|Pandiri, Arun - MICHIGAN STATE UNIVERSITY|
Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 16, 2006
Publication Date: September 1, 2006
Citation: Mays, J.K., Pandiri, A.R., Fadly, A.M. 2006. 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. Avian Diseases. 50:342-347 Interpretive Summary: Avian leukosis virus (ALV) is an economically important virus infection that can cause cancer-like disease and other production problems in chickens. ALV can mutate (change) at a higher rate and has the ability to recombine with other subgroups of ALVs resulting in new forms of the virus. Recently, we isolated from commercial chicken layer flocks a recombinant ALV termed ALV-B/J that contains genetics materials from two different subgroups of ALV, B and J. In this study, we tested the susceptibility of chickens from seven different genetic lines of commercial layers to infection with this new recombinant ALV-B/J. Our data show that chickens from all commercial lines tested were susceptible to ALV-B/J infection and tumors. However, the type of tumors noted in this study (lymphoid leukosis) differed from that noted in the original case (myeloid leukosis) where ALV-B/J was isolated. The data suggest that such differences in type of tumors may be due to difference in genetic makeup of line of chickens. This information should be useful to scientists in academia and industry who are studying the pathogenesis and control of this important virus infection of chickens.
Technical Abstract: Chickens from seven different 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 lines were inoculated with ALV-B. Chickens were tested for ALV viremia and antibody at 0, 4, 8, 16, and 32 weeks post-infection. Chickens from all seven lines 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 eight days of embryonation induced tolerance to ALV with 86-100% of the chickens viremic and only 2/125 (2%) of the chickens producing serum neutralizing antibodies against homologous ALV-B/J recombinant virus at 32 weeks post-infection. In contrast, when infected with the ALV-B/J recombinant virus at hatch, 33-88% of the chickens were viremic and 0-56% were producing serum neutralizing antibodies against homologous ALV-B/J recombinant virus at 32 weeks post-infection. Infection with the ALV-B/J recombinant virus at embryonation and at hatch induced predominately lymphoid leukosis (LL) along with other common ALV neoplasms. 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. 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 line in which ML was first diagnosed and the present commercial layer lines tested.