High-resolution analysis of Merkel Cell Polyomavirus in Merkel Cell Carcinoma reveals distinct integration patterns and suggests NHEJ and MMBIR as underlying mechanisms
Fig 2
MCPyV integration sites detected by capture sequencing.
(A): MCPyV integration sites in the human chromosomes. Depicted in blue is the distance between breakpoints on the host genome. Characteristics of the host genome at the breakpoints are indicated in brackets. (B) and (C): Schematic representation of the two characteristic groups of coverage profiles obtained by the mapping of virus-host fusion reads to the human genome. A schematic of virus-host fusion reads is depicted above the coverage patterns; red arrows indicate the direction of the MCPyV sequence in the fusion reads. (B) represents the first group characterised by short distances (4-18bp) between breakpoints on the host genome and inward-facing orientation of the fused viral sequences (upper panel). The middle panel shows coverage tracks from the cell lines MKL-1 and BroLi as examples. The bottom panel depicts a schematic model of the linear integration pattern deduced from the coverage profiles presented above. (C) represents the second group where host sequences in fusion reads map with large distances (17kbp to 300kbp) on the host genome and viral sequences show an outward-facing orientation. WaGa and MKL-2 coverage tracks are shown as examples with a schematic model of the integration pattern deduced from the coverage profiles above. Large host regions preceding the left virus-host junction are duplicated after the right virus-host breakpoint leading to a “Z” shape of the integration. Coverage tracks from all additional samples are provided in S4 Fig.