## 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
Inheritance of susceptibility to friend mouse leukemia virus. X. Separate genetic control of two viruses in friend virus preparation
✍ Scribed by Takeshi Odaka
- Publisher
- John Wiley and Sons
- Year
- 1973
- Tongue
- French
- Weight
- 580 KB
- Volume
- 11
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
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 more susceptible to LLV of N‐tropic FLV than those with Fv‐1^b^ genotype. This difference in susceptibility to LLV was shown to be controlled by a single gene locus with the recessive allele for susceptibility. Mouse strains congenic except for Fv locus showed marked differences in susceptibility to SFFV according to their Fv genotypes; mice with Fv^s^ genotype were much more susceptible to SFFV than those with Fv^r^ genotype. These results indicate that the innate susceptibility to FLV in mice is under the simultaneous control of two separate gene loci, one locus (probably Fv‐1) for LLV multiplication and the other (Fv or Fv‐2) for proliferation of infected spleen cells (spleen focus formation and splenomegaly induction) as well as SFFV multiplication. All the data obtained support Lilly's interpretation for two‐gene control. Interaction of these two gene loci with respect to multiplication of the two viruses is discussed.
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