem). A: epithelial telomere length; B: stromal telomere length; C: epithelial telomerase activity; D: stromal telomerase activity; E: γ-H2AX; F: Dec1, G: p16; and H: p53. * p<0.05, ** p<0.005, based on Mann-Whitney tests. UC (Ulcerative Colitis) patients with high-grade dysplasia (HGD) low-grade dysplasia (LGD) or cancer (UC Progressors).

This is part one of a series. First and foremost, it is not just cancer that can be a complication of persistent SARS-CoV-2 infection/viral proteins. I’d like to quote a book published early in the pandemic. One which I translated myself to read. Josepth Tritto’s Cina COVID-19: La chimera che ha cambiato il mondo. Early in the book Tritto speaks of a British virologist who wished to remain anonymous that said;

SARS-CoV-2 never lets its victim go.

I took that to heart. It has been reverberating in my mind ever since. And it becomes ever clearer what the virologist meant. Evidence continues to mount that SARS-CoV-2 and its Spike Protein induce a chronic inflammatory disease – that, due to its targeting of the endothelium – is of a systemic nature. I now believe this is what the virologist meant. And it is not just in the manifestation of clinical Long COVID. I believe evidence is now sufficient to suggest that there is also a chronic sub-clinical inflammatory disease state which may develop. And have potentially devastating consequences.

Much has been said about the observed increase in new onset cancers since the emergence of SARS-CoV-2 and its Spike Protein. Today I’d like to examine the possibility that the increased incidence of cancers may be a complication of a new, systemic chronic inflammatory disease. The starting point of our investigation will be a paper from 2011 published in Cancer Research.

The paper we will discuss, in the context of potential emerging SARS-COV-2 related cancers, is Ulcerative colitis-associated colorectal cancer arises in a field of short telomeres, senescence, and inflammation. In this paper, a finding was made that associated leukocyte infiltration with cancer.

Another interesting aspect of this study is the association between infiltrating leukocytes in the lamina propria and progression to dysplasia, supporting a connection between inflammation and cancer. We measured two types of inflammation: active and chronic. Active inflammation is the classical pathological index, which is based on the presence of granulocytes in the epithelium. Chronic inflammation refers to the infiltration of leukocytes (mainly lymphocytes) in the lamina propria. Interestingly, we found that chronic inflammation, but not active inflammation, is associated with tumor progression in UC. Moreover, abundant infiltrating leukocytes were associated with shorter telomeres, increased levels of γ-H2AX, increased levels of Dec1, and reduced p53 expression.

Ulcerative colitis-associated colorectal cancer arises in a field of short telomeres, senescence, and inflammation
https://pmc.ncbi.nlm.nih.gov/articles/PMC3077943/

There they are. Key mechanisms of the Spike Protein we have discussed for over half a decade. Shortened telomeres, reduced p53 expression, and chronic inflammation.

Going back to the association of leukocyte infiltration with cancer, the Spike causes precisely this in the gut.

Cellular deconvolution of Spike+ regions (in colon tissue) revealed a statistically significant focal enrichment of myeloid-derived cells (macrophages, non-classical/intermediate monocytes), plasma cells, and regulatory T cells, coupled with significant enrichment in T-cell-related pathways, including “Antigen processing and presentation,” and “Th1/Th2/Th17 cell differentiation.” The ileum displayed a similar, though less pronounced, signature, demonstrating these statistically significant findings are specific to the colon of LC subjects.

Persistent SARS-CoV-2 Spike is Associated with Localized Immune Dysregulation in Long COVID Gut Biopsies
https://www.biorxiv.org/content/10.64898/2026.03.09.707564v2.full

The pancreas.

Mild lymphocytic infiltration of the endocrine and exocrine pancreas has been documented in some SARS-CoV-2–infected individuals with SARS-CoV-2 infection (65, 105). Such studies reported evidence supporting significant long-term morphological defects of the pancreas upon SARS-CoV-2 infection. For instance, histologic examination of pancreatic sections from postmortem tissues and infected pancreatic tissues showed thrombotic lesions, fibrosis, necroptotic cell death, immune cell infiltration, chronic pancreatitis, and focal acute pancreatitis (55, 65, 121)

Molecular analysis of long COVID and new-onset diabetes mellitus: pathobiological relationships and current mechanistic views
https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2025.1737894/full

The liver.

Some liver biopsy and histopathology specimens that were analyzed from patients with COVID-19 showed moderate microvascular steatosis and mild lobular and portal vein activity. There was evidence of infiltration of lymphocytes, sinusoidal expansion of the central lobule, and patchy necrosis[4].

Liver injury induced by COVID 19 treatment – what do we know?
https://pmc.ncbi.nlm.nih.gov/articles/PMC9753058/

The peripheral nervous system.

Long COVID patients without neurological symptoms did not have overt fiber abnormalities, but importantly, both groups of patients had elevated numbers of corneal dendritic cells compared with controls, suggesting ongoing leukocyte infiltration of the PNS post‐COVID‐19.

Neuroimmune pathophysiology of long COVID
https://pmc.ncbi.nlm.nih.gov/articles/PMC12247276/

The liver.

Conclusions We identified a possible manifestation of an immune-mediated postacute sequel to COVID-19 associated with a characteristic immune infiltrate in children with AHUO. COVID-19 testing should be considered in paediatric AHUO.

Characteristic immune cell interactions in livers of children with acute hepatitis revealed by spatial single-cell analysis identify a possible postacute sequel of COVID-19
https://gut.bmj.com/content/74/9/1486

What does all of this suggest? As stated earlier, the recent increase in cancer diagnoses, particularly among the young, may be a complication of a persistent SARS-CoV-2 infection or persistence of SARS-CoV-2 viral antigens. The blame has been placed on many ludicrous mechanisms in the MSS. However, we know better.

We must determine how prevalent persistent SARS-CoV-2 infection/viral antigens are. This is a de minimis starting point. Thank you, as always, for your readership, dialogue and support. I cannot do this without you. Please have a blessed week.

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