Susceptibility of various parental lines of commercial White Leghorn layers to infection with a naturally occurring recombinant avian leukosis virus containing subgroup B envelope and subgroup J long terminal repeat

Chickens from seven different parental lines of commercial White Leghorn layer flocks from three independent breeders were inoculated with a naturally occurring avian leukosis virus (ALV) containing an ALV-B envelope and an ALV-J long terminal repeat (LTR) termed ALV-B/J. Additional groups of chickens from the same seven parental lines were inoculated with ALV-B. Chickens were tested for ALV viremia and antibody at 0, 4, 8, 16, and 32 wk postinfection. Chickens from all parental lines studied were susceptible to infection with ALV-B with 40%-100% of inoculated chickens positive for ALV at hatch following embryo infection. Similarly, infection of egg layer flocks with the ALV-B/J recombinant virus at 8 days of embryonation induced tolerance to ALV with 86%-100% of the chickens viremic, 40%-75% of the chickens shedding virus, and only 2/125 (2%) of the chickens producing serum-neutralizing antibodies against homologous ALV-B/J recombinant virus at 32 wk postinfection. In contrast, when infected with the ALV-B/J recombinant virus at hatch, 33%-82% of the chickens were viremic, 28%-47% shed virus, and 0%-56% produced serum-neutralizing antibodies against homologous ALV-B/J recombinant virus at 32 wk postinfection. Infection with the ALV-B/J recombinant virus at embryonation and at hatch induced predominately lymphoid leukosis (LL), along with other common ALV neoplasms, including erythroblastosis, osteopetrosis, nephroblastomas, and rhabdosarcomas. No incidence of myeloid leukosis (ML) was observed in any of the commercial White Leghorn egg layer flocks infected with ALV-B/J in the present study. Data suggest that the parental line of commercial layers may influence development of ALV-B/J-induced viremia and antibody, but not tumor type. Differences in type of tumors noted in the present study and those noted in the field case where the ALV-B/J was first isolated may be attributed to differences in the genetics of the commercial layer flock in which ML was first diagnosed and the present commercial layer flocks tested in the present study.