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Genetic control of type C virus of wild mice

Nature volume 259, pages 143–145 (1976)Cite this article

Abstract

THE genetic control of type C virus group-specific (GS) antigen expression1,2, infectious virus3–6, and tumorigenesis6,7 has been described in crosses between strains of inbred laboratory mice with high and low incidence of leukaemia. We described a natural population of wild mice (Mus musculus) near Lake Casitas (LC) in southern California which showed a high level of indigenous type C virus activity in terms of GS antigen and infectious virus throughout their lifetime. When ageing was observed in the laboratory, LC wild mice showed a marked susceptibility to lymphoma8, epithelial tumours9 and a neurogenic hind leg paralysis10. Virus transmission and in vivo neutralisation studies11 established the indigenous type C virus as the critical determinant of the lymphoma and paralysis. To ultimately prevent these diseases by antiviral measures we have attempted to suppress LC virus expression by crossbreeding LC wild mice with a specific inbred laboratory mouse strain C57BL/10 Snell (designated B10). The B10 mouse was selected because of its homozygosity for two non-linked dominant alleles, Fv-1b and MLv-1b, the function of either of which might be expected to restrict virus expression in the hybrid progeny. Laboratory strains of mouse type C virus can be classified according to their in vitro host range as N-, B-, or X(xenotropic)-tropic depending on whether they grow preferentially in NIH Swiss or BALB/c embryo cells or replicate only in non-murine cells12,13. Field isolates from LC mice have an unusually wide in vitro host range (‘amphotropic’) but are N-tropic for mouse cells (S. Rasheed, V.K., and M.B.G., unpublished). B10 mice, within the first year of life, show a low incidence of both N-and B-tropic infectious virus14 and also harbour an endogenous X-tropic genome13. The Fv-1b allele from the B10 parent should limit the replication of N-tropic virus within the LC×B10 progeny15, presumably by interfering with the integration or transcription of the proviral DNA16. The MLv 1b allele, the function of which is unknown, might restrict either N-, B-, or X-tropic virus expression in the progeny since this allele completely suppressed GS antigen expression in B10 crosses with the congenic resistant (58N) strain17. Although the genetic mechanism has yet to be established, our findings indicate that control of type C virus expression can be accomplished by genetic means in wild mice.

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Authors and Affiliations

  1. Departments of Pathology, Microbiology, and Pediatrics, University of Southern California, School of Medicine, Los Angeles, California

    M. B. GARDNER, V. KLEMENT & B. E. HENDERSON

  2. Jackson Memorial Laboratory, Bar Harbor, Maine

    H. MEIER

  3. National Cancer Institute, Bethesda, Maryland

    J. D. ESTES & R. J. HUEBNER

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  1. M. B. GARDNER
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  2. V. KLEMENT
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  6. R. J. HUEBNER
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GARDNER, M., KLEMENT, V., HENDERSON, B. et al. Genetic control of type C virus of wild mice. Nature 259, 143–145 (1976). https://doi.org/10.1038/259143a0

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