Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 25, 2006
Publication Date: N/A
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 the virus is changing (mutating) at a higher rate, however, information regarding the ability of a subgroup of ALV to recombine with another subgroup to form new viruses expressing characteristics of both subgroups is not known. Understanding the molecular structure and relationships among strains of ALV 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 a recombinant ALV, that was isolated from an outbreak of a cancer-like disease termed myelocytomastosis in commercial layer flocks, contains genetic components from two different subgroups, namely subgroups B and J (ALV-B/J). Further molecular and biological characterization of this recombinant ALV suggested that these viruses continue to evolve by recombination generating new viruses with different pathological properties. This information is significant and useful to scientists who are studying the basic principals of tumor formation by ALV; the information should also be useful to industry scientists working on diagnosis and control of ALV.
Technical Abstract: Infection of broiler chickens with subgroup J avian leukosis virus (ALV) results in the induction of myeloid tumors. However, although egg-type chickens are susceptible to infection with ALVJ, the tumor incidence is very low and on rare occasion the tumors observed are of the myeloid lineage. We recently described the isolation of an ALV (AF115-4) from commercial egg-type chickens suffering from myeloid leukosis. AF115-4 was initially identified as an ALV-J isolate based on PCR analysis of the LTR. However, further characterization of the viral envelope indicated that the virus is a recombinant with subgroups B envelope and J LTR. Here, we further characterize this recombinant virus at both the molecular and biological levels. We show that the AF115-4 isolate expresses a recombinant envelope glycoprotein encoded by a subgroup B gp85 region and a subgroup E gp37 region. The host range of AF115-4 was analyzed using cells resistant to infection by subgroups A/B, J or E, and show that no ALV-J was present in the isolates obtained from the affected chickens. Additional antigenic characterization of AF115-4 using chicken sera specific for subgroups B or J indicated that no ALV-J was present in the samples examined. Inoculation of AF115-4 into ALV susceptible 15I5x71 chickens resulted in the induction of lymphoid leukosis but not the expected myeloid leukosis affecting the commercial chickens. These results suggest that differences in the genetic makeup of the chickens from where AF115-4 was isolated and line 15I5x71, used in the present experiments, may be responsible for the differences in pathogenicity observed. In addition, the results suggest that ALV-J continues to evolve by recombination, generating new viruses with different pathological properties.