Merkel Cell Polyomavirus Infection And Persistence Modeled In Skin Organoids

This study utilizes an iPSC-derived hair-bearing skin organoid system to model Merkel cell polyomavirus (MCPyV) infection and persistence, which is crucial for understanding its role in Merkel cell carcinoma. The research demonstrates that MCPyV can efficiently infect and persist in dermal fibroblasts, particularly papillary and dermal sheath fibroblasts, by maintaining a quasi-latency state. The virus evades the innate immune response, but treatments like interferon-beta and ruxolitinib can suppress or stimulate viral replication. This model closely mimics human conditions, providing a valuable platform for studying viral interactions with the immune system and testing potential treatments to control viral reactivation and tumor development.