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Retrovirology 2012
Emv2, the only endogenous ecotropic murine leukemia virus of C57BL/6J miceAbstract: We are writing in regard to the paper by Lee et al. [1], recently published in Retrovirology. We have a number of concerns about the accuracy of this paper that need to be considered.First we would like to ask whether the virus identified is novel or of intact coding potential. In the pioneering study by Jenkins et al. [2], they examined the endogenous ecotropic proviruses (Emv loci) present in the germ line of inbred mice. Different inherited proviruses were defined by Southern hybridization analysis using an ecotropic murine leukemia virus-specific envelope gene probe (pEco) and DNA from different mouse strains cut with several different restriction enzymes to yield a variety of virus-flanking sequence fragments. Different proviruses, integrated at different chromosomal locations, will yield characteristic sets of fragments [2]. Emv2 was found in C57BL/6J and related strains. It was characterized by pEco reactive fragments of 5.2, 7.0, 11.5, 17.0 kb in DNA digested with PvuII, HindIII, XbaI and BclI respectively [2,3]. A number of genetic studies show that Emv2 maps to the distal region of mouse chromosome 8 http://www.informatics.jax.org/searches/mapdata_report_by_marker.cgi?8452 webcite, and whilst not yet annotated on the C57BL/6J reference genome assembly, its location can be ascertained by BLASTn searches of the genomic sequence with the pEco probe sequence. This reveals only a single match in this region of chromosome 8 for the entire C57BL/6J genome. Although a fraction of old C57BL/6 mice express ecotropic virus [4] and a poorly inducible ecotropic virus has been mapped to the distal region of chromosome 8 of both C57BL6 [5] and C57BL/10 [6] mice, transfection studies clearly indicate that the Emv2 provirus is replication defective due to a specific base change in pol that results in an Ala to Pro change in RT [3,7,8]. Presumably correction of this defect is readily and routinely accomplished, perhaps by recombination with another endogenous virus [9].In t
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