Frequent detection of human polyomavirus 6 in keratoacanthomas

Beckervordersandforth, Jan; Pujari, Sreedhar; Rennspiess, Dorit; Speel, Ernst J. M.; Winnepenninckx, Véronique; Díaz, Carlos Guerrero; Weyers, Wolfgang; Haugg, Anke; Kurz, Anna Kordelia; Hausen, Axel zur

doi:10.1186/s13000-016-0509-z

Cited by 32 publications

(37 citation statements)

References 40 publications

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“…In their study, 42.3% of all 59 examined KA were positive for HPyV6 DNA tested by PCR, which also was confirmed with FISH hybridisation. Likewise, higher prevalence numbers of HPyV6 were also reported in basal cell carcinomas, squamous cell carcinomas and trichoblastomas 4. In contrast, in the present study, HPyV6 DNA was not detected in KA or SN.…”

Section: Discussioncontrasting

confidence: 71%

“…Nevertheless, recently Beckervordersandforth et al 4 suggested a link between HPyV6 and KA. In their study, 42.3% of all 59 examined KA were positive for HPyV6 DNA tested by PCR, which also was confirmed with FISH hybridisation.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, attempts have been made to link KA to, for example, mucosal and cutaneous human papillomaviruses, but the results have unfortunately not been convincing 3. Recently, some researchers have instead suggested an association to human polyomaviruses (HPyV), suggesting that especially HPyV6 may play a role in the emergence of KA 4. However, these results are still controversial, and others have reported a lower HPyV6 prevalence in KA 5.…”

Section: Introductionmentioning

confidence: 99%

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Human polyomavirus DNA detection in keratoacanthoma and Spitz naevus: no evidence for a causal role

2016

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Keratoacanthomas (KA) and Spitz naevus (SN) are both lesions with unknown aetiology; therefore, the possibility of a viral involvement, more specifically the involvement of human polyomaviruses (HPyV), was investigated. In total, 22 cases of KA and 25 cases of SN were tested for the presence of HPyVs. DNA was extracted and amplified by multiplex PCR and thereafter tested with a multiplex bead-based assay for HPyVs (BKPyV, JCPyV, KIPyV, WUPyV, MCPyV, TSPyV, HPyV6, 7 and 9) and two primate viruses (SV40 and LPyV). HPyV DNA was found in 20 of the 47 lesions. There was no significant difference in HPyV DNA detection frequency between patients diagnosed with KA and patients diagnosed with SN, nor any over-representation of a specific HPyV type in any of the two patient categories. In conclusion, evidence for a specific aetiological role of any of the above tested HPyVs in either KA or SN was not disclosed.

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Section: Discussioncontrasting

confidence: 71%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Human polyomavirus DNA detection in keratoacanthoma and Spitz naevus: no evidence for a causal role

2016

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“…In contrast to HPyV7, HPyV6 has not yet been linked with specific skin disease. Low levels of HPyV6 DNA have been detected in several types of epithelial neoplasms and a contribution of HPyV6 to these neoplasms has not been excluded 10, 11 .…”

Section: Introductionmentioning

confidence: 99%

Human polyomavirus 6 and 7 are associated with pruritic and dyskeratotic dermatoses

Nguyen

Lee

Yue

et al. 2017

Journal of the American Academy of Dermatology

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Background Human Polyomavirus 6 (HPyV6) and Human Polyomavirus 7 (HPyV7) are shed chronically from human skin. HPyV7, but not HPyV6, has been linked to a pruritic skin eruption of immunosuppression. Objective We determined whether biopsies showing a characteristic pattern of dyskeratosis and parakeratosis might be associated with polyomavirus infection. Methods We screened biopsies showing “peacock plumage” histology by PCR for human polyomaviruses. Cases positive for HPyV 6 or 7 were then analyzed by immunohistochemistry, electron microscopy (EM), immunofluorescence, quantitative PCR, and complete sequencing, including unbiased, next generation sequencing (NGS). Results We identified three additional cases of HPyV6 or 7 skin infections. Expression of T antigen and viral capsid was abundant in lesional skin. Dual immunofluorescence staining experiments confirmed that HPyV7 primarily infects keratinocytes. High viral loads in lesional skin compared to normal skin and the identification of intact virions by both EM and NGS support a role for active viral infections in these skin diseases. Limitation This was a small case-series of archived materials. Conclusion We have found that HPyV6 and HPyV7 are associated with rare, pruritic skin eruptions with a unique histologic pattern and describe this entity as “HPyV6- and HPyV7-associated pruritic and dyskeratotic dermatosis (H6PD and H7PD).”

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“…Viral loads of HPyV6 tend to be much higher than those of HPyV7, with significantly higher viral burdens of both species found in individuals over 80 years of age . HPyV6 and HPyV7 can be detected using PCR on DNA extracted from skin scrapings or biopsies …”

Section: Human Polyomaviruses 6 Andmentioning

confidence: 99%

Polyomaviruses of the skin: integrating molecular and clinical advances in an emerging class of viruses

Tran

Rády²,

Dao

et al. 2019

Br J Dermatol

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Summary Background Human polyomaviruses (HPyVs) are small, nonenveloped, double‐stranded DNA viruses that express tumour antigen proteins. Fourteen species of polyomaviruses have been discovered in humans, and since the 2008 discovery of the first cutaneous polyomavirus – Merkel cell polyomavirus (MCPyV) – six more species have been detected in the skin: trichodysplasia spinulosa‐associated polyomavirus (TSPyV), HPyV6, HPyV7, HPyV9, HPyV10 and HPyV13. Of these cutaneous species, only MCPyV, TSPyV, HPyV6 and HPyV7 have been definitively associated with diseases of the skin, most commonly in immunocompromised individuals. MCPyV is a predominant aetiology in Merkel cell carcinomas. TSPyV is one of the aetiological factors of trichodysplasia spinulosa. HPyV6 and HPyV7 have been recently linked to pruritic skin eruptions. The roles of HPyV9, HPyV10 and HPyV13 in pathogenesis, if any, are still unknown, but their molecular features have provided some insight into their functional biology. Results In this review, we summarize the known molecular mechanisms, clinical presentation and targeted therapies of each of the eight cutaneous HPyVs. Conclusions We hope that heightened awareness and clinical recognition of HPyVs will lead to increased reports of HPyV‐associated diseases and, consequently, a more robust understanding of how to diagnose and treat these conditions.

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Frequent detection of human polyomavirus 6 in keratoacanthomas

Cited by 32 publications

References 40 publications

Human polyomavirus DNA detection in keratoacanthoma and Spitz naevus: no evidence for a causal role

Human polyomavirus DNA detection in keratoacanthoma and Spitz naevus: no evidence for a causal role

Human polyomavirus 6 and 7 are associated with pruritic and dyskeratotic dermatoses

Polyomaviruses of the skin: integrating molecular and clinical advances in an emerging class of viruses

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