Erratum: Type C Viruses of Wild Mice: Characterization and Natural History of Amphotropic, Ecotropic, and Xenotropic MuLV
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Following the discovery by Gross in 1950 of type C murine leukemia virus (MuLV) (Gross, 1951), considerable knowledge about these viruses in laboratory strains of mice has accumulated (for review, see Sarma and Gazdar, 1974). Only in the last few years, however, has information been obtained about type C viruses in outbred, feral-living Mus musculus, the progenitor of the laboratory mouse. An understanding of the natural history of these viruses in wild mice is important because in laboratory mice they could represent to some extent an artifact of inbreeding and laboratory selection. The wild mouse might also prove a useful model for humans, an outbred species in which some involvement with RNA tumor virus genomes is suspected (for review, see Hehlman, 1976). The first indication that these viruses were present in wild mice was the detection of virus group specific antigen in the tissues of Maryland wild mice bred in captivity (Huebner et al., 1970). Type C viruses were subsequently found in multiple populations of wild mice in southern California and were shown to be lymphomagenic under natural and experimental conditions. Completely unanticipated, however, was the discovery of an independent etiologic involvement of these agents with a naturally occurring neurogenic hind leg paralytic disease of wild mice, which in several aspects is similar to amyotrophic lateral sclerosis in humans. In retrospect, however, a similar type C virus induced paralytic disease may have been observed in the early 1960s in Balb/c mice bearing Moloney leukemia virus-induced lymphoma transplants (Stansly, 1965).