Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 28, 2009
Publication Date: June 1, 2010
Citation: Pandiri, A.R., Mays, J.K., Silva, R.F., Hunt, H.D., Reed, W.M., Fadly, A.M. 2010. Subgroup J Avian Leukosis Virus Neutralizing Antibody Escape Variants Contribute to Viral Persistence in Meat-Type Chickens. Avian Diseases. 54(2):848-856. Interpretive Summary: Avian leukosis virus (ALV) is an economically important virus infection that can cause cancer like disease and other production problems in chickens. Previous observations suggest that chickens that are persistently viremic in the presence of antibody (harbor the virus for extended period of time although they test positive for antibody) may develop tumors and pass the virus to next generation. The reason for establishment of this particular infection profile (virus +, antibody +) in chickens is not clearly understood. We used a molecular clone (genetically engineered) ALV named ADOL pR5-4 to study the phenomenon of developing virus+, antibody + status in chickens. Our results indicated that the emergence ALV that survive the presence of neutralizing antibodies (Nab) termed NAb escape variants exhibited distinct molecular changes within the envelope (coat) region, suggesting viral evolution to escape the host immune response. Further, these results demonstrate that the emergence of NAb escape variants in chickens contributes to the establishment of ALV persistence viremic status. This new information is significant and useful to scientists in academia and industry who are interested in understanding the basic principals of ALV infection profiles, an integral part of any program to control this important viral infection of chickens.
Technical Abstract: We have previously demonstrated a high incidence of chickens with persistent viremia even in the presence of neutralizing antibodies (NAb) against the inoculated parental virus (V+A+) in commercial meat-type chickens inoculated at hatch with Subgroup J avian leukosis virus (ALV J) field isolates. In this study, using an ALV J molecular clone ADOL pR5-4, we have confirmed a similar high incidence of V+A+ profile in commercial meat-type chickens. In addition, we have demonstrated that NAb escape variants contribute to the high V+A+ infection profile in meat-type chickens. In experiment#1, 50 meat-type chickens and 100 ADOL line 0 chickens were infected with ADOL pR5-4 at hatch and 22 meat-type chickens were added as sentinels (contact exposed). In experiment #2, 30 commercial meat-type chickens were inoculated with ADOL pR5-4 at 1 week post hatch and housed individually in 30 Horsfall-Bauer units. The emergence of NAb escape variants was evaluated by sequential autologous virus neutralization (VN) (between virus and antibody from the same sampling period) and heterologous VN (between virus and antibody from preceding and succeeding sampling periods). Sequential virus isolates and corresponding antisera from 18 chickens were examined by VN matrix. In all chickens, autologous virus isolates were not neutralized by corresponding antisera. However, some of these resilient autologous virus isolates were neutralized by antibodies from subsequent sampling intervals. Nucleotide sequence analysis of consecutive isolates from three individually housed chickens with V+A+ infection profile revealed distinct changes within the envelope region suggesting viral evolution to escape the host immune response. These results demonstrate that the emergence of antibody escape variants in commercial meat-type chickens contributes to ALV J persistence.