Acutely transforming avian leukosis virus subgroup J strain 966: Defectivegenome encodes a 72-kilodalton gag-myc fusion protein

Avian leukosis virus subgroup J (ALV-J), the most recent member of the avia n retroviruses, is predominantly associated with myeloid leukosis in meat-t ype chickens. We have previously demonstrated that the acutely transforming virus strain 966, isolated from an ALV-J-induced tumor, transformed periph eral blood monocyte and bone marrow cells in vitro and induced rapid-onset tumors, suggesting transduction of oncogenes (L. N, Payne, A. M, Gillespie, and K, Howes, Avian Dis, 37:438-450, 1993), In order to understand the mol ecular basis for the rapid transformation and tumor induction, we have dete rmined the complete genomic structure of the provirus of the 966 strain. Th e sequence of the 966 provirus clone revealed that its genome is closely re lated to that of HPRS-103 but is defective, with the entire pol and parts o f the gag and ear genes replaced by a 1,491-bp sequence representing exons 2 and 3 of the c-myc gene. LSTC-IAH30, a stable cell line derived from turk ey monocyte cultures transformed by the 966 strain of ALV-J, expressed a 72 -kDa Gag-Myc fusion protein. The identification of the myc gene in 966 viru s as well as in several other ALV-J-induced tumors suggested that the induc tion of myeloid tumors by this new subgroup of ALV occurs through mechanism s involving the activation of the c-myc oncogene.