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Article Dans Une Revue Histopathology Année : 2023

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

Marie-Laure Jullie
  • Fonction : Auteur
Pierre Sohier
Arno Rütten
  • Fonction : Auteur
Patricia Berthon
Yannick Le Corre
  • Fonction : Auteur
Ewa Hainaut-Wierzbicka
  • Fonction : Auteur
Nathalie Beneton
  • Fonction : Auteur
Charline Nardin
  • Fonction : Auteur
Francois Aubin
  • Fonction : Auteur
Monica Dinulescu
  • Fonction : Auteur
Sebastien Visée
  • Fonction : Auteur
Antoine Touzé

Résumé

Aims: Merkel 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. Methods and results: Whole-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. Conclusion: The data presented here suggest the presence of wildtype MCPyV genomes and VP1 transcription in a subset of MCC.
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Dates et versions

hal-04325836 , version 1 (06-12-2023)

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Paternité - Pas d'utilisation commerciale - Pas de modification

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Thibault Kervarrec, Silke Appenzeller, Anne Tallet, Marie-Laure Jullie, Pierre Sohier, et al.. Detection of wildtype Merkel cell polyomavirus genomic sequence and VP1 transcription in a subset of Merkel cell carcinoma. Histopathology, 2023, 84 (2), pp.356-368. ⟨10.1111/his.15068⟩. ⟨hal-04325836⟩
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