Long COVID and Cancer Risk: What the Evidence Shows About Cancer Stem Cells, Viral Reactivation, and Spike Protein (2026)

By Editorial Team -
⚠ Medical Disclaimer — Please Read First
This article is for educational purposes only and does not constitute medical advice, diagnosis, or treatment. It synthesizes published, preprint, and retracted research to give an accurate, evidence-tiered picture of a scientifically unsettled topic. Cancer survivors, immunocompromised individuals, and anyone with concerns about infection or vaccination should discuss their individual risk with their treating oncologist or physician.

Immune Systems Advisor · Evidence Review · Published: September 2026 · By Editorial Team
Reviewed against peer-reviewed literature, preprints, and retraction/correction notices current as of September 5, 2026

A scope note: this review focuses on infection — acute COVID-19 and Long COVID — and its relationship to dormant cancer cell biology. Readers looking for our separate evaluation of vaccine-specific "turbo cancer" claims will find that here; the two questions are related but scientifically distinct, and this article does not re-litigate the vaccine debate.

QUICK ANSWER

A 2025 Nature study provides solid, peer-reviewed evidence that respiratory viral infections — COVID-19 and influenza alike — can wake up dormant cancer cells and worsen outcomes for cancer survivors, through IL-6-driven inflammation, not through any spike-protein-specific mechanism. Whether the SARS-CoV-2 spike protein itself directly reprograms cells toward a cancer-stem-cell-like state is a separate, far weaker claim: the single most-cited paper making that argument (spike protein blocking BRCA1/53BP1 DNA repair) was retracted in 2022 for flawed methodology, and other preclinical findings on spike protein and cancer cells are mixed — some show pro-tumor effects, at least one shows anti-tumor effects. The practical, well-supported takeaway for cancer survivors is about infection generally: minimizing respiratory infection risk (including through vaccination, per ASCO/NCCN guidance) and keeping up with screening matters more than any specific fear of the spike protein.

Evidence Tier Key
TIER 1RCT / systematic review
TIER 2Observational / cohort (peer-reviewed)
TIER 3In vitro / mechanistic / animal model (peer-reviewed)
TIER 4Expert consensus / clinical observation / preprint (not yet peer-reviewed)
RETRACTEDFormally withdrawn by the journal — not valid evidence for any claim

1. Cancer Stem Cells and Tumor Dormancy, Briefly

Most cells inside a tumor are relatively short-lived and divide the way ordinary cancer cells do. A minority subpopulation, however, behaves differently. These cancer stem cells (CSCs) can self-renew, sit quietly without dividing for long stretches (quiescence), and rebuild an entire tumor from a single surviving cell. They are disproportionately responsible for treatment resistance, relapse after apparent remission, and metastasis.[1,2]

CSCs are closely linked to a process called epithelial-mesenchymal transition (EMT), in which cancer cells shed their epithelial identity, become more migratory, and pick up stem-like transcription factors such as Oct4, Sox2, and Nanog, alongside surface markers like CD44, CD24, and ALDH1 depending on cancer type.[3,4] A related and, for this article, more directly relevant concept is the disseminated cancer cell (DCC) — a cell that broke away from the original tumor years or even decades earlier, lodged in a distant organ (commonly the lungs, bone marrow, or liver), and has remained dormant ever since. DCCs share the quiescence and self-renewal features of CSCs, and a growing body of work treats "waking up" a dormant DCC as functionally the same problem as CSC activation: both describe a rare cell converting from a sleeping, treatment-resistant state into an actively dividing one.[5,6]

This distinction matters for the rest of this article, because the strongest new evidence connecting viral infection to cancer relapse is a dormancy-reactivation story, not a de novo carcinogenesis story — it is about disease patients already carry, not about a virus creating cancer from scratch.

2. The Landmark Finding: Respiratory Infection Reawakens Dormant Cancer Cells

TIER 2/3 — Nature, July 2025. Researchers at the University of Colorado Anschutz Medical Campus, the Montefiore Einstein Comprehensive Cancer Center, and Utrecht University published a study combining mouse experiments with two large human datasets (UK Biobank and the Flatiron Health oncology database).[7] The trigger for the research was a documented rise in cancer deaths during the first two years of the pandemic that could not be fully explained by COVID-19 deaths or by delayed screening alone — prompting the hypothesis that the infections themselves were doing something biologically active.[7]

In mice, both influenza and a mouse-adapted SARS-CoV-2 virus caused dormant breast cancer cells already lodged in the lungs to switch into a proliferative state within days, expanding roughly 100-fold into metastatic lesions within two weeks. The mechanism centered on interleukin-6 (IL-6), a cytokine released during the inflammatory response to infection, and on a shift in local T-cell behavior in which CD4+ T cells suppressed the cancer-killing activity of CD8+ T cells, allowing the reactivated cells to escape immune control.[7] Critically, this pathway was general to respiratory viral infection — it was not specific to any SARS-CoV-2 protein, and influenza produced the same effect.

