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Volume 32, Number 10—October 2026
Research Letter
Evaluation of Trichodysplasia Spinulosa Polyomavirus in Skin Biopsies, United States
Suggested citation for this article
Abstract
Trichodysplasia spinulosa polyomavirus (TSPyV) has been identified in human endothelial cell tumors. We evaluated 25 clinical cases of various inflammatory dermatoses in California, USA, for TSPyV by using RNAscope in situ hybridization. We did not detect TSPyV in any of the biopsy samples, suggesting that endothelial TSPyV is uncommon in inflammatory dermatoses.
Trichodysplasia spinulosa polyomavirus (TSPyV) typically causes folliculocentric cutaneous eruptions, usually on the face, although the virus has been detected in tonsillar tissue, blood, urine, cerebrospinal fluid, and respiratory specimens (1–4). Recently, TSPyV was identified within the endothelial cells of tumors from 3 separate patients by analyzing off-target next-generation sequencing reads (5). Subsequently, in situ hybridization demonstrated the localization of TSPyV to intratumoral endothelial cells. The significance of TSPyV within endothelial cells in those cases is uncertain. Of note, all 3 patients received corticosteroids immediately before tumor resection.
We hypothesized that TSPyV might be found in vasculitides or other cutaneous inflammatory conditions. We evaluated skin biopsy samples from 25 patients with inflammatory dermatologic conditions. Of the 25 patients, 13 received corticosteroids before skin biopsy. Among those patients, 10 were treated with corticosteroids within 10 days of the biopsy. Three patients had longer intervals between the corticosteroid dose and the biopsy, with intervals of 108 days, 1,494 days, and 1949 days between the corticosteroid administration and the biopsy. The biopsy samples included leukocytoclastic vasculitis (n = 5), medium-vessel vasculitis (n = 1), interface dermatitis (n = 6), perniosis (n = 2), tumid lupus (n = 1), erythema nodosum (n = 4), calciphylaxis (n = 1), and nonspecific epidermal dermatoses (n =5). In addition, 1 sample of trichodysplasia spinulosa was included as a positive control.
Figure
We performed in situ hybridization by using a custom RNAScope probe (5) targeting the complete TSPyV genome on tumor-associated endothelial cells within 25 dermatologic samples representing a range of inflammatory conditions. We used a peptidylprolyl isomerase B RNA probe as a positive control for RNA integrity in all specimens (Figure). We did not detect TSPyV in endothelial cells in any of the 25 inflammatory skin biopsy samples. In contrast, the trichodysplasia spinulosa control had positive staining, and peptidylprolyl isomerase B staining was present in all samples (Table).
We found no evidence of TSPyV infection in endothelial cells in this survey of cutaneous inflammatory conditions, suggesting that TSPyV does not play a role in the cutaneous inflammatory conditions we included. Of note, our cohort is small compared with that of the previous study, which initially led to the identification of TSPyV in 3 cases from 252 specimens (3). Therefore, the prevalence of TSPyV infection of endothelial cells might be too low to be detected in a cohort of only 25 cases. Our findings provide evidence that endothelial TSPyV infection is not commonly detected in inflammatory skin biopsy specimens and helps refine the spectrum of tissues and clinical settings in which TSPyV should be considered.
Dr. Espinal is a fourth-year anatomic and clinical pathology resident at Stanford University and an incoming gastrointestinal pathology fellow. His research interests include gastrointestinal, hematologic, and microbiologic pathology.
Acknowledgment
Evaluation and reporting of these cases were performed under research protocols approved by the institutional review board of Stanford University. The patients provided informed consent for the research.
References
- Lawrence L, Wang A, Charville G, Liu CL, Garofalo A, Alizadeh A, et al. Identification and confirmation via in situ hybridization of Merkel cell polyomavirus in rare cases of posttransplant cutaneous T-cell lymphoma. J Cutan Pathol. 2023;50:835–44. DOIPubMedGoogle Scholar
- Sadeghi M, Aaltonen LM, Hedman L, Chen T, Söderlund-Venermo M, Hedman K. Detection of TS polyomavirus DNA in tonsillar tissues of children and adults: evidence for site of viral latency. J Clin Virol. 2014;59:55–8. DOIPubMedGoogle Scholar
- van der Meijden E, Horváth B, Nijland M, de Vries K, Rácz EK, Diercks GF, et al. Primary polyomavirus infection, not reactivation, as the cause of trichodysplasia spinulosa in immunocompromised patients. J Infect Dis. 2017;215:1080–4.PubMedGoogle Scholar
- Borgogna C, Albertini S, Zavattaro E, Veronese F, Peruzzi L, van der Meijden E, et al. Primary trichodysplasia spinulosa polyomavirus infection in a kidney transplant child displaying virus-infected decoy cells in the urine. J Med Virol. 2019;91:1896–900. DOIPubMedGoogle Scholar
- Lawrence L, Wang A, Charville G, Toland A, Pinsky B, Natkunam Y, et al. Trichodysplasia spinulosa polyomavirus endothelial infection, California, USA. Emerg Infect Dis. 2022;28:1935–7. DOIPubMedGoogle Scholar
Figure
Table
Suggested citation for this article: Espinal IM, Charville GW, Lawrence L, Brown RA, Rieger KE, Fernandez-Pol S. Evaluation of trichodysplasia spinulosa polyomavirus in skin biopsies. Emerg Infect Dis. 2026 Oct [date cited]. https://doi.org/10.3201/eid3210.261264
Original Publication Date: September 21, 2026
Table of Contents – Volume 32, Number 10—October 2026
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Please use the form below to submit correspondence to the authors or contact them at the following address:
Sebastian Fernandez-Pol, Department of Pathology, Stanford University School of Medicine, 300 Pasteur Dr, Rm H2110, Stanford, CA 94305, USA
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