Area of research
Virology · Molecular Biology
Research interest
Research interests include HIV Research and Treatment, Single-cell and spatial transcriptomics, Immune Cell Function and Interaction, and Gene Regulatory Network Analysis.
Gene expression and chromatin conformation of microglia in virally suppressed people with HIV
Brain expression quantitative trait locus and network analyses reveal downstream effects and putative drivers for brain-related diseases
RANK ligand converts the NCoR/HDAC3 co-repressor to a PGC1β- and RNA-dependent co-activator of osteoclast gene expression
Niche-Specific Reprogramming of Epigenetic Landscapes Drives Myeloid Cell Diversity in Nonalcoholic Steatohepatitis
Transcriptomic and epigenetic mechanisms underlying myeloid diversity in the lung
Chronic Peripheral Inflammation Causes a Region-Specific Myeloid Response in the Central Nervous System
Immunological Fingerprints of Controllers Developing Neutralizing HIV-1 Antibodies
Liver-Derived Signals Sequentially Reprogram Myeloid Enhancers to Initiate and Maintain Kupffer Cell Identity
<i>Cx3cr1-</i>deficient microglia exhibit a premature aging transcriptome
ALS/FTD-Linked Mutation in FUS Suppresses Intra-axonal Protein Synthesis and Drives Disease Without Nuclear Loss-of-Function of FUS
A Reproducibility-Based Computational Framework Identifies an Inducible, Enhanced Antiviral State in Dendritic Cells from HIV-1 Elite Controllers
Metabolic pathway activation distinguishes transcriptional signatures of CD8+ T cells from HIV-1 elite controllers
Clonal expansion of genome-intact HIV-1 in functionally polarized Th1 CD4+ T cells
Circulating CXCR5+CXCR3+PD-1lo Tfh-like cells in HIV-1 controllers with neutralizing antibody breadth
Innate Immune Activity Correlates with CD4 T Cell-Associated HIV-1 DNA Decline during Latency-Reversing Treatment with Panobinostat
Potent Cell-Intrinsic Immune Responses in Dendritic Cells Facilitate HIV-1-Specific T Cell Immunity in HIV-1 Elite Controllers
Long-Term Antiretroviral Treatment Initiated at Primary HIV-1 Infection Affects the Size, Composition, and Decay Kinetics of the Reservoir of HIV-1-Infected CD4 T Cells