Rauscher virus (RV) induces acute erythroleukaemia and a myeloproliferative disease in adult mice. It consists of a replication-competent murine leukaemia virus (R-MuLV) which acts as a helper virus and a defective transforming component which causes spleen focus formation, Rauscher spleen focus-forming virus (R-SFFV). The integrated proviral DNA of R-SFFV was cloned molecularly. The cloned R-SFFV was compared to that of other viral components which are associated with RV-induced disease and also to the cloned Friend SFFV (F-SFFV) and the myeloproliferative sarcoma virus (MPSV), both of which expand the erythroid (F-SFFV, MPSV) and myeloid (MPSV) compartment on infection of adult mice. The genome of R-SFFV differs, if analysed by restriction enzymes, from R-MuLV in the 3′ end of the genome between the gene and the long terminal repeat. The difference is most likely an alteration in the 3′ part of the gp70-coding region of the gene. Comparison with Rauscher mink cell focus-inducing virus (R-MCF) suggests that R-SFFV is derived from R-MCF by substitution of the 3′ half of the gene with a sequence of unknown origin. The molecularly cloned R-SFFV pseudotyped with Friend MuLV induces an increase in late erythroid precursor cells which still require erythropoietin for maturation. Host range studies of the molecularly cloned R-SFFV prove that the locus is required but not sufficient to restrict RV-induced haemopoiesis in adult mice, thus suggesting that R-SFFV has a different target cell range than F-SFFV and is similar to MPSV.


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