Genetic cellular resistance to subgroup E avian leukosis virus in slow-feathering dams reduces congenital transmission of an endogenous retrovirus encoded at locus ev21.

The gene ev21, which encodes an infectious endogenous subgroup E avian leukosis virus (ALV-E), designated EV21, is closely linked to the sex-linked, slow-feathering (SF) gene K. To address the relationship between congenital transmission of EV21 and host susceptibility to ALV-E infection, SF roosters that were heterozygous for the dominant gene for susceptibility to ALV-E were mated with ev-negative rapid-feathering (RF), subgroup E-resistant dams to produce SF and RF progeny. The SF female progeny that were heterozygous ALV-E susceptible were viremic at hatch and, when mature, consistently shed the ALV group-specific antigen, p27, in the egg albumen they produced. In contrast, SF females that were homozygous ALV-E resistant were neither viremic at hatch nor shedders of ALV p27. Infectious ALV-E assays of progeny from susceptible and resistant SF dams confirmed that maternal cellular resistance to ALV-E limited congenital transmission of EV21. It is proposed that, in progeny, immunologic tolerance toward exogenous ALV infection due to congenital transmission of antigenically related endogenous viruses may be abrogated by selection for cellular resistance to ALV-E in SF lines used as female parents of feather-sexed crosses.