Research interests
We study herpesviruses — a family of large, double stranded DNA viruses.
After primary infection, herpesviruses stay inside their host for life. There are no therapeutic agents which can clear or cure infection. We lack vaccines for all but one (VZV) species of herpesvirus.
Nine different species of herpesviruses infect humans. Most individuals are infected with 3-5 different species by adulthood.
Herpesvirus infection drives significant disease including oral and genital lesions, encephalitis (brain inflammation), keratitis (infectious blindness), congenital defects, and cancer (Kaposi sarcoma, Burkitt's Lymphoma).
RNA damage and repair
Herpesviruses depend on their host’s gene expression machinery.
Herpesviruses infect cells and deliver their genome to the nucleus. Once inside they need to synthesize viral products (DNA, RNA, protein) to reproduce and spread to new cells.
To successfully replicate, the virus has to express their >80 different genes, while combatting (and outpacing) immune detection.
Herpesviruses mount distinct gene expression profiles depending on the cell type they infection. The virus alternates between persistent “latent” and replicative “lytic” gene expression profiles.
Alternative splicing
Our research investigates core mechanisms that define the RNA landscape and how these pathways and their products are remodeled during viral infection. Ongoing projects center on:
Pol III-dependent transcription
