## Abstract The effect of the __Fv__ locus on the pathogenesis of Friend virus‐induced leukemia was studied with two pairs of mouse strains which are congenic except for the locus. The rapid spleen enlargement or spleen focus formation which is characteristic of Friend virus infection occurred in t
Inheritance of susceptibility to friend mouse leukemia virus. XII. Effects of the Fv-1 locus
✍ Scribed by Takeshi Odaka
- Publisher
- John Wiley and Sons
- Year
- 1974
- Tongue
- French
- Weight
- 429 KB
- Volume
- 14
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
The genetic control of susceptibility to the Friend leukemia virus (FLV) complex was studied under conditions which excluded the effect of the Fv locus. From hybrids between two mouse lines which have the same Fv genotype, but differ from each other in response to FLV infection, partially inbred lines were established by selecting for high or low ability to support multiplication of the N‐tropic FLV complex. The results indicated that the Fv‐1 locus controls multiplication of the FLV complex and of the lymphatic leukemia virus (a viral component of FLV complex) and also the development of late splenomegaly. Gene interaction between Fv and Fv‐1 in determining the susceptibility to FLV complex was discussed.
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## Abstract Based on the previous observation that a single major autosomal locus controls susceptibility to Friend leukemia virus in mice, an attempt was made to place the gene for resistance, Fv^r^, from resistant C57Bl/6 mice into the genetic background of susceptible D D D mice. The cross‐inter
## Abstract Genetic control of splenomegaly which occurs at a late stage of Friend leukemia virus infection was studied in hybrid mice between DDD‐Fv^r^ and C57BL/6. It was demonstrated that this late splenomegaly was mainly controlled by a single autosomal locus with the dominant allele for resist
## Abstract Susceptibility of mice to viral components present in Friend leukemia virus (FLV) preparation, lymphatic leukemia virus (LLV) and spleen focus‐forming virus (SFFV), was studied by separately determining end point for infection of each component. Mice with __Fv‐1^n^__ genotype were much
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## Abstract A murine sarcoma virus‐transformed S+L—3T3FL cell line has previously been shown to be equally susceptible to infection with both N‐ and B‐tropic variants of murine leukemia virus, unlike all other mouse cells so far described (Krontiris et al., 1973). Transformed S+L—‐BALB/3T3 and S+L‐