## Abstract Susceptibility of mice to viral components present in Friend leukemia virus (FLV) preparation, lymphatic leukemia virus (LLV) and spleen focusβforming virus (SFFV), was studied by separately determining end point for infection of each component. Mice with __Fvβ1^n^__ genotype were much
Inheritance of susceptibility to friend mouse leukemia virus. XI. Genetic control of late splenomegaly
β Scribed by Takeshi Odaka
- Publisher
- John Wiley and Sons
- Year
- 1973
- Tongue
- French
- Weight
- 326 KB
- Volume
- 12
- Category
- Article
- ISSN
- 0020-7136
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β¦ Synopsis
Abstract
Genetic control of splenomegaly which occurs at a late stage of Friend leukemia virus infection was studied in hybrid mice between DDDβFv^r^ and C57BL/6. It was demonstrated that this late splenomegaly was mainly controlled by a single autosomal locus with the dominant allele for resistance. This locus may be idential with or genetically linked with the locus which controls the level of virus multiplication at an early stage of infection. Considered together with previous findings, splenomegaly induced by Friend leukemia virus in mice is classified into two types, early and late, both being controlled by two separate gene loci.
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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 crossβinter
## Abstract The effect of the __Fv__ locus on the pathogenesis of Friend virusβinduced 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
## 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, partial
## Abstract It has previously been shown that DBA/2 mice protected against the development of Friend leukemia virus (FLV)^4^βinduced disease by the passive administration of heterologous antisera directed against disrupted virions or the major viral envelope glycoprotein (gp71) fail to undergo the