Trichodysplasia Spinulosa Small T Antigen Drives Ectopic Hair Follicle Development in Adult Transgenic Mice

    Li-Jyun Syu, D. Wilbert, E. van der Meijden, Mariet C.W. Feltkamp, Andrzej A. Dlugosz
    TLDR The Trichodysplasia spinulosa virus protein can cause abnormal hair growth in mice.
    The study investigated the role of the Trichodysplasia spinulosa polyomavirus (TSPyV) small T antigen (sTAg) in hair follicle development by generating transgenic mice with a Cre-inducible TS sTAg transgene. Expression of sTAg in adult mice skin led to the formation of numerous dysmorphic hair follicles, even in normally hairless areas, indicating ectopic hair follicle development. These follicles showed activation of the Wnt and Hedgehog signaling pathways, as evidenced by high levels of beta-catenin, nuclear Lef1, and GLI1. The study also found similar beta-catenin accumulation in human TS cases. This research provided the first evidence of a polyomavirus early protein engaging specific signaling pathways crucial for hair follicle development, suggesting a mechanism for productive viral infection in TS.
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