The human data lent real-world weight to the mouse findings. In the UK Biobank, cancer survivors who later tested positive for COVID-19 had close to double the risk of cancer-related death compared with survivors who were never infected.[8,9] In the Flatiron Health breast-cancer cohort (more than 36,000 women), COVID-19 infection was associated with roughly a 40% higher rate of subsequent lung metastasis in an unadjusted analysis; after adjusting for comorbidities and estrogen-receptor status, the effect size was similar in direction (hazard ratio approximately 1.4) but no longer reached statistical significance, which the authors themselves flagged as a limitation warranting larger studies.[7]

Why this is the strongest evidence in this entire topic area: it is published in a top-tier peer-reviewed journal, it combines mechanism with epidemiology, and it doesn't depend on any speculative spike-protein pathway — inflammation from infection is a well-established driver of cancer progression independent of which virus caused it.[10]

3. Does the Spike Protein Specifically Drive This? Separating Mechanism from Speculation

The question people are usually really asking is narrower: not "can infection worsen cancer" (reasonably well supported, as above) but "does the spike protein itself — as opposed to the infection or inflammation in general — reprogram cells toward stemness." Here the evidence is thinner, more contested, and considerably more mixed.

Tumor-suppressor interference (TIER 3, preliminary). A 2024 cell-based study found that SARS-CoV-2 spike protein can interrupt the interaction between p53 (a central tumor-suppressor protein) and MDM2 (the enzyme that normally degrades p53), and that spike-expressing cancer cells showed blunted activation of p53 target genes after chemotherapy exposure along with altered DNA-damage signaling.[11,12] The authors were careful to frame this as a preliminary, hypothesis-generating observation warranting further study, not a demonstrated mechanism of human carcinogenesis.

Contradictory in vitro evidence. A 2026 study in Scientific Reports found the opposite effect in a different cancer cell line: SARS-CoV-2 spike protein exposure actually suppressed proliferation and triggered apoptosis in A549 lung cancer cells, associated with changes in two long non-coding RNAs.[13] This illustrates a broader problem with the "spike protein promotes cancer stemness" narrative: effects appear highly dependent on cell type, spike concentration, and experimental design, and do not point in one consistent direction.

The ACE2 receptor itself is not a stemness switch. Since spike protein enters cells via the ACE2 receptor, some commentary assumes that ACE2 engagement is inherently pro-tumorigenic. A pan-cancer analysis of Cancer Genome Atlas data across 13 cancer types found the opposite correlation: higher ACE2 expression was associated with lower tumor stemness scores, less EMT activity, and better survival across most cancer types studied.[14] This is a correlative bioinformatics finding, not a causal experiment, but it undercuts the simple assumption that spike-ACE2 binding automatically pushes tumor cells toward a stem-like phenotype.

Hematopoietic and immune-cell effects (TIER 3). Separately, spike protein exposure has been shown to trigger pyroptosis (an inflammatory form of cell death) in CD34+ hematopoietic stem/progenitor cells via the NLRP3 inflammasome in ex vivo experiments, and to stimulate immune cells to release cytokine-release-syndrome-associated cytokines.[15,16] These findings are relevant to blood-cell biology and inflammation, but they describe cell damage and immune activation, not a coherent pathway toward cancer-stem-cell-like transformation.

Net assessment: a direct, reproducible, spike-protein-specific pathway to cancer stemness has not been established. What exists is a scatter of preliminary, sometimes contradictory in vitro findings — some suggesting pro-tumor effects on specific pathways, one suggesting anti-tumor effects, and correlative data arguing against a simple ACE2-to-stemness link. This is meaningfully different from the infection-and-inflammation pathway in Section 2, which is far better supported.

