Can COVID-19 and Influenza Awaken Dormant Cancer Cells?

Introduction

As the world continues to manage the long-term consequences of the COVID-19 pandemic, scientists are uncovering complex and sometimes alarming connections between respiratory viruses and chronic diseases. Among the most concerning discoveries is the potential for common respiratory infections—particularly COVID-19 and influenza—to reactivate dormant cancer cells.

New research indicates that patients who have been in remission from cancers such as breast cancer may remain vulnerable to disease resurgence years or even decades after successful treatment. This risk appears to increase following infections with certain respiratory viruses, which may act as a biological trigger that "awakens" silent cancer cells hidden in organs like the lungs.

These findings carry profound implications for how we think about viral infections and cancer recurrence, especially in a post-pandemic world. Could a simple case of the flu be enough to reignite cancer in someone thought to be cured? Let’s dive into the emerging science.

Dormant Cancer Cells: The Hidden Threat

After successful treatment, many cancer survivors carry residual cancer cells in their bodies—cells that have not been destroyed by chemotherapy, radiation, or surgery but instead enter a dormant state. These disseminated cancer cells (DCCs) can remain inactive for years, evading detection by the immune system and medical imaging. In breast cancer, particularly, these DCCs are often found in tissues like the lungs, liver, or bone marrow.

The biggest concern is that, under certain conditions, these dormant cells can become active again, leading to cancer recurrence or metastasis, often with more aggressive behavior than the original tumor.

The COVID-19 Clue

The connection between respiratory viruses and dormant cancer cells came into sharper focus during and after the COVID-19 pandemic. Researchers, including Dr. James DeGregori, a molecular geneticist at the University of Colorado, began noticing a suspicious increase in cancer-related deaths following waves of SARS-CoV-2 infections.

According to a study published in 2025, cancer survivors who contracted COVID-19 were found to be twice as likely to die from cancer than those who avoided infection. This surprising correlation sparked deeper investigations into the potential relationship between viral infections and cancer reactivation.

As Dr. DeGregori noted, “These dormant cancer cells are like embers buried under ash. A virus like COVID-19 can act like a strong wind, fanning them back into flame.”

Influenza and Other Viruses: Not Innocent Bystanders

While SARS-CoV-2 drew the initial attention, researchers also discovered similar patterns with influenza viruses, particularly Influenza A. Animal studies using mouse models demonstrated that both influenza and COVID-19 infections can activate dormant breast cancer cells in the lungs. Infected mice showed rapid cancer progression—tumors grew 100 times faster within two weeks of infection.

What was especially revealing in these studies was that the cancers did not appear to be caused by the viruses directly. Rather, the immune response to infection, particularly the inflammatory response, created an environment in which dormant cells could “wake up” and proliferate.

Inflammation: The Silent Catalyst

One of the most critical mechanisms behind this phenomenon appears to be inflammation. When the body fights a viral infection, it releases cytokines, proteins that mediate and regulate immunity, inflammation, and hematopoiesis. Among these, interleukin-6 (IL-6) plays a particularly influential role.

Increased levels of IL-6, as seen in both COVID-19 and severe influenza infections, have been shown to activate dormant cancer cells in mice. These findings suggest that it’s not necessarily the virus itself, but the body’s inflammatory response to the virus, that can tip the balance from dormancy to disease.

This idea is not entirely new. IL-6 has been implicated in various cancers for years, but its role in reawakening previously treated cancers is a more recent revelation.

Supporting Evidence from Human Data

In addition to animal studies, human epidemiological data supports these findings. An analysis of the UK Biobank, a large health database, revealed that individuals previously treated for cancer and later infected with SARS-CoV-2 had a significantly higher rate of cancer-related mortality.

Another U.S.-based study involving over 37,000 breast cancer patients found that those who had COVID-19 had a 40% higher risk of experiencing lung metastases—a common site for dormant breast cancer cells to reactivate.

Roel Vermeulen, an epidemiologist at Utrecht University, emphasized, “This level of increased risk is almost unprecedented in cancer epidemiology.”

A Broader Pattern: Other Cancer-Linked Viruses

The relationship between viruses and cancer is not without precedent. Several viruses have long been associated with cancer initiation and progression. For example:

Epstein-Barr virus (EBV) is linked to lymphomas and nasopharyngeal cancer.

Human papillomavirus (HPV) is the leading cause of cervical cancer.

Hepatitis B and C viruses are major risk factors for liver cancer.

In breast cancer research, scientists have been searching since the 1930s for a viral link. While conclusive proof has remained elusive, EBV has been found in breast cancer tissue at five times the rate found in normal tissue, suggesting a possible connection.

How Respiratory Viruses May Influence Cancer Recurrence

To understand how respiratory viruses might reawaken cancer, researchers are exploring several biological pathways:

Immune Suppression and Exhaustion
Viral infections can weaken or confuse the immune system, reducing its ability to suppress dormant cells.

Inflammatory Cytokine Storms
Respiratory viruses often trigger cytokine storms, especially IL-6, which can act as a growth signal for DCCs.

Microenvironment Changes
Infected tissues may undergo changes in oxygenation, blood flow, and immune surveillance, making them more hospitable to cancer growth.

Epigenetic Shifts
Some viruses can influence gene expression in host cells, potentially “unlocking” dormant traits in cancer cells.

Implications for Cancer Survivors

These findings bring up urgent questions for the millions of people living in remission from cancer:

Should cancer survivors take extra precautions during flu season?

Are COVID-19 and flu vaccines enough to prevent this phenomenon?

Could new therapies be developed to specifically suppress dormant cell activation?

Dr. DeGregori emphasizes the importance of continued vigilance:
“If you’re someone who has been treated for cancer and still has dormant cells, you could live a normal life and never be affected. But if you get a respiratory infection like COVID or the flu, the odds of a dangerous reactivation increase significantly.”

The Road Ahead: Research and Prevention

While the research is compelling, scientists caution that more work is needed to fully understand the mechanisms and risks involved. Specifically, clinical trials are needed to determine whether vaccines against COVID-19 and influenza can reduce the risk of cancer recurrence in those with dormant cells.

Moreover, studies are now underway to explore:

Whether anti-inflammatory therapies might be effective in preventing reactivation.

How long dormant cells remain susceptible to viral reactivation.

Whether certain cancers are more vulnerable to this effect than others.

What Can Patients Do?

For now, experts recommend that cancer survivors take practical steps to protect themselves, especially during viral outbreaks:

Get vaccinated against respiratory viruses like influenza and COVID-19.

Avoid crowded or high-risk environments during flu and cold seasons.

Consult oncologists about personalized risk assessments.

Monitor for unusual symptoms, even long after remission.

Conclusion

The idea that a common viral infection could awaken a long-silent cancer may sound like science fiction, but it is becoming an increasingly well-supported scientific reality. As researchers continue to probe this connection, the medical community may need to rethink long-held assumptions about cancer remission and recurrence.

For survivors of cancers like breast cancer, the end of treatment is not the end of vigilance. With viruses like COVID-19 and influenza potentially acting as triggers for recurrence, the fight may continue in quieter, hidden ways—requiring new strategies for monitoring, prevention, and protection.

Understanding and addressing this hidden risk could transform survivorship care and save countless lives in the decades to come.