Deletions within the U3 long terminal repeat alter the tumorigenic potential of myeloblastosis associated virus type 1(N).

The molecularly cloned myeloblastosis-associated virus type-1(N) (MAV-1(N)) strain induces specifically nephroblastomas in chicken. MAV-induced nephroblastoma constitutes a unique animal model of the human Wilms' tumor. We have previously shown that the MAV-1(N) long terminal repeats (LTR) were necessary and sufficient for nephroblastoma induction. Since major determinants for oncogenesis have been mapped in the U3 region of several other retroviruses, we have analyzed the tumorigenic potential of five recombinant viruses partially deleted in their U3 region. The results obtained indicated that deletions of the LTRs resulted in a modification of the pathogenic spectrum of MAV-1(N) and a decreased efficiency for nephroblastoma induction.