Our research program sits at the intersection of virology, evolutionary genomics, and stem cell biology, united by a central question: how do viruses and hosts co-evolve to shape disease and development? We combine molecular genetics, biochemical assays, computational phylogenomics, and patient-derived cellular models to decode the regulatory networks that govern viral latency, innate immunity, and autoimmune pathogenesis. By bridging deep evolutionary time with modern cellular reprogramming, we aim to uncover fundamental principles of host defense and translate them into therapeutic strategies for viral-associated cancers and immune disorders.

Viral Oncogenesis and Innate Immune Regulation

Virus–host interactions permeate every aspect of biology, and we integrate virology, molecular and cellular biology, immunology, pathology, and evolutionary genomics to study host defense and pathogenesis. A primary focus is Epstein-Barr virus (EBV), a human herpesvirus linked to multiple cancers and autoimmune conditions such as multiple sclerosis (MS). Building on Dr. Zhang's discovery of IRF-7 as a master regulator of innate immunity and viral transformation, we employ genetic and biochemical approaches to dissect how cellular signaling pathways control Interferon Regulatory Factors (IRFs). Our goal is to precisely define their context-dependent roles in establishing viral latency, driving EBV-mediated oncogenesis, and triggering autoimmune pathology.

Evolutionary and Experimental Genomics

We investigate the genomic architecture and evolutionary dynamics that underpinned major animal transitions. Our work merges computational phylogenomics with wet-lab experimental validation to explore how ancient cellular predator–prey interactions drove early animal body-plan diversification and how sexual reproduction was shaped by evolutionary pressures. To bridge molecular mechanisms with macroevolution, we apply single-cell genomics and experimental infection assays—including direct tests of viral infection in gametes—to examine viral latency, genomic integration, and the co-evolutionary arms race between host immune defenses and viral counter-strategies.

Virus–Stem Cell Interactions and Personalized Disease Models

We are developing a personalized hiPSC-based genetic platform to enable precise genomic modification for a wide range of translational applications. Using iPSC-derived stem cell lineages, we model viral infection and pathogenesis in a patient-specific context. This system allows us to interrogate how host genetic variation influences susceptibility to viral entry, replication, and immune evasion, and to test novel antiviral or immunomodulatory interventions in physiologically relevant human cell types.