Nancie M. Archin

This paper identifies the ENL-USP7 complex as a host factor that stabilizes BRD4 to maintain HIV-1 latency and shows that disrupting this complex reactivates latent HIV.

This study uses single-nucleus multi-omic analysis to show cannabis use in HIV patients alters gene expression and chromatin accessibility in immune cell types, with cell-type-specific effects on inflammation and transcription factor regulation.

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 shows that BRD4 degraders are less effective than BET inhibitors in reactivating latent HIV in CD4+ T-cells, highlighting the importance of BRD4's role in disrupting 7SK and P-TEFb.

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