| Autor: |
Passerini S; Department of Public Health and Infectious Diseases, 'Sapienza' University of Rome, 00185 Rome, Italy., Prezioso C; Laboratory of Microbiology of Chronic-Neurodegenerative Diseases, IRCCS San Raffaele Roma, 00166 Rome, Italy., Babini G; Department of Public Health and Infectious Diseases, 'Sapienza' University of Rome, 00185 Rome, Italy., Ferlosio A; Anatomic Pathology, Department of Biomedicine and Prevention, Tor Vergata University of Rome, 00133 Rome, Italy., Cosio T; Dermatologic Unit, Department of Systems Medicine, Tor Vergata University of Rome, 00133 Rome, Italy.; Department of Experimental Medicine, Tor Vergata University of Rome, 00133 Rome, Italy., Campione E; Dermatologic Unit, Department of Systems Medicine, Tor Vergata University of Rome, 00133 Rome, Italy., Moens U; Department of Medical Biology, Faculty of Health Sciences, University of Tromsø-The Arctic University of Norway, 9037 Tromsø, Norway., Ciotti M; Virology Unit, Polyclinic Tor Vergata Foundation, 00133 Rome, Italy., Pietropaolo V; Department of Public Health and Infectious Diseases, 'Sapienza' University of Rome, 00185 Rome, Italy. |
| Abstrakt: |
Merkel cell polyomavirus (MCPyV) is the etiological agent of the majority of Merkel cell carcinoma (MCC): a rare skin tumor. To improve our understanding of the role of MCPyV in MCCs, the detection and analysis of MCPyV DNA and transcripts were performed on primary tumors and regional lymph nodes from two MCC patients: one metastatic and one non-metastatic. MCPyV-DNA was searched by a quantitative polymerase chain reaction (qPCR), followed by the amplification of a Large T Antigen (LTAg), Viral Protein 1 (VP1) and Non-Coding Control Region (NCCR). LTAg and VP1 transcripts were investigated by reverse-transcription PCR (RT-PCR). Viral integration was also studied, and full-length LTAg sequencing was performed. qPCR revealed that the primary tumor of both patients and the lymph node of one patient was positive for the small t-antigen, with an average value of 7.0 × 10 2 copies/µg. The same samples harbored LTAg, NCCR and VP1 DNA. Sequencing results showed truncated LTAg with the conserved retinoblastoma (Rb) protein binding motif and VP1 and NCCR sequences identical to the MCC350 strain. RT-PCR detected LTAg but not VP1 transcripts. The MCPyV genome was integrated into the primary tumor of both patients. The results confirmed the connection between MCPyV and MCC, assuming integration, LTAg truncation and Rb sequestration as key players in MCPyV-mediated oncogenesis. |
