Could a Common Flu or COVID-19 Trigger Cancer Recurrence Years Later? New Study Raises Concerns

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Study Suggests Flu and COVID-19 Could Trigger Cancer Recurrence Years After Remission

Recovering from cancer is often seen as the end of a long and gruelling battle. However, new research indicates that common respiratory infections like influenza and COVID-19 could potentially reactivate cancer cells years—even decades—after successful treatment.

A study published in Nature on July 30, 2025, sheds light on why cancer can return long after patients are declared cancer-free. Researchers found that viral infections may “wake up” dormant cancer cells—disseminated cancer cells (DCCs)—that have spread to other organs and remained inactive.

Dormant cancer cells and metastasis
After treatment, some cancer cells migrate to organs such as the lungs, bones, or liver, where they can remain in a “sleeping” state for years, evading detection. Until now, what triggers these dormant cells to reactivate remained unclear.

Viruses as a trigger
Led by Dr. James DeGregori at the University of Colorado Anschutz Medical Campus, researchers studied mouse models of breast cancer. They found that influenza or COVID-19 infection dramatically increased the number of dormant cancer cells in the lungs. Within days, these cells multiplied rapidly, and alarmingly, remained active months after the virus had cleared.

In one experiment, mice with dormant breast cancer cells infected with influenza A saw cancer cell numbers increase between 100 and 1,000 times in just 15 days. Similar results were observed with COVID-19 infections.

Inflammation and IL-6 drive reactivation
The study identified interleukin-6 (IL-6), a protein produced during infections, as a key factor. IL-6 promotes tumor growth and reduces dormancy in cancer cells. Mice unable to produce IL-6 showed significantly less cancer activity post-infection, highlighting its critical role.

Immune cells may aid cancer growth
Dormant cancer cells clustered near CD4+ T cells in the lungs. Removing these CD4+ cells reduced cancer activity, while CD8+ T cells, which attack cancer cells, became more effective—suggesting that some immune responses may unintentionally support cancer growth.

Human data supports the findings
Analyses of nearly 5,000 cancer survivors in the UK Biobank revealed that those who contracted COVID-19 had almost double the risk of dying from cancer. In another dataset of 36,000 women with breast cancer, COVID-19 infection increased the risk of lung metastasis by around 40%.

Implications for survivors
The findings may explain the rise in cancer deaths during the pandemic and highlight why recurrence can occur long after recovery. Potential strategies include targeting IL-6 or managing inflammation during infections.

Dr. DeGregori explained, “Dormant cancer cells are like embers in an abandoned campfire, and respiratory viruses are like a strong wind that reignites the flames.” Experts emphasize the need for cancer survivors to be protected from infections and monitored closely, even years after treatment.

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