Breast cancer survivors have lived with a guarded sense of relief. Even after beating the disease, the possibility of recurrence remains a faint shadow but new research has raised an alarming possibility- respiratory viruses, including common ones like influenza and SARS-CoV-2, may act as a catalyst, reawakening dormant breast cancer cells that linger quietly in the lungs long after remission.In a new study published in Nature, researchers from the University of Colorado and Utrecht University have found that viral infections can reignite cancer’s flame literally. Dormant cancer cells are like the embers left in an abandoned campfire, and respiratory viruses are like a strong wind that reignites the flames.This study marks a crucial turning point in how we understand long-term remission and highlights the importance of continued vigilance among cancer survivors.Also Read: Legionnaires Outbreak: All That You Need To Know About The Disease That Killed 1 And Left 22 Sick In New YorkWhy COVID-19 Infection Is First Red Flag?The investigation kicked off in the aftermath of the COVID-19 pandemic. Clinicians and researchers began to notice an uptick in metastatic cancer cases, especially among individuals previously in remission. Something wasn’t adding up. Cancer recurrences were occurring at an unusual rate and too often to be dismissed as coincidence.The researchers turned to two key data sources: the UK Biobank and a large U.S. breast cancer database with over 37,000 patient records. In the UK Biobank cohort, survivors who had contracted COVID-19 exhibited a twofold increase in cancer-related mortality. In the U.S. dataset, those with prior SARS-CoV-2 infection faced a more than 40% increase in metastatic breast cancer, particularly in the lungs.The extent of this increased risk is almost unheard of in cancer epidemiology, it’s a significant effect.What’s Happening in the Body?To understand the mechanics, the researchers turned to mouse models—long used as reliable proxies for studying human disease behavior. When the mice with previously dormant breast cancer cells were infected with either SARS-CoV-2 or influenza A, it took only days for those latent cells to wake up. Within two weeks, there was a more than 100-fold increase in metastatic tumor burden in the lungs.Here’s the crucial insight, the cancer cells didn’t reawaken because the virus directly interacted with them. Instead, the viruses triggered an inflammatory immune response, rich in signaling proteins called cytokines—especially interleukin-6 (IL-6). This cytokine storm appeared to create an environment ripe for dormant cancer cells to start proliferating again.According to lead researcher Shi Chia from the University of Colorado, “Although species differences warrant caution in interpreting mouse data… collectively, these findings underscore the substantial metastatic risk COVID-19 posed to cancer survivors.”Role of Viruses in Cancer BiologyThe link between viruses and cancer isn’t new. Human papillomavirus (HPV) has long been known to cause cervical and other cancers. The Epstein-Barr virus (EBV) has been implicated in several types of lymphoma. In fact, EBV has been found in five times higher concentrations in breast cancer tissue compared to healthy tissue.The idea that viruses could influence cancer development or recurrence has been around since the 1930s, particularly in mouse models. But this new research is among the first to show how non-oncogenic, respiratory viruses—those not traditionally associated with cancer—might still play a key role in its resurgence.Role of Inflammation and the Immune SystemOne of the most compelling parts of the study is the insight into how the immune system's response, not the virus itself, may be the real driver of cancer recurrence.After remission, it’s common for a few cancer cells known as dormant disseminated cancer cells (DCCs), to remain hidden in tissues like the lung, bone, or liver. These DCCs are typically inactive, posing no threat unless triggered.Inflammatory responses to infections, especially those that involve cytokines like IL-6, appear to disturb this dormancy. In simple terms, inflammation acts like a wake-up call for these sleeping cells.The researchers demonstrated that only when the viral infections resulted in elevated levels of inflammatory markers did the dormant cells awaken. This opens up new avenues for therapeutic research focused on blocking inflammation, rather than targeting cancer cells directly.What This Means for Breast Cancer Survivors?This is not a reason for panic but it is a call for caution. As DeGregori explains, “If you are a cancer patient who has these dormant cells, you may end up living a normal life and dying with these dormant cells, instead of dying because those dormant cells awakened. But if you get a respiratory virus like influenza or COVID, your chance of dying from those dormant cells awakening is much greater.”Millions of breast cancer survivors around the world, many of whom are years or even decades into remission—could unknowingly carry dormant cells. For them, a common respiratory illness may no longer be just an inconvenience; it may be a risk factor for relapse.Could Vaccination Be Protective?Can we reduce this risk with vaccines? It’s too early to say definitively, but the idea is promising. If viral infections act as a trigger, then preventing infection might, in turn, prevent relapse.DeGregori’s team is now exploring whether flu and COVID-19 vaccinations could lower the likelihood of dormant cell reactivation. This would have wide-ranging implications not just for cancer survivors, but for public health policy as a whole. The idea that a respiratory virus could reignite cancer long after remission is unsettling but not entirely surprising. As science continues to unravel the complex relationship between our immune system, viruses, and cancer, this study offers one clear message:Remission isn’t always the end and staying healthy may mean more than avoiding recurrence it could mean avoiding infection altogether.