An early start to long-term antiretroviral therapy limits the size of the HIV-1 reservoir more effectively than treatment that starts later.

Building on previous work (Zanini et al, 2015), deep-sequencing is used to show that HIV persistence during suppressive antiretroviral therapy, the main hurdle for HIV cure, is due to homeostatic proliferation and longevity of infected cells rather than ongoing virus replication.

HIV-specific T cells remain detectable for years in HIV-infected individuals on antiretroviral therapy and importantly, mostly (68%) recognize HIV viruses that have the capacity to rebound following treatment interruption.

Inflamasomme inhibition prevents immune activation, HIV-1 pathogenesis and the splenic content of HIV-1 total DNA in humanized mice when administrated early after HIV-1 infection.

Genome-intact HIV-1 proviruses were detected in autopsy samples from the brain of ART-treated persons living with HIV, indicating that the virus can persist in the central nervous system.

Measuring HIV-1 DNA levels at the time of stopping antiretroviral therapy (when initiated during primary infection) predicts clinical progression and the time taken for plasma viraemia to become detectable.

USP49 can increase A3G protein expression and enhance its anti-HIV-1 activity, which is also correlated with hypermutations and affects the HIV-1 latent reservoir.

The frequency of SIV reactivation from latency after treatment interruption is not directly related to measures of SIV DNA, RNA, immune activation or immune response in peripheral blood.

TRIM28 was found to be a versatile dual-function latency contributor by bridging both suppressive epigenetic modifications and RNAP II transcriptional-pausing, and can be a novel target to develop latency-reversing agents.