4. The Retracted BRCA1/53BP1 Paper — What Happened, and Why It Still Gets Cited

No discussion of "spike protein and cancer" is complete without addressing the single most widely circulated citation behind it: a 2021 paper in the journal Viruses (Jiang & Mei) reporting that spike protein localizes to the cell nucleus and blocks recruitment of BRCA1 and 53BP1 — two key DNA-damage-repair proteins — and separately impairs V(D)J recombination, the process that generates diverse antibodies and T-cell receptors.[17]

This paper was retracted in May 2022. Following an investigation prompted by the paper's own first author, the journal found that the experimental design used a spike-protein construct and a GFP-reporter overexpression system in a way that could have introduced significant ambiguity into the results, undermining confidence in the findings. The retraction notice also states explicitly that the study performed no adaptive-immunity experiments and did not examine full-length, vaccine-relevant spike protein — meaning any conclusions about vaccine safety drawn from the paper were, in the journal's own words, unvalidated and unsupported by the data presented.[18,19]

Despite the retraction, the paper continues to be cited — including in some outlets and reviews that either omit the retraction or cite it before the retraction was issued — as mechanistic support for claims that spike protein (from infection or vaccination) causes DNA damage that leads to cancer. Independent researchers analyzing how scientific findings get misrepresented in health-misinformation content have specifically flagged this paper as a commonly misused source.[20] Any content — including older content on this network — that cites BRCA1/53BP1 suppression by spike protein as established fact should be understood as resting on a retracted foundation unless it separately cites newer, non-retracted work.

5. Long COVID's Immune Signature and Tumor Surveillance

A more plausible and better-evidenced bridge between Long COVID specifically (as opposed to acute infection) and cancer risk runs through immune dysfunction rather than any single viral protein. Long COVID is consistently characterized, across multiple peer-reviewed cohorts, by:

  • T-cell exhaustion — sustained expression of inhibitory receptors (PD-1, TIM-3, LAG-3, CTLA-4) on CD4+ and CD8+ T cells, a phenotype associated with reduced ability to clear infected or abnormal cells.[21,22]
  • NK-cell dysfunction — reduced natural killer cell numbers and impaired cytotoxic function, reported in a 2025 Frontiers in Immunology cohort of Long COVID patients.[23] NK cells are a first-line defense against both virus-infected and early neoplastic cells, so their impairment is mechanistically relevant to tumor immune surveillance.
  • Persistent chronic inflammation — a 2025 Nature Immunology study found sustained upregulation of IL-1, IL-6, JAK-STAT, and interferon-gamma signaling pathways in Long COVID patients for more than 180 days after infection, alongside markers of T-cell exhaustion.[24]

A 2025 peer-reviewed review synthesizing this literature specifically proposes that Long COVID may impair tumor immune surveillance through metabolic reprogramming of immune cells and reactivation of dormant disseminated cancer cells, converging with the mechanism described in Section 2 but extending it to the chronic, months-to-years timescale of Long COVID rather than just the acute infection window.[25] This is a coherent, biologically plausible hypothesis built on published immunology — but it remains, at this stage, a synthesis and framework rather than a proven causal chain with its own dedicated outcomes data.

6. Persistent Spike Protein in Long COVID: A Biomarker, Not Yet a Mechanism

Separately from the mechanistic debate above, several small studies have detected circulating spike protein (or its S1 subunit) in the blood of a majority of Long COVID patients tested, in some cases up to a year after the initial infection, while it was undetectable in fully recovered patients.[26,27] The leading interpretation is that this reflects a persistent tissue reservoir of viral antigen — not necessarily active viral replication — that continues to stimulate the immune system and may help explain ongoing symptoms.[26]

A more recent (2026) preprint extended this by comparing gut tissue regions with and without detectable spike protein in Long COVID patients, finding a distinct, more inflammatory gene-expression signature — including some genes associated with tumorigenesis — specifically in the spike-positive regions.[28] This is an intriguing, mechanistically suggestive finding, but it is a preprint that has not completed peer review, based on a small, localized tissue sample, and it demonstrates an association between antigen persistence and altered gene expression — not a demonstrated increase in actual cancer incidence. It belongs squarely in Tier 4 until replicated and peer-reviewed.

7. What This Means for Cancer Survivors and High-Risk Patients

Taken together, the most defensible practical conclusion is not about the spike protein specifically — it is about respiratory infection in general, for people carrying dormant disease:

  • Infection prevention matters for cancer survivors. Because the best-supported mechanism (Section 2) is infection-triggered inflammation rather than a spike-specific pathway, and because influenza produced the same dormancy-reactivation effect as SARS-CoV-2 in the landmark study, reducing exposure to any respiratory viral infection — not singling out COVID-19 — is the relevant risk-reduction principle.
  • Don't let pandemic-era screening gaps persist. Independent of any viral mechanism, delayed cancer screening and treatment during 2020–2021 produced measurable stage migration — modeling studies estimate meaningfully higher rates of later-stage diagnosis and excess mortality from delays as short as three to six months, across breast, lung, colorectal, gastric, and cervical cancers.[31,32,33] Anyone who deferred screening during the pandemic should catch up.
  • Report unusual symptoms after any respiratory infection promptly, especially in remission. Given the dormancy-reactivation mechanism, cancer survivors who develop new symptoms in the weeks following a COVID-19 or influenza infection have a reasonable basis for flagging this to their oncologist rather than waiting.

