Last Updated:
A study published in the journal Nature on July 30, 2025, shed light on why cancer can suddenly return long after patients are declared cancer-free
Using mouse models of breast cancer, scientists studied the effects of influenza and Covid-19 infection on dormant cancer cells in the lungs.
Recovering from cancer is often seen as the end of a long and gruelling battle. But new scientific evidence suggests that common respiratory infections such as influenza and Covid-19 could reignite cancer years, even decades, after successful treatment.
A study published in the journal Nature on July 30, 2025, shed light on why cancer can suddenly return long after patients are declared cancer-free. Researchers said viral infections may awaken “sleeping” cancer cells that have quietly spread to other organs and remained dormant.
How cancer hides after treatment
Cancer cells can break away from the original tumour and travel to distant organs, a process known as metastasis. These cells, called disseminated cancer cells (DCCs), often settle in organs such as the lungs, bones or liver. In many cases, they remain inactive for years or even decades, evading detection and causing no symptoms. What causes these dormant cells to awaken has remained a mystery, until now.
Viral infections act as a trigger
A research team led by Dr James DeGregori at the University of Colorado Anschutz Medical Campus investigated whether respiratory viruses could be the missing trigger. Using mouse models of breast cancer, scientists studied the effects of influenza and Covid-19 infection on dormant cancer cells in the lungs.
Before infection, only a small number of isolated DCCs were present. But within just three days of influenza infection, the number of cancer cells in the lungs rose sharply. Over the next two weeks, these cells multiplied rapidly, and alarmingly, they remained active even nine months after the virus had cleared. Similar effects were seen in mice infected with Covid.
In experiments conducted on mice, researchers observed dramatic changes. Mice carrying dormant breast cancer cells in their lungs were infected with the influenza A virus. Within just 15 days, the number of cancer cells in their lungs increased between 100 and 1,000 times. The viral infection altered the lung environment in a way that made it more favourable for cancer growth. Alarmingly, even two months after the virus had cleared from the body, the cancer cells remained active.
The infection didn’t just increase cancer cell numbers; it also reduced the proportion of cells that were dormant, effectively pushing them back into an active, tumour-forming state. Researchers from Harvard University and Albert Einstein College of Medicine found that after treatment, some breast cancer cells do not disappear entirely. Instead, they migrate to other organs such as the lungs, bones or liver, where they enter a “sleeping” state. These cells can remain inactive for years and often escape detection through routine medical tests.
The role of inflammation and IL-6
Scientists found that this reawakening was driven by inflammation, particularly by a protein called interleukin-6 (IL-6), which the body produces during infections. Mice that were unable to produce IL-6 showed far less cancer cell growth after infection, with more cancer cells remaining dormant.
Further lab experiments showed that IL-6 directly promoted tumour growth. When breast tissue organoids were treated with IL-6, their growth increased significantly, reinforcing the protein’s role as a key driver.
Immune cells may help cancer grow
The study also uncovered a surprising role played by immune cells. Dormant cancer cells were found clustering near CD4+ T cells in the lungs. When these CD4+ T cells were removed, fewer cancer cells stayed active a month after infection.
At the same time, levels of CD8+ T cells (immune cells that kill cancer and virus-infected cells) increased. These CD8+ cells were also more effective at destroying breast cancer cells, suggesting that CD4+ T cells may indirectly help cancer grow by suppressing the body’s natural cancer-fighting response.
Human data backs the findings
The risk is not limited to animal models. Researchers analysed health records from the UK Biobank, focusing on nearly 5,000 people who had previously had cancer and were believed to be in remission. Those who tested positive for Covid-19 had nearly double the risk of dying from cancer compared to those who did not.
In a separate dataset involving over 36,000 women with breast cancer, Covid-19 infection increased the risk of cancer spreading to the lungs by about 40%.
What this means for cancer survivors
Scientists say these findings help explain why cancer deaths increased during the pandemic and why recurrence can occur years after recovery. The research also points to potential preventive strategies, including therapies that block IL-6 or reduce harmful inflammation during infections.
Explaining the discovery, Dr DeGregori said dormant cancer cells are “like embers left in an abandoned campfire, and respiratory viruses are like a strong wind that reignites the flames”.
Experts stress that more research is needed, but the study highlights the importance of protecting cancer survivors from severe infections and closely monitoring them even long after treatment ends.
December 24, 2025, 21:22 IST
