Edward P. Browne

In ART-suppressed human brain, an SPP1+ activated microglial subset holds most detected HIV RNA and shows chronic interferon-I and MHC-I signatures, alongside complement signaling and neuronal loss.

This study identifies chromatin regulators of HIV latency and reactivation using RelB proximity proteomics and CRISPR screening, revealing key acetyltransferases involved in noncanonical NF-κB pathway activation.

The paper analyzes HIV integration sites and expression in CD4 T cells, finding no significant variation in viral expression based on integration site features but identifying insertional activation of host genes in some cells.

The paper identifies TAF1 as a novel regulator of HIV latency through a chemical screen and genetic experiments, showing its role in maintaining viral transcriptional silence.

This study investigates how THC affects HIV-infected CD4 T cells using single-cell multiomic analysis, finding no effect on HIV reactivation but altered gene expression and chromatin accessibility.

This study identifies Vpr's transcription-promoting activity in HIV-1 latency, showing it is inhibited by HDACs and contributes to reservoir formation in CD4+ T cells.

This study identifies INTS12 knockout as a method to enhance HIV latency reversal by overcoming a transcriptional block, improving reactivation in CD4 T cells from HIV-positive individuals.

This paper identifies ETS1 as a regulator of HIV latency through a CRISPR screen and shows it has opposing roles in actively and latently infected CD4 T cells.

This study identifies transcriptomic clusters in HIV patients on ART linked to immune recovery and inflammation markers, revealing novel subgroups with distinct immunological profiles.

This study shows that SETD2 inhibition reduces HIV gene expression and latency by altering viral RNA splicing, not transcription.

The paper uses machine learning to analyze HIV reservoir and immunology data to identify immune signatures associated with total and intact HIV DNA levels during ART.

The paper introduces a high-throughput microwell outgrowth assay to quantify and characterize HIV-infected cells with high sensitivity and precision.

The paper identifies HDAC inhibitors as agents that prevent HIV latency by maintaining viral expression and altering memory T cell phenotypes in infected cells.

The paper demonstrates that AZD5582, a SMACm mimic, effectively reverses HIV latency in patient-derived cells without significant off-target effects.