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© A-M. Pais-Correia, M-I. Thoulouze, A. Alcover, A. Gessain
Mise en évidence de structures de type "biofilm ", formées par le rétrovirus HTLV-1 générés par des cellules infectées (cellules du haut), qui ont été transmis à un autre lymphocyte (cellule du bas). Micrographie en microscopie électronique à balayage. Image colorisée.
Publication : Virology

Genetic variability and integration of Merkel cell polyomavirus in Merkel cell carcinoma

Team: Oncogenic Virus Epidemiology and Pathophysiology
Team: Archived: Experimental neuropathology
Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Virology - 16 Feb 2012

Martel-Jantin C, Filippone C, Cassar O, Peter M, Tomasic G, Vielh P, Brière J, Petrella T, Aubriot-Lorton MH, Mortier L, Jouvion G, Sastre-Garau X, Robert C, Gessain A

Link to Pubmed [PMID] – 22342276

Virology 2012 May;426(2):134-42

Merkel cell polyomavirus (MCPyV) is associated to Merkel cell carcinoma (MCC). We studied 113 MCC tumoral skin lesions originating from 97 patients. MCPyV detection was higher in fresh-frozen (FF) biopsies (94%) than in formalin-fixed paraffin-embedded biopsies (39-47%). Mean viral load in FF tumor was of 7.5 copies per cell with a very wide range (0.01-95.4). Nineteen complete sequences of LTAg were obtained, mainly from FF biopsies when the viral load was high. Seventeen showed stop codons, all localized downstream of the pRb protein binding domain. Sequence comparison and phylogenetic analysis showed that all sequences clustered in the large C clade of MCPyV strains. MCPyV integration was demonstrated in 19 out of 27 FF MCC DNA biopsies without evidence of specific host cellular genome integration site. In 13/19 cases, the viral junction was located within the second exon of the LTAg, after the pRB binding domain.