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Analysis of HIV integration sites from induced and non-induced latently infected populations reveals the role of genomic localization and chromatin context in the fate of HIV-1 infection and the reversal of viral latency.

An improved dual-color reporter reveals how the fate of latent HIV-1 depends on where it integrates in the human genome.

In two independent cohorts, NNRTI-based cART regimens are associated with significantly lower cell-associated HIV RNA levels than PI-based regimens, suggesting more potent suppression of residual virus replication by NNRTI-based regimens.

Computational evolutionary model to predict the efficacy of broadly neutralizing antibodies (bNAbs) in suppressing HIV and to design optimal combination therapy with bNAbs.

The expression of CD32 in HIV-reservoir cells prevents the binding of specific anti-HIV antibodies conferring resistance to NK cell-mediated death, and gives the cell the potential to proliferate in the presence of immune complexes.

Dimension reduction and machine learning tools were used to identify novel associations between the HIV reservoir and the immune systems of people with HIV.

Uracil/adenine base pairs in HIV-1 DNA are attacked by the uracil base excision repair machinery in macrophages, which leads to HIV restriction and viral genome diversification by transcription-associated mutagenesis.

An in-depth view of the in vivo blood and tissue HIV reservoir is presented highlighting shared phenotypic features between individuals, thus enabling marked ex vivo enrichment of replication-competent latent cells.

A gaseous signaling molecule hydrogen sulfide stimulates mitochondrial bioenergetics, maintains glutathione redox poise, and suppresses ROS to subvert viral rebound in latently infected CD4⁺ T cells from HIV subjects.