Smith, E.J., USDA, Avian Disease and Oncology Laboratory, East Lansing, Michigan 48823.
Fadly, A.M., USDA, Avian Disease and Oncology Laboratory, East Lansing, Michigan 48823.
Levin, I., USDA, Avian Disease and Oncology Laboratory, East Lansing, Michigan 48823.
Crittenden, L.B., USDA, Avian Disease and Oncology Laboratory, East Lansing, Michigan 48823.

Endogenous virus (EV) locus ev6 encodes only virus envelope glycoprotein. The influence of ev6 on the immune response to contact infection with hatchmates infected with avian leukosis virus (ALV) was compared in replicate hatches. The ALV Subgroup E-resistant, rapid-feathering (RF) female chickens produced by slow-feathering (SF) and RF dams with and without ev6 were exposed at hatch to hatchmates infected with ALV Subgroup A (Strain RPL-40). The RPL-40 viremia, shedding, and virus neutralizing antibodies were measured among pullets from two hatches at 22 wk of age. Although significant (P less than .05) differences between hatches in the immune response to contact infection were noted among ev6+ pullets, significantly fewer ev6+ pullets seroconverted than their ev6- hatchmates. At 22 wk of age, significantly more lymphomas were also found among ev6+ pullets than among ev6- hatchmates. In flocks wherein both parents and progeny were homozygous resistant to Subgroup E virus, there was no deterimental maternal effect on RF progeny from SF dams that carried ev21. These results also confirm that selection for genetic cellular resistance to Subgroup E ALV infection eliminates congenital transmission of EV21.