Submitted to: Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 22, 2000
Publication Date: N/A
Interpretive Summary: Subgroup J avian leukosis virus (ALV-J) is an emerging economically important virus infection that can cause cancer-like disease and other production problems in meat-type chickens. Previous observations suggest that the virus is changing (mutating) at a high rate; however, information regarding the ability of ALV-J to recombine with other subgroups of ALV viruses is not known. Understanding the molecular structure and relationships among strains of ALV-J that are able to recombine with other subgroups of ALV is an important component of any effort to develop specific diagnostics and effective control programs. Our data show that two strains of ALV-J, that had been isolated from broiler breeder flocks in the United States, are indeed able to recombine with another subgroup of ALV, namely subgroup A and developed into a hybrid virus having the characteristics of both subgroups, A and J. This new information is significant and useful to scientists who are studying the basic principles of tumor formation by this emerging virus; the information should also be useful to industry scientists working on ALV-J vaccines and diagnostic kits.
Technical Abstract: Three recombinant Avian leukosis subgroup J viruses, ADOL 5701A, ADOL 5701A DELTA and ADOL 6803A, carrying a subgroup A envelope have been isolated and characterized. These viruses were identified by their ability to replicate in DF-1/J, a recombinant chicken embryo fibroblast (CEF) cell line expressing the subgroup J envelope that is resistant to subgroup J replication. Flow cytometric analysis of DF-1/J cells infected with ADOL 5701 and ADOL 6803, two subgroup J isolates, indicated cross reactivity with subgroup A chicken polyclonal serum. The envelope and LTR of these viruses was amplified using primers specific for subgroup A envelope and subgroup J LTR. Sequence analysis of the PCR products indicated that these viruses had a subgroup A gp85, a subgroup E gp37 and a subgroup J LTR. These results indicate that these three recombinant viruses arose by recombination between exogenous subgroup J isolates and a defective endogenous virus with subgroup A gp85 and subgroup E gp37 present in alv6 cells.