HIV eradication faces a major obstacle that is viral persistence in latent reservoir cells despite antiretroviral therapy. Epigenetic repression plays a central role in viral transgene latency and several epigenetic regulators have been involved in this process. Among them, the "Human Silencing Hub" or HUSH complex, composed of Tasor, MPP8 and periphilin, has been shown to recruit the H3K9me3 methyltransferase "SET domain bifurcated 1" (SETDB1) and is therefore responsible for genes' epigenetic repression. Our recent results highlight the ability of Vpx from HIV-2/SIVsmm to counteract HUSH and to reactivate latent viruses in a latency model. We propose here to study HUSH activity along pathogenesis.
Study Type
OBSERVATIONAL
Enrollment
50
Peripheral blood sampling on EDTA
Hôpital Bicêtre
Le Kremlin-Bicêtre, France
NOT_YET_RECRUITINGHôtel-Dieu
Paris, France
RECRUITINGHôpital Necker
Paris, France
NOT_YET_RECRUITINGViremia
Intracellular HIV RNA load expressed in number of copies / ml
Time frame: Baseline
Total HIV DNA and integrated HIV DNA
Quantification by qPCR
Time frame: Baseline
Hush activity
Transcription rate of cellular genes targeted by HUSH by qRT-PCR
Time frame: Baseline
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