Bladder cancer might trace its origins not just to smoking or chemical exposure — but to a very common virus most people catch in childhood, according to new research led by scientists at University of York. The findings, published in Science Advances, suggest that the body’s own immune response to the virus — rather than the virus itself — could trigger DNA damage in bladder cells, setting the stage for cancer decades later.
The virus in question, BK virus, typically infects most people in childhood and then remains dormant in the kidneys. Under certain conditions — such as weakened immunity with age — it can reactivate. The researchers exposed human urothelial cells (the tissue lining the bladder and urinary tract) to BK virus in a lab setting and observed what happened.
During the immune battle against BK virus, cells activate a group of antiviral enzymes designed to disable the virus. But these enzymes appear to hit the cell’s own DNA as collateral damage. Over time, this “friendly fire” leaves mutations in patterns that resemble those found in the DNA of bladder cancer cells.
Unexpectedly, the DNA damage affected not only cells directly infected by the virus — but also neighboring cells that remained virus-free. This “bystander effect” may help explain a decades-old mystery: many bladder cancers show no trace of BK virus when diagnosed, even if the virus could have triggered the initial mutation.
Although around 95% of adults have been exposed to BK virus during childhood, bladder cancer remains comparatively rare — the study notes roughly 10,000 new diagnoses per year in the UK, most in older adults. Nonetheless, individuals such as kidney transplant recipients — whose immune systems are intentionally suppressed — face substantially higher risk, which has long been linked with BK reactivation.
The researchers are now calling for follow-up clinical studies to examine whether BK virus exposure — combined with other risk factors like smoking — indeed raises the chance of later bladder cancer. If the link is confirmed, it could open new avenues for early intervention, possibly even prevention, by targeting initial viral infections rather than waiting to treat full-blown cancer.
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