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1 April 2003 Pathogenicity of Two Recombinant Avian Leukosis Viruses
Blanca Lupiani, Susan M. Williams, Robert F. Silva, Henry D. Hunt, Aly M. Fadly
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We have recently described the isolation and molecular characteristics of two recombinant avian leukosis subgroup J viruses (ALV J) with an avian leukosis virus subgroup 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 1515 × 71 were inoculated at 1 day of age with r5701A, r6803A, Rous-associated virus type 1 (RAV-1), or strain ADOL-Hcl of ALV-J. At 2, 4, 10, 18, and 32 wk postinoculation (PI), chickens were tested for avian leukosis virus (ALV)-induced viremia, shedding, and neutralizing antibodies. All except one chicken inoculated with the recombinant viruses (98%) developed neutralizing antibodies by 10 wk PI compared with only 16% and 46% of the ADOL-Hcl and RAV-1–inoculated birds, respectively. ALV-induced tumors 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-Hcl. 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.

Blanca Lupiani, Susan M. Williams, Robert F. Silva, Henry D. Hunt, and Aly M. Fadly "Pathogenicity of Two Recombinant Avian Leukosis Viruses," Avian Diseases 47(2), 425-432, (1 April 2003).[0425:POTRAL]2.0.CO;2
Received: 20 September 2002; Published: 1 April 2003

lymphoid leukosis
myeloid leukosis
recombinant ALV
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