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Rauscher Spleen Focus-forming Virus: Biological Properties and Relationship to Helper Viruses

¹ Department of Genetics, Free University, De Boelelan 1087, 1007 Amsterdam, The Netherlands
² Heinrich-Pette-Institut, University of Hamburg, Martinistrasse 52, 2000 Hamburg 20, Federal Republic of Germany
³ Johns Hopkins Oncology Center, 600 N. Wolfe Street, Baltimore, Maryland, U.S.A.
and⁴ Institute of Pathology, Faculty of Medicine, Erasmus University, P.O. Box 1738, Rotterdam, The Netherlands

A Rauscher virus (RV)-transformed erythroid cell line, RA-1, was shown to be a non-producer cell line. RA-1 cells express not only gp51–54 env-related glycoprotein, but also gp70, which is more closely related to gp51–54 coded by a recombinant env gene than to the MuLV-R gp70. RA-1 cells could be infected by Friend, Moloney and Gross viruses, but not by the homologous Rauscher murine leukaemia virus. Rescue of spleen focus-forming activity was obtained on infection of these cells with MuLV-F or MuLV-Mol, but not with MuLV-Gross. The RNA of the RV complex resembles closely that of Friend virus (FV). It contains a 32S, presumably defective, genome, which most likely is responsible for spleen focus formation, and a 35S helper virus genome. Oligonucleotide fingerprint data suggest that RV has evolved independently of FV. Erythroid early BFU-E cells of mice infected with RV of Friend helper virus-infected RA-1 cells were shown to require no addition of conditioned medium to form large erythroid colonies (BFU-E) in the presence of only small amounts of erythropoietin.

Keywords: Rauscher virus, Friend virus, spleen focus-forming virus, BPA independence

Received 26 March 1982; accepted 8 June 1982.