COVID Reinfections and Cancer: Respiratory Infections Prime Accelerated Lung Cancer Growth: Broader Turbocancer Implications

The average reinfection rate for Influenza is once every FIVE years. The CDC notes that COVID reinfection may occur within several weeks.

Readers of my X account know that from the very beginning of the pandemic, I asserted that reinfections with COVID would be possible and, in some cases, frequent. This prediction was harshly criticized by most academics and dismissed as “impossible.” Of course, unfortunately, I was proven correct.

Why does reinfection with COVID concern me so much? One may say that even if I am right about frequent COVID reinfections, what does it matter? So what if you get a “cold” several times a year?

The reason this is concerning is what COVID does to the epigenetic landscape of our bodies every time we become infected with it. It creates an environment that is pro-tumorigenic. This is what I have called “cancer without tumors.”

Chronic inflammation is widely recognized as a key driver of cancer development, including lung tumorigenesis.10,11 COVID-19, particularly PASC, elicits persistent immune activation characterized by the overproduction of inflammatory cytokines such as IL-6, IL-1β, and TNF.12–14 This sustained inflammatory milieu may cause oxidative stress, DNA damage and genomic instability to potentially facilitate cell transformation.15 Persistent immune dysregulation in post-viral syndromes may also compromise immune surveillance, allowing pre-malignant cells to escape recognition and evolve into malignant phenotypes.16 Furthermore, inflammation-driven changes in the lung microenvironment may create favorable systemic or local conditions for tumor progression.

Respiratory viral infections prime accelerated lung cancer growth
https://www.biorxiv.org/content/10.1101/2025.09.02.672566v1.full

What was recently discovered (published September 3^rd) is that previous viral lung infections contribute towards a tumorigenic environment. The cause may be SARS-CoV-2 or the flu. The result is similar.

Here, we investigate whether and how prior severe respiratory viral infections shape the lung environment to promote tumorigenesis. Combining retrospective clinical analysis in a large clinical database with mechanistic studies in multiple murine lung cancer models, we define the long-term lung remodeling process following viral pneumonia including SARS-CoV-2 and influenza that accelerates tumorigenesis and cancer growth. Using single-cell transcriptomic and epigenomic profiling, functional immune analyses and therapeutic interventions, we revealed that persistent epigenetic changes in inflammatory cytokine loci after infection established a lung microenvironment prone to cancer, driven in large part by elevated pro-tumor neutrophil activity in situ.

Respiratory viral infections prime accelerated lung cancer growth
https://www.biorxiv.org/content/10.1101/2025.09.02.672566v1.full

This has broader implications. For example, the deluge of so-called “turbocancers” we are observing. What I believe these actually are, are a set of SARS-CoV-2/Spike Protein induced Rapid-Onset Cancers. A very interesting paper published in June of this year lays out the groundwork for rapid-onset cancers post viral infection.

Human cancers are generally thought to develop over the course of decades. Such slow progression is well documented for a variety of cancers that we designate “slow-onset” cancers. “Rapid-onset” cancers, in contrast, can develop in a matter of months in humans or in as little as 9 days in mice. These cancers often develop under conditions that might be expected to accelerate cancer development: early development, immune deficiency, or viral infection.

Rapid-onset cancer
https://www.sciencedirect.com/science/article/pii/S2666679024000363

It is astonishing how quickly a virus may induce cancer. Be prepared.

Whereas slow-onset, chemically induced malignancy in small animals requires 4 months or more (see above), virus-induced cancers can develop within little over a week. Many of these animal studies, as well as cases of human patients with rapid-onset viral cancer, have involved infection under conditions where one of the hallmarks of cancer might be achieved without mutation, with developing tumors benefitting from the rapid proliferation associated with embryonic or early postnatal tissue growth, the natural invasiveness of infected immune cells, or the susceptibility of immune-deficiency [36,[79], [80], [81]].

Rapid-onset cancer https://www.sciencedirect.com/science/article/pii/S2666679024000363

So, from the above referenced article, we know Influenza may be responsible for priming or inducing cancer. But how often do we actually get infected with Influenza? The answer is: not very often. The average for an individual over 30 is only twice a decade.

Frequency of influenza infection.

(A) Number of infections per decade at risk. For each participant, this is calculated by dividing the estimated total number of infections by whichever value is smaller: participant age or 41 (total years between appearance of A(H3N2) in 1968 and test in 2009). Points give median of the posterior distribution; vertical lines show 95% credible interval. (B) Distribution of time between sequential infections, conditional on having at least two infections, across all participants and strains.

Estimating the Life Course of Influenza A(H3N2) Antibody Responses from Cross-Sectional Data
https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1002082#pbio-1002082-g004

However, according the the CDC, reinfection with COVID can happen more frequently than that – much more frequently.

As the virus evolves, new variants with the ability to evade your existing immunity can appear. This can increase your risk of reinfection. Reinfection can occur as early as several weeks after a previous infection, although this is rare.

About Reinfection
https://www.cdc.gov/covid/about/reinfection.html

Is it rare? All of us know individuals who have had diagnosed COVID 2-3 times a year.

Then there is the Spike Protein, which induces similar systemic inflammatory changes (the pro-tumorigenic environment) after exposure (mRNA).

After follow-up, a significant increase in weight and body mass index was observed overall (p = 0.003 and p = 0.002, respectively). Postvaccination, significant increases were observed in several cytokines, including basic fibroblast growth factor 2 (p < 0.001), interferon gamma (IFNγ) (p = 0.005), interleukin-1 beta (IL1β) (p < 0.001), IL4 (p < 0.001), IL6 (p = 0.003), IL7 (p = 0.001), IL17E (p < 0.001), monocyte chemoattractant protein-1 (MCP1) (p = 0.03), MCP3 (p = 0.001), tumor necrosis factor alpha (TNFα) (p < 0.001), and VEGFA (p < 0.001).

Altered Circulating Cytokine Profile Among mRNA-Vaccinated Young Adults: A Year-Long Follow-Up Study
https://onlinelibrary.wiley.com/doi/10.1002/iid3.70194

So, if individuals are being infected with SARS-CoV-2 on a regular (certainly more than once every five years, perhaps much more often) basis and they are experiencing the same effects on a yearly (or more often) mRNA basis, is it any surprise that, given the post COVID and post COVID mRNA inflammatory profiles are identical to those of cancer promotion, that we are witnessing an incredible increase in turbocancers? Unfortunately, at 30,000 ft, what we see unfolding is all too logical.

I will continue to search for therapeutics to mitigate the damage done to us by SARS-CoV-2 and its Spike Protein. Please have a blessed week.

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