A common childhood virus you probably never think about may be linked to bladder cancer, and new research is beginning to map the chain of events that could connect the two.
It's established that people who receive kidney transplants have about three times the risk of developing bladder cancer compared with the general population. One idea is that, because transplant patients take immunosuppressive drugs, dormant viruses can wake up and contribute to disease processes.
In a study published December 3 in Science Advances, scientists demonstrated that this particular virus can trigger the kind of DNA damage seen in bladder cancer that appears later in life. Notably, the damage seems to arise from the body's own immune response rather than from direct mutations caused by the virus itself.
Dr. Patrick Moore, a tumor virology researcher at the University of Pittsburgh who was not involved in the study, commented that the work represents a solid laboratory exploration of how BK virus (BKV) could play a larger role in bladder cancer than previously thought.
Connecting the dots
Numerous viral infections can lead to cancer. Some viruses, such as HPV, hijack host cells and insert viral genetic material into the human genome, driving cancer development. In other cancers, including many bladder cancers, no virus is detectable in tumor tissue, yet signs of past viral infection are present in the genetic record.
Senior study author Simon Baker, a cancer researcher at the University of York, notes that traditional views have long credited smoking and industrial exposures as major causes of bladder cancer. However, the pattern of DNA mutations in these cancers does not align with what chemical carcinogens typically cause.
Instead, bladder tumors tend to show mutational signatures associated with a family of enzymes called APOBEC. Normally, APOBEC enzymes help defend against viruses by editing genetic material. Baker explains that these APOBEC signatures are a hallmark of the body’s antiviral defenses.
In the experiments, researchers exposed healthy human bladder cells to BK virus in the lab. The cells accumulated mutations similar to those found in bladder cancer and showed heightened activity of APOBEC3, an enzyme that targets viral genomes during infection.
Crucially, when APOBEC3 was disabled, subsequent BK virus infection did not produce the same DNA damage. This points to the host’s own APOBEC3 enzyme—driven by the immune response—as the culprit behind the cancer-like mutations, rather than the virus directly causing those mutations.
The team also observed increased APOBEC3 expression and cancer-like genetic changes in nearby cells that were not infected by BK virus themselves, suggesting that a local infection can influence distant cells to accumulate mutations.
That was unexpected, Baker says, but it makes sense given that bladder cancers often lack detectable viruses. This line of evidence helps explain how an infection early in life might contribute to cancers diagnosed many years later.
A starting point for future work
These findings are significant but preliminary. Moore emphasizes the need to determine whether bladder cancer patients show higher rates of BK virus infection than people without cancer.
The idea is intriguing, but more work is necessary to establish how important this mechanism truly is for human cancer.
BK virus typically causes mild cold-like symptoms in childhood and then remains dormant in the kidneys and urinary tract. For most individuals, it never causes trouble and is not routinely tested outside hospital settings.
For transplant patients, immunosuppressive therapy designed to prevent organ rejection can reactivate BK virus. This reactivation may harm the kidneys, ureters, and bladder.
Tim Tavender, a kidney transplant recipient from Southampton, developed BK virus after his transplant and later bladder cancer. He told The Independent that the new research offers hope that scientists can find ways to control BK virus, potentially sparing others from similar experiences.
Disclaimer: This article is for informational purposes and does not constitute medical advice.
Jennifer Zieba earned a PhD in human genetics from UCLA. She now works as a project scientist in UCLA’s orthopedic surgery department, focusing on identifying mutations and potential treatments for rare genetic musculoskeletal disorders. She enjoys translating complex science for a broad audience and writes as a freelance contributor for various outlets.
