Abstract
MA/MyJ mice express a natural antibody to the highly oncogenic polyoma virus. C57BR/cdJ mice lack this antibody but mount an adaptive T-cell response to the virus. Analysis of F2 progeny of a cross between these strains reveals a pattern of inheritance of expression of the natural antibody involving two genes in an epistatic relationship.
Highlights
Two forms of resistance in inbred strains of mice to the oncogenic effects of polyoma virus emerged in the course of studies of the effects of ionizing radiation on development of virus-induced tumors (Carroll et al 1999)
A hemagglutination-inhibition (HA-I) assay (Carroll et al 2007) based on serial twofold dilutions of sera reveals the presence of this natural antibody
We report the use of genome-wide single nucleotide polymorphism (SNP) analysis of the F2 progeny of a cross between MA and BR to identify the genetic loci controlling production of the natural antibody
Summary
Two forms of resistance in inbred strains of mice to the oncogenic effects of polyoma virus emerged in the course of studies of the effects of ionizing radiation on development of virus-induced tumors (Carroll et al 1999). Sera from normal MA mice show high levels of a natural antibody capable of neutralizing the virus. The neutralizing activity of sera from uninfected MA is roughly an order of magnitude lower than that found in experimentally or naturally infected mice (Carroll et al 2007).
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