On the 13th, Professor Shadmehr Demehri and his research team from the Cancer and Immunology Center at Massachusetts General Hospital (MGH), affiliated with Harvard University, announced in the international journal Cancer Cell that they have demonstrated that the virus beta HPV present in the skin activates T cells, aiding in the recovery of skin damaged by ultraviolet light. /Courtesy of News1

The representative cause of skin cancer is exposure to ultraviolet rays. Prolonged exposure damages DNA, leading to mutations in cells that cause cancer. A study by U.S. researchers suggests that human papillomavirus (HPV), which resides in human skin, can destroy mutated cells caused by ultraviolet exposure, potentially preventing skin cancer. The virus, previously thought to induce cancer, actually plays a role in preventing it.

Researchers from the Cancer and Immunology Center at Massachusetts General Hospital (MGH), affiliated with Harvard University, noted on the 13th in the international journal Cancer Cell that 'beta HPV activates immune cells called T cells to restore skin damaged by ultraviolet radiation.'

Skin cancer is a rapidly increasing cancer. Due to aging populations and skin aging from global warming, the ozone layer, which used to block ultraviolet rays, has been destroyed, leading to a more than doubling of patients worldwide. The situation in South Korea is similar. According to data from the National Health Insurance Service, the number of patients visiting hospitals for skin cancer increased by 34% from 23,605 in 2018 to 31,661 in 2022.

There are over 200 types of HPV. Among them, alpha HPV infects mucous membranes, such as the throat and cervix, causing cancer. Research has also indicated that beta HPV can induce squamous cell carcinoma, a type of skin cancer.

However, according to the researchers, beta HPV quickly multiplies in skin damaged by ultraviolet rays, encouraging the immune system to eliminate damaged cells. Professor Demehri's team previously found that mice infected with beta HPV are less likely to develop skin cancer when exposed to ultraviolet rays compared to other mice.

The researchers further studied the effects of beta HPV in this research. They conducted comparisons using hairless mice commonly used for skin studies, dividing them into two groups: one infected with beta HPV and the other not infected, both of which were exposed to ultraviolet radiation for several months.

In the experimental results, both groups of mice showed mutated cells in their skin, but the group infected with beta HPV had significantly smaller mutated cells. The researchers explained that these results indicate that beta HPV suppresses cancer-causing mutated cells. In fact, examination of the skin of the mice infected with beta HPV revealed a greater presence of cytotoxic T cells, immune cells capable of killing cancer cells.

The effect of inhibiting skin cancer appeared only in cases infected with beta HPV. When the researchers infected mice with another skin virus, polyomavirus, and exposed them to ultraviolet rays, there was no significant difference from the group not infected with the virus.

Professor Demehri's team is currently researching additional methods for enhancing T cell responses against HPV to help people prevent skin cancer. They have also recently filed a patent related to this approach.

Other scientists have expressed a cautious attitude, indicating that further research is needed. Richard Roden, a virologist at Johns Hopkins University, said, 'This study contrasts with earlier research that suggested beta HPV causes skin cancer, and for now, both sides are compelling.' Johann Gudjonsson, a professor at the University of Michigan, noted, 'This study is impressive, but we need to investigate whether the mechanism applies only to the skin or can occur in other tissues.'

Reference materials

Cancer Cell (2024), DOI; https://doi.org/10.1016/j.ccell.2024.11.013

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