[en] First human retrovirus discovered, HTLV-1 infects approximately twenty million individuals worldwide. HTLV-1 is the causative agent of different diseases that include adult T-cell leukemia (ATL) and a neurodegenerative disorder called HAM/TSP (Human associated myelopathy/ Tropical spastic paraparesis). We are interested in the mechanisms of transformation by the viral Tax oncoprotein. We previously showed that Tax interacts with the minichromosome maintenance MCM2-7 helicase and affects host cell replication (Boxus et al, 2012 Blood 119:151). In this project, we focused on the role of the MCM2-7 complex in transcription. We first show by chromatin immunoprecipitation that the MCM2-7 is recruited onto the 5'-LTR promoter. The 5’-LTR does however not act as a DNA replication origin. In contrast, MCM2-7 activates viral transcription as revealed by luciferase reporter assays. Interaction between Tax and MCM2-7 also affect expression of cellular genes. Together, our data thus demonstrate that the viral promoter is not a replication origin and that interaction between Tax and MCM2-7 is involved in the viral transcription.