Readers using nattokinase, bromelain, and curcumin-based spike-clearance protocols for other Long COVID symptoms (see our Base Spike Detox protocol review) should note that no dedicated evidence currently links that protocol to cancer-specific outcomes; it should not be substituted for oncology follow-up or interpreted as cancer prevention.

8. Evidence Tier Summary Table

Claim Tier Status
Respiratory infection (COVID-19 or flu) reactivates dormant cancer cells via IL-6 inflammation2/3Peer-reviewed, Nature 2025 — mechanism + epidemiology
COVID-19 survivors with cancer history have elevated cancer-mortality risk2Peer-reviewed cohort data (UK Biobank)
Spike protein disrupts p53-MDM2 interaction in cancer cells3Peer-reviewed, preliminary, authors urge caution
Spike protein suppresses (not promotes) growth in A549 lung cancer cells3Peer-reviewed, contradicts pro-cancer narrative
Higher ACE2 expression correlates with lower tumor stemness3Peer-reviewed, correlative/bioinformatic
Spike protein blocks BRCA1/53BP1 DNA repairRETRACTEDWithdrawn 2022 — flawed methodology, unsupported vaccine claims
Long COVID immune exhaustion (T-cell, NK-cell) impairs tumor surveillance2/4Immune findings peer-reviewed; tumor-surveillance link is a proposed synthesis
Persistent spike antigen in Long COVID tissue linked to tumorigenesis-gene expression4Preprint, not peer-reviewed, small sample
Pandemic-era screening delays worsened cancer stage at diagnosis2/3Peer-reviewed modeling and registry studies, multiple countries

9. FAQ

Does the COVID-19 spike protein cause cancer?
No study has established that spike protein causes cancer in humans. The best-supported infection-cancer link is that respiratory viral infection generally (COVID-19 or influenza) can reactivate dormant cancer cells through inflammation — a mechanism that doesn't depend on the spike protein specifically.

What is a cancer stem cell, in simple terms?
A rare cell within a tumor that can self-renew, lie dormant for long periods, and regenerate an entire tumor from a single cell — making these cells disproportionately responsible for relapse, treatment resistance, and metastasis.

Is the BRCA1/53BP1 spike protein study still valid?
No. That paper (Jiang & Mei, 2021, Viruses) was formally retracted in 2022 due to flawed experimental design, and the retraction explicitly states its vaccine-safety conclusions were not supported by the data.

Can having COVID-19 make a cancer in remission come back?
A 2025 Nature study found that in mice, both COVID-19 and influenza infection reactivated dormant breast cancer cells, and human cohort data showed cancer survivors who tested positive for COVID-19 had substantially higher cancer-mortality risk than those who didn't. This is a genuine, peer-reviewed finding, though the exact human effect size (especially for metastasis specifically) is still being refined.

Does this mean COVID-19 vaccination increases cancer risk?
That is a separate claim from what this article addresses. This review covers infection-related biology; our companion article evaluates vaccine-specific "turbo cancer" claims and the state of registry evidence on that question separately.

What can cancer survivors realistically do?
Keep up with cancer screening and surveillance schedules (including catching up on anything delayed during the pandemic), and flag new or unusual symptoms to an oncologist promptly, especially following a respiratory infection.

10. AI Personalization Guide

If you're asking an AI assistant to help you think through your own situation, here's how to get a more useful answer from each:

Claude / ChatGPT: Share your cancer type, stage, treatment status, and any recent respiratory infections, and ask for questions to bring to your oncologist rather than a risk verdict — these models can help you organize what's known versus speculative, but shouldn't be used to self-diagnose reactivation risk.

Gemini: Useful for pulling the latest PubMed-indexed studies on dormancy reactivation or Long COVID immunology if you ask it to search and cite primary sources rather than summarize secondary commentary.

Perplexity: Good for quickly checking whether a specific claim you've encountered (e.g., about a particular mechanism) has a retraction or correction attached — ask it directly to check for retraction notices before treating a cited study as current.

