New research reveals viruses may reactivate dormant cancer cells

Understanding the Link Between Viral Infections and Cancer Relapse

Breast cancer survivors often live with the fear that the disease may return. This anxiety is understandable, as many relapses and cases of metastatic cancer are not caused by new tumors but by dormant cancer cells that were previously inactive. These sleeper cells can reside in areas like the lungs or bones, waiting for the right conditions to become active again.

For years, scientists have sought to understand what triggers these dormant cells to awaken. There were hints that chronic inflammation, such as that caused by smoking or aging, might play a role. However, recent research has provided new insights, suggesting that common respiratory infections like the flu or COVID-19 can also act as triggers.

The Role of Immune Response in Cancer Cell Reactivation

In a groundbreaking study, researchers used mice with engineered breast cancer cells that mimic the behavior of dormant human cancer cells in the lungs. They infected these mice with either the influenza virus or the SARS-CoV-2 virus. What they found was both revealing and concerning: within days of infection, the previously inactive cancer cells began to multiply rapidly and form new metastatic lesions in the lungs.

Surprisingly, it wasn’t the viruses themselves that caused this reaction. Instead, the immune response to the infection was responsible. The body’s immune system releases a molecule called interleukin-6 (IL-6), which normally helps fight off invaders. However, during viral infections, IL-6 levels can spike, creating an environment that allows dormant cancer cells to become active.

The Impact of IL-6 on Cancer Cells

When the researchers disabled IL-6 in the mice, the dormant cancer cells did not multiply as much when exposed to the virus. This suggests that IL-6 acts as a crucial switch, enabling cancer cells to transition from a dormant state to an active, proliferative one.

The reawakening of cancer cells does not last indefinitely. After about two weeks, the activity typically subsides, and the cells often return to dormancy. However, each infection leaves behind more awakened cancer cells, increasing the risk of future relapses. This creates a cycle where each episode amplifies the threat.

The Role of Helper T Cells

Another factor in this process involves helper T cells, a type of immune cell. Rather than destroying the cancer cells, these cells seem to protect them from other immune attacks. This highlights how cancer can exploit the body's defenses, turning them into allies rather than enemies.

Real-World Implications

While the experiments were conducted on mice, researchers also analyzed data from thousands of cancer survivors in the UK and the U.S. during the COVID-19 pandemic. They found that patients who had recently experienced respiratory infections faced nearly double the risk of dying from cancer compared to those who did not get infected. This pattern was most evident in the months following infection, aligning with the findings from the mouse studies.

This link between viral infections, inflammation, and cancer relapse could explain why cancer death rates increased early in the pandemic, particularly among those with a history of breast or other cancers.

Preventive Measures and Future Research

These findings underscore the importance of protecting against respiratory infections for cancer survivors. Measures such as vaccination and prompt treatment of infections could become essential components of long-term care. Additionally, drugs targeting IL-6, already used for conditions like Castleman’s disease and COVID, may offer potential benefits for cancer survivors.

While this research is still in its early stages, it offers hope for new strategies to prevent cancer relapses. By understanding and intercepting the signals that awaken dormant cancer cells, it may one day be possible to stop relapses before they occur, significantly improving outcomes for survivors.