title: Susceptibility of nude mice carrying the Fv-4 gene to Friend murine leukemia virus infection.
abstract: Fv-4 is a mouse gene that dominantly confers resistance to infection with Friend murine leukemia virus (F-MuLV) (S. Suzuki, Jpn. J. Exp. Med. 45:473-478, 1975). Despite complete resistance to ecotropic MuLV infection in mice carrying the Fv-4 gene, it is known that cells carrying the resistance gene in tissue culture do not always show resistance as extensive as that in vivo (H. Yoshikura and T. Odaka, JNCI 61:461-463, 1978). To investigate the immunological effect on resistance in vivo, we introduced the Fv-4 gene into BALB/c nude mice (Fv-4-/- nude[nu/nu]) by mating them with Fv-4 congenic BALB/c mice (Fv-4r/r nude+/+) and examined the susceptibility of the F2 progeny to F-MuLV. All BALB/c nude mice without the Fv-4 gene (Fv-4-/- nude[nu/nu]) were permissive to F-MuLV and developed erythroleukemia within 2 weeks after virus inoculation. The BALB/c nude mice with the Fv-4 gene (Fv-4r/r nude[nu/nu]) did not develop leukemia, and no or little virus was detected in the spleen 7 weeks after virus inoculation. The resistance to F-MuLV was dominant in (Fv-4 congenic BALB/c x BALB/c nude) F1 mice with the Fv-4r/- nude(nu/+) genotype as strictly as in (Fv-4 congenic BALB/c x BALB/c) F1 mice with the Fv-4r/- nude+/+ genotype. However, almost all BALB/c nude mice with the Fv-4r/- nude(nu/nu) genotype developed the disease within 7 weeks, and the virus was detected in all of their spleens even in the mice without leukemia. These results show that the resistance caused by the Fv-4 gene is recessive in nude mice and dominant in BALB/c mice. Some immunological effects, perhaps cell-mediated immunity, may play important roles in the resistance to F-MuLV infection in vivo in addition to the dosage effect of the Fv-4 product.
authors.affiliation: Department of Viral Oncology, Institute for Virus Research, Kyoto University, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Higo
authors.forename: Y
authors.initials: Y
authors.lastname: Kubo
authors.forename: Y
authors.initials: Y
authors.lastname: Iwatani
authors.forename: T
authors.initials: T
authors.lastname: Ono
authors.forename: M
authors.initials: M
authors.lastname: Maeda
authors.forename: H
authors.initials: H
authors.lastname: Hiai
authors.forename: T
authors.initials: T
authors.lastname: Masuda
authors.forename: K
authors.initials: K
authors.lastname: Kuribayashi
authors.forename: F
authors.initials: F
authors.lastname: Zhang
authors.forename: T Y
authors.initials: TY
authors.lastname: Lamin
authors.forename: A
authors.initials: A
authors.lastname: Adachi
authors.forename: A
authors.initials: A
authors.lastname: Ishimoto
mesh_terms: D000818:Animals; D004198:Disease Susceptibility / Q000276:immunology*; D005260:Female; D005622:Friend murine leukemia virus / Q000254:growth & development / Q000276:immunology*; D020022:Genetic Predisposition to Disease; D007942:Leukemia, Experimental / Q000276:immunology* / Q000821:virology; D008297:Male; D051379:Mice; D008819:Mice, Nude; D012192:Retroviridae Infections / Q000276:immunology* / Q000821:virology; D013154:Spleen / Q000276:immunology*; D014412:Tumor Virus Infections / Q000276:immunology* / Q000821:virology