Submitted to: Avian Diseases
Publication Type: Peer reviewed journal
Publication Acceptance Date: 1/25/2005
Publication Date: 6/1/2005
Citation: Mays, J.K., Bacon, L.D., Pandiri, A.P., Fadly, A.M. 2005. Response of white leghorn chickens of various B haplotypes to infection at hatch with subgroup J avian leukosis virus. Avian Diseases. 49(2):214-219. Interpretive Summary: Avian leukosis subgroup J (ALV-J) virus, a virus that can induce cancer-like disease and other production problems in chickens, continues to be a very costly disease for the commercial broiler breeder industry to control and eradicate. Broiler breeder companies have instituted expensive programs to reduce or eliminate ALV-J infection in elite breeding stock by identification and removal of dams that are likely to transmit virus to progeny chicks. However, identification of transmitter dams in broilers is difficult and even rigorous testing may not identify all transmitter dams. In addition, genetic factors involved in resistance to ALV-J infection have not been identified. This makes eradication and control of ALV-J very difficult. The B haplotype (a genetic component) has been linked to disease resistance and susceptibility against a few avian pathogens. In this study, we analyzed the role of B haplotype in resistance and susceptibility to infection with ALV-J. We found that within a line of chickens termed 15.B congenic there was no significant difference in susceptibility to ALV-J infection between the seven different B haplotypes. In fact, infection with ALV-J at hatch, resulted in viremia (virus in blood) in all chickens with little to no antibodies against ALV-J. In contrast, infection of a semicongenic line of chickens termed 0.B with ALV-J at hatch resulted in a transient viremia in which chickens with the B*21 haplotype responded earlier and cleared the virus earlier than chickens with a haplotype known as B*13. Thus additional genetic factors beyond the B haplotype play a role in resistance to ALV-J. This important information on the genetic mechanisms of control of ALV-J infection is essential and should be helpful to poultry breeders in their efforts to eradicate ALV-J.
Technical Abstract: White Leghorn chickens from seven 15.B congenic lines (genetically similar except for genes linked to the MHC B haplotype) and two Line 0.B semicongenic lines were infected at hatch with strain ADOL Hc-1 of subgroup J Avian Leukosis virus (ALV-J). At 5, 8, 16, and 36 wks of age, chickens were tested for viremia, serum neutralizing antibody, and cloacal shedding. Chickens were also monitored for development of neoplasia. In the 15.B congenic lines (B*2, B*5, B*12, B*13, B*15, B*19, and B*21) there were no significant differences in the incidence of viremia between B haplotypes. In fact, infection at hatch in all of the 15.B congenic lines induced tolerance to ALV-J since 100% were viremic and transient circulating serum neutralizing antibody was detected in only a few chickens throughout the 36 wk experiment. However, at 16 weeks of age more B*15 chickens had antibody and fewer B*15 chickens shed virus than B*2, B*5, or B*13 chickens. Moreover, a higher percentage of B*13 chickens consistently shed virus compared with B*15 chickens from 8 weeks post-infection to termination at 36 weeks post-infection. The B haplotype had a transient effect on viral clearance in line 0.B semicongenics as more B*13 chickens remained viremic through 5 weeks of age than B*21 chickens. Very few (0-18%) of the line 0.B semicongenic chickens shed virus. By 36 weeks of age, all line 0 B*13 and B*21 chickens produced serum neutralizing antibodies and cleared the virus. These results show that following ALV-J infection at hatch the immune response is influenced transiently by the B haplotype and strongly by the line of chicken. We discuss the probability that endogenous virus expression likely reduced immunity to ALV-J in line 15I5 in contrast to line 0, and propose that endogenous viral expression and B haplotype should be evaluated for an influence on immunity to ALV-J in broilers.