TWO independent-autosomal-recessive genes (tvar, tvbr) control resistance to subgroups A and B of the avian leukosis-sarcoma group of viruses, respectively (Crittenden et al., 1967). Resistance to subgroup A serves to exclude the viral genome from the host cell (Piraino, 1967; Crittenden, 1968), and resistance to subgroup B appears to operate by a similar mechanism (Vogt and Ishizaki, 1965). The excluded genome can induce neither viral replication nor neoplastic development in a host whose cells do not allow penetration. Therefore, breeding for resistance controlled by these genes should not only reduce disease but also reduce the prevalence of the causal virus. Payne et al. (1968) showed that resistance at the tva locus did, indeed, reduce the incidence of acute neoplasms and lymphoid leukosis after inoculation of embryos with subgroup A leukosis viruses, but had little or no effect on the response to mixtures of subgroups A and B. The results presented…
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Crittenden et al. (1969) studied this question.
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