References

  1. Krawczyk N, et al. Expression of Stem Cell and EMT Markers in Circulating Tumor Cells of Breast Cancer Patients. BioMed Research International, 2014.
  2. Ge Y, et al. Epithelial-mesenchymal transition: a hallmark in pancreatic cancer stem cell migration, metastasis, and drug resistance. PMC, 2021.
  3. Nieto MA, et al. Epithelial-Mesenchymal Transition in Cancer: A Historical Overview. ScienceDirect.
  4. Chickarmane V, et al., as cited in Hu J, et al. Cancer Stem Cell Marker Endoglin (CD105) Induces EMT. 2019.
  5. Analysis of Dormancy-Associated Transcriptional Networks Reveals a Shared Quiescence Signature in Lung and Colorectal Cancer. PMC, 2022.
  6. Epithelial-Mesenchymal Transition in Metastatic Cancer Cell Populations Affects Tumor Dormancy in a Simple Mathematical Model. PMC.
  7. [Authors]. Respiratory viral infections awaken metastatic breast cancer cells in lungs. Nature, July 30, 2025. DOI: 10.1038/s41586-025-09332-0.
  8. Dormant cancers can be reawakened by flu, COVID: Study coverage. LiveNOW/FOX, 2025.
  9. COVID significantly increases risk of death from metastatic cancer. Radiology Business, 2025.
  10. Coussens LM, Werb Z. Inflammation and cancer — foundational framework cited throughout the infection-cancer literature.
  11. SARS-CoV-2 spike S2 subunit inhibits p53 activation of p21(WAF1), TRAIL Death Receptor DR5 and MDM2 proteins in cancer cells. bioRxiv, 2024.
  12. Transfected SARS-CoV-2 spike DNA inhibits p53 activation and increases cancer cell viability after chemotherapy. PMC11073320.
  13. SARS-CoV-2 spike protein exerts an anti-cancer effect in A549 cells in association with MEG3 and BCYRN1 regulation. Scientific Reports, 2026.
  14. The SARS-CoV-2 host cell receptor ACE2 correlates positively with immunotherapy response and is a potential protective factor for cancer progression. Science Partner Journal, 2020.
  15. An evidence that SARS-CoV-2/COVID-19 spike protein damages hematopoietic stem/progenitor cells via pyroptosis in an Nlrp3 inflammasome-dependent manner. Leukemia (Nature), 2021.
  16. SARS-CoV-2 spike protein induces cytokine release syndrome by stimulating T cells to produce IL-2. PMC.
  17. Jiang H, Mei Y-F. SARS-CoV-2 Spike Impairs DNA Damage Repair and Inhibits V(D)J Recombination In Vitro. Viruses 2021, 13, 2056. [RETRACTED]
  18. Retraction notice: Viruses 2022, 14, 1011. DOI: 10.3390/v14051011.
  19. Expression of Concern: Viruses 2021, 14, 12. DOI: 10.3390/v14010012.
  20. Missci: Reconstructing Fallacies in Misrepresented Science (annotation of Jiang & Mei misuse in health misinformation). arXiv, 2024.
  21. T-cell exhaustion in COVID-19: what do we know? PMC12605343.
  22. Immune exhaustion in ME/CFS and long COVID. JCI Insight.
  23. Long COVID Immune Dysfunction Linked to NK Cells. Frontiers in Immunology coverage, Autoimmune Institute.
  24. Barouch D, et al. Long COVID involves activation of proinflammatory and immune exhaustion pathways. Nature Immunology, 2025.
  25. Post-COVID-19 pandemic Inflammatory Insights into Cancer. ScienceDirect, 2025.
  26. Long COVID linked to persistence of SARS-CoV-2 spike protein in blood. News-Medical.net, coverage of Swank et al. preprint, 2022.
  27. Persistent spike protein may account for long COVID. Hospital Healthcare Europe.
  28. Persistent SARS-CoV-2 Spike is Associated with Localized Immune Dysregulation in gut tissue. bioRxiv preprint, 2026.
  29. ASCO Updates Guidelines on Vaccines in Patients with Cancer. Targeted Oncology / ASCO guideline, 2026.
  30. NCCN Guidelines: Cancer and COVID-19 Vaccination, Vaccination Advisory Committee.
  31. Modelling the impact of the COVID-19 pandemic on cancer stage migration and excess mortality in Ireland. PMC11924935, 2024.
  32. Delays and disruptions in cervical cancer care during COVID-19 — real-world data from India. medRxiv, 2025.
  33. Reduced Cancer Screening Due to Lockdowns of the COVID-19 Pandemic. PMC9372444.

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