Poster de conférence
Résumé : Bovine leukemia virus (BLV) is a B-lymphotropic oncogenic deltaretrovirus infecting cattle and closely related to human T-cell leukemia viruses I and II (HTLV-I and II). Despite the well-established repression of the 5'LTR-driven viral gene expression, we and others have discovered and characterized two alternative viral promoters[1][2][3][4], allowing a high expression of viral miRNAs[2][3] and antisense viral transcripts[4], potentially contributing to tumor progression and to escape from the host immune system. In addition, our data have suggested a collision phenomenon between the RNAPIII transcribing the miRNA cluster and the RNAPII coming in an antisense orientation from the 3’LTR[1] with, as a result, a stalling of both RNA polymerase complexes. These latter results have indicated that transcriptional interference could be seen as a new mechanism used by BLV to regulate its three transcriptional activities.In this work, we investigated the interplay and self-regulation between the three BLV promoter activities and showed putative critical functions of the transcriptional interference to drive or repress BLV transcriptional activities. In addition, we highlighted the implication of new transcription factors in BLV transcriptional and epigenetic regulations but also in BLV-mediated pathogenesis. Overall in this study, we further investigated new alternative ways used by BLV to regulate its transcriptional and epigenetic status and provided new fundamental insights into BLV transcriptional and epigenetic regulations which could explain the escape from the host immune system and/or the BLV-induced pathogenesis.