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The persistence of latently infected HIV cell reservoirs harbouring replication-competent proviruses, despite prolonged treatment with HAART (Highly Active Anti-Retroviral Therapy), represents a major obstacle to the eradication of the virus. These latently infected cells are insensitive to HAART treatment and escape the host immune response. They are a permanent source of virus reactivation and lead to a rebound in viral load after HAART has been interrupted. Activation of HIV gene expression in these cells, combined with effective HAART, has been proposed as an adjuvant therapy that could lead to the elimination of reservoirs of latent infection.

We are studying the molecular mechanisms regulating the transcriptional latency and reactivation of HIV-1, in its natural context represented by the provirus integrated into the cellular genome and organised in chromatin. More specifically, our investigations focus on the cellular transcription factor CTIP2 and its functions in the formation and persistence of latently infected reservoirs.