Among normal tissue with oncogenic somatic mutations, sun-exposed skin has the highest mutational burden caused by UV exposure. While immunosuppression disrupts normal skin homeostasis, raising the risk of skin cancer development, the precise role of the immune system in this progression was previously unclear. Now, Son et al. find that commensal papillomavirus maintains homeostasis and suppresses mutant clone expansion in sun-damaged skin.

To further assess the role of CD8+ T cells, B6 nude mice, which lack functional T cells, were injected with CD8+ memory T cells from wild-type B6 mice infected with MmuPV1or VLP. The B6 nude mice were then infected with MmuPV1 or VLP, and upon exposure to UV, virus-specific CD8+ T cells could target and block the expansion of mutant p53 clones.