Table 1.
Clinical data of MCC patients.
Figure 1.
Kaplan Meier analysis of survival in complete remission relative to primary tumour MCPyV load.
Patients with ≥1 genome copy per cell (n = 15, black curve) had longer survival in complete remission than patients with <1 genome copy per cell (n = 9, grey curve). VL : viral load. Open circles indicate patients censored at last follow-up visit.
Figure 2.
Kaplan Meier analysis of overall survival relative to MCPyV detection in PBMC.
Patients who had all MCPyV-negative PBMC (n = 14, black curve) had a longer survival than patients who had at least one MCPyV-positive PBMC (n = 14, grey curve). Open circles indicate patients censored at last follow-up visit.
Table 2.
Identification of four novel integration sites of MCPyV DNA in MCC genome.
Figure 3.
Characterization of MCC patients' strain and tumour signature in MCPyV LT.
A. Direct PCR sequencing of the second exon of MCPyV LT in MCC tumours. Twelve distinct representative cases (case number indicated on the left) are represented. Sequences from MCC (black), nasal swab (blue), urine (green) and PBMC (red) tissues reveal single nucleotide polymorphisms (SNPs), and tumour-specific mutations: open circle, synonymous; filled circle, non synonymous; black cross, premature stop codon; filled box, deletions. In cases 1 and 20, weak viral load in PBMC and nasal swab respectively prevented full length amplification of LT. Base pair designation as in Table 2. B. Diagram representation of main functional domains encoded by the second exon of LT (Rb = Rb binding domain, NLS = nuclear localization signal, OBD = origin binding domain and helicase domain). Arrows indicate premature truncating mutations determined by direct sequencing and arrowheads indicate the site of integrated viral DNA determined by 3′ DIPS-PCR. GenBank accession number: HM587427-HM587448.