Scientists are investigating a common childhood infection that may be linked to bladder cancer, uncovering the chain reaction that could connect the two conditions.
People who receive kidney transplants are three times more likely to develop bladder cancer than the general population. Researchers have long suspected that immunosuppression in transplant patients allows dormant viruses in the body to reactivate.
One of these viruses is BK virus (BKV), also called human polyomavirus type I, a cold-like virus that infects roughly 95% of people during childhood. After initial infection, BKV remains dormant in the kidneys. This raises a question: can the virus trigger cancer years later?
A study published Dec. 3 in Science Advances suggests it can. The research shows that BKV can induce DNA damage resembling that found in bladder cancer. Surprisingly, the damage appears to result not directly from the virus, but from the body’s immune response.
“This is a nicely done laboratory study showing a possible way that BKV could play a larger role in bladder cancer than previously thought,” said Dr. Patrick Moore, a tumor virologist at the University of Pittsburgh, who was not involved in the study.
How a Virus Can Lead to Cancer
Some viruses, like HPV, can trigger cancer by inserting their genetic material into human cells. But many bladder cancers show no traces of a virus, despite carrying genetic signs of past viral infection.
“Since the 1950s, the prevailing view has been that smoking and industrial exposures are the main causes of bladder cancer,” said senior author Simon Baker, a cancer researcher at the University of York in the U.K. However, DNA mutations in bladder cancer differ from those caused by chemicals. Instead, they show patterns linked to enzymes called APOBECs, which normally defend the body against viruses.
Baker’s team infected healthy human bladder cells with BKV in the lab. The cells showed mutations similar to bladder cancer and increased activity of APOBEC3, an enzyme that attacks viral genomes. When APOBEC3 was deactivated, the DNA damage disappeared, indicating the enzyme, not the virus, caused the mutations.
The researchers also found that neighboring “bystander” cells that were not infected exhibited similar genetic damage. “This makes sense because bladder cancers don’t contain viruses,” Baker explained. The finding sheds light on how early-life viral infections could contribute to cancers decades later.
Related topic：
