Primary Polyomavirus Infection, Not Reactivation, as the Cause of Trichodysplasia Spinulosa in Immunocompromised Patients. (30th August 2016)

• Record Type: Journal Article
• Authors: van der Meijden, Els; Horváth, Barbara; Nijland, Marcel; de Vries, Karin; Rácz, Emo˝ke; Diercks, Gilles F.; de Weerd, Annelies E.; Clahsen-van Groningen, Marian C.; van der Blij-de Brouwer, Caroline S.; van der Zon, Arnulfo J.; Kroes, Aloys C. M.; Hedman, Klaus; van Kampen, Jeroen J. A.; Riezebos-Brilman, Annelies; Feltkamp, Mariet C. W.
• Is Part Of: Journal of infectious diseases. Volume 215:Number 7(2017:Apr. 01)
• Page Start: 1080
• Page End: 1084
• Publication Date: 2016-08-30
• Subjects: polyomavirus -- trichodysplasia spinulosa -- primary infection -- reactivation -- dissemination -- viral load -- cidofovir; Communicable diseases -- Periodicals; Diseases -- Causes and theories of causation -- Periodicals; Medicine -- Periodicals; Communicable Diseases -- Periodicals; Electronic journals; 616.9
• DOI: 10.1093/infdis/jiw403
• Languages: English
• ISSNs: 0022-1899

Abstract

Abstract: 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.