This Article Full Text Full Text (PDF) Other Versions of this Article: JVI.01058-07v1 81/18/10195    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Florins, A. Articles by Willems, L. Search for Related Content PubMed PubMed Citation Articles by Florins, A. Articles by Willems, L.

 Previous Article  |  Next Article 

Journal of Virology, September 2007, p. 10195-10200, Vol. 81, No. 18
0022-538X/07/$08.00+0     doi:10.1128/JVI.01058-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Even Attenuated Bovine Leukemia Virus Proviruses Can Be Pathogenic in Sheep

Cellular and Molecular Biology, FNRS-FUSAGx, Gembloux, Belgium,¹ Veterinary and Agrochemical Research Centre, Uccle, Belgium²

Received 16 May 2007/ Accepted 29 June 2007

Based on a reverse genetics approach, we previously reported that bovine leukemia virus (BLV) mutants harboring deletions in the accessory R3 and G4 genes persist at very low proviral loads and are unable to induce leukemia or lymphoma in sheep, indicating that these R3 and G4 gene sequences are required for pathogenesis. We now show that lymphoma can occur, albeit infrequently (1 case of 20) and after extended periods of latency (7 years). Direct sequencing and reinfection experiments demonstrated that lymphomagenesis was not due to the reversion of the mutant to the wild type. Similar observations with another type of attenuated mutant impaired in the transmembrane protein (TM) YXXL signaling motifs were made. We conclude that the R3 and G4 genes and the TM YXXL motifs are not strictly required for pathogenesis but that their integrity contributes to disease frequency and latency.

Published ahead of print on 11 July 2007.