Primary polyomavirus infection, not reactivation, as the cause of trichodysplasia spinulosa in immunocompromised patients
Classic human polyomaviruses (JC and BK viruses) become pathogenic when reactivating from latency. For the rare skin disease trichodysplasia spinulosa, we show that manifestations of the causative polyomavirus (TSPyV) occur during primary infection of the immunosuppressed host. High TSPyV loads in blood and cerebrospinal fluid, sometimes coinciding with cerebral lesions and neuroendocrine symptoms, marked the acute phase of trichodysplasia spinulosa, whereas initiation and maturation of TSPyV seroresponses occurred in the convalescent phase. TSPyV genomes lacked the rearrangements typical for reactivating polyomaviruses. These findings demonstrate the clinical importance of primary infection with this rapidly expanding group of human viruses and explain the rarity of some novel polyomavirus-associated diseases.
|Keywords||Cidofovir, Dissemination, Polyomavirus, Primary infection, Reactivation, Trichodysplasia spinulosa, Viral load|
|Persistent URL||dx.doi.org/10.1093/infdis/jiw403, hdl.handle.net/1765/100370|
|Journal||The Journal of Infectious Diseases|
van der Meijden, E, Horváth, B. (Barbara), Nijland, M. (Marcel), de Vries, K, Rácz, E, Diercks, G.F. (Gilles F.), … Feltkamp, M.C.W. (2017). Primary polyomavirus infection, not reactivation, as the cause of trichodysplasia spinulosa in immunocompromised patients. The Journal of Infectious Diseases, 215(7), 1080–1084. doi:10.1093/infdis/jiw403