Submitted to: Avian Diseases
Publication Type: Peer reviewed journal
Publication Acceptance Date: 12/28/2002
Publication Date: 1/1/2003
Citation: Lupiani, B., Williams, S.M., Silva, R.F., Hunt, H.D., Fadly, A.M. 2003. Pathogenicity of two recombinant avian leukosis viruses. Avian Diseases. 47:425-432. Interpretive Summary: Subgroup J avian leukosis virus (ALV-J) is an 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 mutating at a higher rate, however, information regarding the effect of genetic recombination among various subgroups of ALV on its disease-inducing potential is not known. Understanding the molecular structure and relationships among recombinant strains of ALV-J is an important component of any effort to develop specific diagnostics and effective control programs. Our data show that the disease-inducing potential of two recombinant ALVs containing genetic components of two subgroups namely, A and J differed from that of the parental strains. This new information is significant and should be useful to scientists in academia and industry who are studying the basic principals of mutation, recombination and transmission of this economically important virus of chickens.
Technical Abstract: We have recently described the isolation and molecular characteristics of two recombinant avian leukosis subgroup J viruses (ALV-J) with an ALV-A envelope (r5701A and r6803A). In the present study, we examined the role of the subgroup A envelope in the pathogenesis of these recombinant viruses. Chickens of line 15I5X71 were inoculated at one day of age with r5701A, r6803A, Rous associated virus-1 (RAV-1), or strain ADOL-Hc1 of ALV-J. At 2, 4, 10, 18 and 32 weeks post inoculation (PI), chickens were tested for ALV-induced viremia, shedding and neutralizing antibodies. All except one chicken inoculated with the recombinant viruses (98%) developed neutralizing antibodies by 10 weeks PI compared to only 16 and 46% of the ADOL-Hc1 and RAV-1 inoculated birds, respectively. ALV-induced tumor and mortality in the two groups inoculated with recombinant viruses were different. The incidence of tumors in groups inoculated with r5701A or RAV-1 was 100%, compared with only 9% in the groups inoculated with r6803A or ADOL-Hc1. The data suggest that differences in pathogenicity between the two recombinant viruses might be due to differences in the sequence of the 3' untranslated region (presence or absence of the E element), and therefore, not only the envelope but also other elements of the viral genome play an important role in the pathogenesis of ALV.