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.

Inclusion Criteria for group 1:

• Symptomatic or asymptomatic acute HIV1 infection
• Age above 15 years old
• No ARV treatment prior inclusion (excepted as prophylaxis pre or post exposure)

Inclusion Criteria for group 2:

• Chronic HIV1 infection
• Age above 18 years old
• No ARV treatment since at least 3 month (regardless the reason)

Inclusion Criteria for group 3:

• HIV2 Infection
• Age above 18 years old
• No ARV treatment since at least 3 month (regardless the reason)

Exclusion Criteria for all groups:

• HIV1 and HIV2 co-infection
• Evolutive intercurrent pathology, in particular active co-infection (i.e. HBV, HCV, tuberculosis, HTLV1)
• Life-threatening pathology

Population infected either by HIV1 or HIV2