We aim to discover the molecular mechanisms how HIV transcription machinery is regulated during active HIV transcription and during HIV latency. The ultimate goal in our lab is to translate our understanding of transcription and latency of HIV into therapeutic intervention.

We recently discovered that a previously unrecognized epigenetic modification called histone crotonylation is involved in an efficient transcription of HIV. The induction of crotonylation disrupted HIV latency. In combination with other latency reversal agents (LRAs), the disruption of HIV latency is highly achieved compared with a single LRA. We are particularly interested whether and how crotonylation of histone and non-histone proteins integrates into canonical and non-canonical NF-κB pathways for the initiation of HIV transcription.
We recently established a novel HIV deep latency model in which not only a deep latency can be induced but also sustained. We are actively investigating the molecular mechanisms underlying the induction and maintenance of deep latency and extending it to patient models.
We are interested in how cells in deep tissue are infected by HIV, such as CNS, lymph node, kidney, GALT and skin. For example, how the unique interaction among HIV, immune cells, vascular cells, and neuron cells contributes to the initial seeding of latent reservoirs in the CNS, and whether we can target the unique viral infection and latency signaling pathways to attack HIV reservoirs in CNS therefore control HIV-1 infection and HIV-associated neurocognitive disorders (HAND).

Funding support:
Our lab is actively supported by Qura Therapeutics, UNC Center for AIDS Research, NIMH and CARE Program.