Mutations in the env gene of friend spleen focus-forming virus overcome Fv-2(r)-mediated resistance to friend virus-induced erythroleukemia

M. K. Majumdar, C. L. Cho, M. T. Fox, K. L. Eckner, S. Kozak, D. Kabat, R. W. Geib

Research output: Contribution to journalArticle

14 Scopus citations

Abstract

Although Fv-2(r) homozygous mice are resistant to leukemias induced either by an erythropoietin-encoding virus or by wild-type Friend virus (FV) (M. E. Hoatlin, S. L. Kozak, F. Lilly, A. Chakraborti, C. A. Kozak, and D. Kabat, Proc. Natl. Acad. Sci. USA 87:9985-9989, 1990), they are susceptible to some variants of FV (R. A. Steeves, E. A. Mirand, A. Bulba, and P. J. Trudel, Int. J. Cancer 5:349-356, 1970; R. W. Geib, M. B. Seaward, M. L. Stevens, C.-L. Cho, and M. Majumdar, Virus Res. 14:161-174, 1989). To localize the virus gene involved in influencing the host range, we cloned and sequenced the env gene of the BB6 variant of FV (Steeves et al., Int. J. Cancer 5:349-356, 1970). In comparison with the wild-type env gene, the BB6 variant contains a 159-bp deletion that eliminates the membrane-proximal portion of the extracellular domain and 58 point mutations resulting in 13 amino acid changes. Substitution of the variant env gene for the wild-type env gene resulted in a recombinant virus that produced a Friend virus-like disease in Fv-2(r) homozygotes. Our results identify the spleen focus-forming virus env gene as the viral gene involved in this virus-host interaction. Additionally, they suggest that the product of the Fv-2(r) gene modifies the interaction between the spleen focus-forming virus envelope protein and the erythropoietin receptor.

Original languageEnglish (US)
Pages (from-to)3652-3660
Number of pages9
JournalJournal of virology
Volume66
Issue number6
DOIs
StatePublished - 1992

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

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