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Published on: October 7, 2011
Friend viral pathogenesis in C57BL/6 reversible DBA/2 allophenic mice
Abstract:
Infection of mice with Friend erythroleukemia virus initially causes massive proliferation of erythroid precursors accompanied by splenomegaly and reticulocytosis. Strains of mice differ among themselves in susceptibility to Friend virus and one of the major genes affecting the early response to viral infection is Fv-2. Allophenic mice compounded from a resistant strain C57BL/6 (Fv-2rr) and a susceptible one DBA/2 (Fv-2ss) were infected with the polycythemic strain of Friend virus to determine whether susceptibility/resistance was limited to cells of the respective genotypes or if there was an influence across the genotypic barriers. The manifestations of viral pathogenesis monitored were splenomegaly, reticulocytosis and leukocytosis. In addition, the proportion of red cells of the two genotypes in each animal was monitored before and after viral infection by analyses for strain specific electrophoretic variants of hemoglobin and glucose phosphate isomerase. The group of allophenic mice with 25% or more susceptible-strain red blood cells all developed symptoms of virus-induced disease and also revealed dramatic increases in the number of red cells of the susceptible-strain genotype. Thus, no evidence for protection of susceptible-strain cells by ones of the resistant strain could be observed and the disease developed primarily in susceptible strain cells. On the other hand infected animals with 15% or less DBA/2 red cells were severely retarded in the development of Friend disease. Under these circumstances susceptible strain target cells might fail to undergo viral induced replication as a result of direct protection by resistant strain cells. Alternatively, other more complex mechanisms might be involved such as protective anti-viral immune reactions.
Insights
Friend virus infection causes disease primarily in susceptible mouse cells, with resistant cells offering no protection. However, resistant cells may protect susceptible cells when present in high numbers, slowing disease development.
Area of Science:
- Virology
- Immunology
- Genetics
Background:
- Friend erythroleukemia virus infection in mice leads to erythroid precursor proliferation, splenomegaly, and reticulocytosis.
- Mouse strain susceptibility to Friend virus varies, with the Fv-2 gene significantly influencing the early response to infection.
Purpose of the Study:
- To investigate whether Friend virus susceptibility/resistance is cell-autonomous or influenced by interactions between cells of different genotypes.
- To determine the role of Fv-2 genotype in Friend virus pathogenesis using allophenic mice.
Main Methods:
- Allophenic mice, created from resistant (C57BL/6, Fv-2rr) and susceptible (DBA/2, Fv-2ss) mouse strains, were infected with Friend virus.
- Viral pathogenesis was monitored by splenomegaly, reticulocytosis, and leukocytosis.
- Red blood cell genotype proportions were analyzed using strain-specific electrophoretic variants of hemoglobin and glucose phosphate isomerase.
Main Results:
- Allophenic mice with ≥25% susceptible-strain red blood cells developed Friend virus disease, with increased susceptible-strain red cells.
- No evidence of resistant-strain cells protecting susceptible-strain cells was observed when susceptible cells predominated.
- Mice with ≤15% susceptible-strain red blood cells showed significantly retarded Friend disease development.
Conclusions:
- Friend virus disease development is primarily driven by susceptible-strain cells, with no protective effect from resistant-strain cells when susceptible cells are abundant.
- Resistant-strain cells may offer protection to susceptible-strain cells, potentially inhibiting viral replication or involving immune mechanisms, when resistant cells are in the majority.
- The Fv-2 genotype plays a critical role in determining the cellular response to Friend virus infection.
