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

Archive ouverte

Kervarrec, Thibault | Appenzeller, Silke | Tallet, Anne | Jullie, Marie-Laure | Sohier, Pierre | Guillonneau, Francois | Rütten, Arno | Berthon, Patricia | Le Corre, Yannick | Hainaut-Wierzbicka, Ewa | Blom, Astrid | Beneton, Nathalie | Bens, Guido | Nardin, Charline | Aubin, Francois | Dinulescu, Monica | Visée, Sebastien | Herfs, Michael | Touzé, Antoine | Guyétant, Serge | Samimi, Mahtab | Houben, Roland | Schrama, David

Edité par CCSD ; Wiley -

International audience. 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.

• Description
• Sujet/Public
• Outil
• Outil d'anticipation
• Mémoire et thèse
• Gestion