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In this study, human dermal fibroblasts were identified as natural host cells that support productive Merkel cell polyomavirus infection, and the MEK antagonist trametinib was introduced as an effective inhibitor to control the virus.

This study found that the development of Merkel cell carcinoma from hair follicles in mice can be driven by in vivo reprogramming with ATOH1 and relies on p53 loss for progression.

This study suggests that Merkel cell polyomavirus T antigen-positive cells resembling Merkel cell carcinoma may originate from epithelial cells in human hair follicles, potentially informing future transgenic mouse models for this cancer.

This study demonstrates that an iPSC-derived skin organoid model effectively supports Merkel cell polyomavirus infection, persistence, and immune evasion, providing a valuable platform for studying viral tumorigenesis and testing treatment strategies.

This review summarizes current evidence on how beta-human papillomavirus and Merkel cell polyomavirus may contribute to the development of nonmelanoma and Merkel cell skin carcinomas, respectively, but it reports no new clinical findings.