Papillomaviruses cause non-melanoma skin cancer

UV radiation has been known for a long time to be a risk factor for the development of skin cancer. Simultaneous infection with human papillomaviruses (HPV) has also been suspected to promote skin cancer, particularly in organ transplant recipients.

Papillomaviruses associated with UV light promote the development of non-melanoma skin cancer. The investigators provide an explanation why the viruses can be detected in benign human cancer precursors but not in advanced carcinoma.
Everyone is infected with skin-typical ("cutaneous") human papillomaviruses (HPV) at some point in their lives, usually in early childhood.

In healthy people, the immune system can fight off the viruses, but this often changes in older age. Recipients of organ transplants whose immune system is suppressed by long-term drug therapy to prevent transplant rejection are particularly at risk. Ultraviolet radiation exposure is generally known to be a major risk factor for skin cancer. Non-melanoma skin cancer occurs primarily on sun-exposed sites of the body.

Researchers used a specific species of mice that usually contracts infection with papillomaviruses shortly after birth, like humans. They compared the virus-infected animals with control animals that were raised in a completely virus-free environment. They exposed the animals to UV radiation at a dose that could be expected during a vacation in Mediterranean regions.

Subsequently, only virus-infected animals developed non-melanoma skin cancer (squamous cell carcinoma ) while the virus-free control animals did not. They noticed a glance that a group of tumors was keratinizing while the other one was not. The keratinizing tumors contained large amounts of viruses - a situation that is also found in precursors of cancer (so-called "actinic keratosis") in humans.

This is a condition where cells of the upper skin layers have started to grow excessively while still resembling the original structure of the skin. The researchers demonstrated that the viruses affect the stability of the host cell's DNA, thus promoting the accumulation of UV-related damage.
By contrast, the second group of tumors did not contain any viruses. This is also the case in patients with advanced carcinoma.

However, tests for antibodies in the animals' blood revealed prior infection with the virus. These tumors exhibited a striking rate of mutations in a gene called p53, which is crucially important for the cell and is regarded the "guardian of the genome". This gene is also defective in many cases of human squamous cell carcinoma, leading to uncontrolled cellular growth.

When the cells grow out of control, the tumor turns more cancerous. The viruses, which are now no longer needed for the tumor to grow, are thus prevented from replicating further. Up until now, the loss of viruses in advanced cases of carcinoma has been a major argument against a role of cutaneous papillomaviruses in the development of cancer.
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