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. Author manuscript; available in PMC: 2011 Aug 1.
Published in final edited form as: Virology. 2010 May 6;403(2):103–110. doi: 10.1016/j.virol.2010.04.011

Figure 4.

Figure 4

Schematic representation of the recombination junctions identified in the SU genes of FeLV-B viruses amplified from tumor DNA of the indicated animals. Depicted for comparison are the SU genes of exogenous viruses FeLV-A/61E (solid bar) and FeLV-945 (gray bar) and endogenous FeLV-related provirus CFE-6 (open bar). A deletion within FeLV-A/61E relative to CFE-6 is indicated (vv). Shown diagrammatically are the positions of previously identified preferred recombination sites A – G (Sheets et al., 1992). Also indicated is the infectivity of genomic DNA for canine-D17 cells, presumably representing polytropic FeLV-B replication.