Human Papillomaviruses (HPV) are small double-stranded DNA tumor viruses which infect cutaneous and mucosal epithelia. HPV is the most common sexual transmitted disease in the United States and there are no treatments after virus infection. The viral genome replicative program consists of three different stages: initial replication after infection, genome maintenance, and genome amplification, which are linked to the differentiation status of the infected epithelium. HPV replication is mediated by the viral E1 DNA helicase and activator E2 protein. The E2 protein recognizes and binds to DNA sites within the viral genome to initiate replication. The participation of cellular factors at each of these stages remains largely unknown. The goal of my laboratory is to identify the host factors responsible for the molecular switches which tightly regulate the different modes of HPV replication. Furthermore, cellular origin licensing and genome replication is difficult to study in mammalian cells. The PV genome acts like mini-chromosome with defined origins of replication and therefore represents a tractable model for examining this fundamental process.
The incidence of HPV-positive oropharyngeal cancers has dramatically increased over the last decade and it is now the most common HPV related cancer in the United States. Our goal is to fully understand the role of the viral lifecycle in the context of mammalian disease. PVs are species specific and will not infect any host that is not its own. My short-term goal is to develop a mouse PV model in the oropharyngeal cavity to study the PV lifecycle from infection to cancer progression. We will use these mouse PV models to study how E2 and host factors regulate and drive viral replication and tumor initiation and transformation.
Post-doctoral Fellowship - Indiana University School of Medicine, Indianapolis, IN 12/2018
Ph.D. - Purdue University, West Lafayette, IN 05/2012