Cover Image: Detection of hair follicle-associated Merkel cell polyomavirus in an immunocompromised host with follicular spicules and alopecia

Nemeth, Michael J.; Görög, Anna; Mezey, Éva; Pintér, Dóra; Kuroli, Enikő; Hársing, Judit; Kovács, László; Fischer, Max; Rády, Peter L.; Silló, Pálma; Tyring, Stephen K.; Kárpáti, Sarolta

doi:10.1111/bjd.15039

Cited by 4 publications

(5 citation statements)

References 1 publication

(1 reference statement)

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“…MCPyV‐induced transformation of skin appendage‐derived cells or even directly of cells from the hair follicle or other appendages suggests that MCPyV is able to infect these cells. Interestingly, expression of MCPyV T antigens in hair follicles has been reported in a case of alopecia 48 . In addition, we also describe LT/VP1 expression in hair follicle cells in the current study.…”

Section: Discussionsupporting

confidence: 65%

“…Interestingly, expression of MCPyV T antigens in hair follicles has been reported in a case of alopecia. 48 In addition, we also describe LT/VP1 expression in hair follicle cells in the current study. The respective small-sized (1.2 mm diameter) MCC sample may represent a "young" tumour, which, due to its visible location on the face, was excised early enough to still display initial steps of MCC development allowing detection of a follicular "in situ" MCC component as well as adjacent MCPyV-infected hair follicle cells.…”

Section: Discussionmentioning

confidence: 86%

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Detection of wildtype Merkel cell polyomavirus genomic sequence and VP1 transcription in a subset of Merkel cell carcinoma

Kervarrec,

Appenzeller,

Tallet

et al. 2023

Histopathology

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AimsMerkel cell carcinoma (MCC) is frequently caused by the Merkel cell polyomavirus (MCPyV). Characteristic for these virus‐positive (VP) MCC is MCPyV integration into the host genome and truncation of the viral oncogene Large T antigen (LT), with full‐length LT expression considered as incompatible with MCC growth. Genetic analysis of a VP‐MCC/trichoblastoma combined tumour demonstrated that virus‐driven MCC can arise from an epithelial cell. Here we describe two further cases of VP‐MCC combined with an adnexal tumour, i.e. one trichoblastoma and one poroma.Methods and resultsWhole‐genome sequencing of MCC/trichoblastoma again provided evidence of a trichoblastoma‐derived MCC. Although an MCC‐typical LT‐truncating mutation was detected, we could not determine an integration site and we additionally detected a wildtype sequence encoding full‐length LT. Similarly, Sanger sequencing of the combined MCC/poroma revealed coding sequences for both truncated and full‐length LT. Moreover, in situ RNA hybridization demonstrated expression of a late region mRNA encoding the viral capsid protein VP1 in both combined as well as in a few cases of pure MCC.ConclusionThe data presented here suggest the presence of wildtype MCPyV genomes and VP1 transcription in a subset of MCC.

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Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 86%

Detection of wildtype Merkel cell polyomavirus genomic sequence and VP1 transcription in a subset of Merkel cell carcinoma

Kervarrec,

Appenzeller,

Tallet

et al. 2023

Histopathology

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“…A subsequent report of cryoglobulins accumulation in follicular content obtained from a patient with multiple myeloma supports this finding [3]. Besides, there has been speculation that Merkel cell polyomavirus, Propionibacterium acne , and Demodex folliculorum are the causes of the disease [15, 19, 20, 21, 22, 23]. However, there is a lack of evidence to support that these microorganisms play a role in the disease pathogenesis.…”

Section: Discussionmentioning

confidence: 87%

“…To our knowledge, our patient is the second reported case of idiopathic follicular hyperkeratotic spicules. Previously reported cases of this disorder are demonstrated in Table 1 and Table 2 [1, 2, 3, 5, 6, 7, 8, 9, 10, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23].…”

Section: Discussionmentioning

confidence: 99%

A Case Report of Idiopathic Follicular Hyperkeratotic Spicules and Literature Review

2019

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Follicular hyperkeratotic spicules is a rare skin disorder that is usually associated with multiple myeloma. The condition typically presents with tiny hyperkeratotic spicules in follicular distribution and predominantly on the face. To our knowledge, there has been one reported case of this condition without underlying disease. We herein report the second case of idiopathic follicular hyperkeratotic spicules in a 54-year-old Thai woman presenting with multiple follicular horn-like spicules on her face and neck.

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“…The potential of skin fibroblasts to be reprogrammed to MCC cells is supported by the recent finding that expression of MCPyV LT-t in these cells can induce the neuroendocrine-like growth characteristics of MCC (98). Alternatively, MCPyV actively replicating in the dermal fibroblasts may unintentionally enter the precursor cells of Merkel cells residing in their immediate vicinity, either within the basal layer of the epidermis or inside hair follicles (99). The nonpermissive propagation environment created as these cells develop into Merkel cells may force the replication-defective MCPyV genome to integrate into the host cell genome, eventually leading to oncogenesis (Figure 4).…”

Section: The Cell Origin Of Merkel Cell Carcinomamentioning

confidence: 98%

Molecular Mechanisms of Merkel Cell Polyomavirus Transformation and Replication

Liu

You

2020

Annu. Rev. Virol.

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Viral infection underlies a significant share of the global cancer burden. Merkel cell polyomavirus (MCPyV) is the newest member of the human oncogenic virus family. Its discovery over a decade ago marked the beginning of an exciting era in human tumor virology. Since then, significant evidences have emerged to support the etiologic role of MCPyV in Merkel cell carcinoma (MCC), an extremely lethal form of skin cancer. MCPyV infection is widespread in the general population. MCC diagnoses have tripled over the past 20 years, but effective treatments are currently lacking. In this review, we highlight recent discoveries that have shaped our understanding of MCPyV oncogenic mechanism and host cellular tropism, as well as the molecular events occurring in the viral infectious life cycle. These insights will guide future efforts in developing novel virus-targeted therapeutic strategies for treating the devastating human cancers associated with this new tumorigenic virus. Expected final online publication date for the Annual Review of Virology, Volume 7 is September 29, 2020. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

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Cover Image: Detection of hair follicle-associated Merkel cell polyomavirus in an immunocompromised host with follicular spicules and alopecia

Cited by 4 publications

References 1 publication

Detection of wildtype Merkel cell polyomavirus genomic sequence and VP1 transcription in a subset of Merkel cell carcinoma

Detection of wildtype Merkel cell polyomavirus genomic sequence and VP1 transcription in a subset of Merkel cell carcinoma

A Case Report of Idiopathic Follicular Hyperkeratotic Spicules and Literature Review

Molecular Mechanisms of Merkel Cell Polyomavirus Transformation and Replication

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