Our group studies polyomaviruses. A great majority of healthy adults chronically shed polyomavirus virions in their urine and from the surface of their skin. Although these lifelong infections generally aren't known to cause symptoms in healthy individuals, under conditions of immune impairment polyomaviruses  can cause disease. For example, BK polyomavirus (BKV) causes kidney and bladder damage in organ transplant patients, while its close relative JCV causes a lethal brain disease in patients on immunosuppressive therapies and in individuals suffering from HIV/AIDS. An increasingly compelling body of evidence indicates that BKV and JCV cause bladder cancer, at least in rare cases.

Virus discovery efforts led by our lab have uncovered the existence of several human polyomavirus species (HPyVs 6, 7, 10, and 16). The organizing focus of work in the lab is the functional biology of viral capsids. By applying basic-science knowledge of capsid biology, our group has pioneered the development of polyomavirus-based gene transfer vectors. These vectors (also known as pseudoviruses) deliver encapsidated reporter plasmids to the cell nucleus via pathways that resemble the infectious entry of authentic virions. In addition to their utility for studying the mechanics of infectious entry, these tools have a variety of other applications. For example, we use pseudoviruses to perform high-throughput analyses of neutralizing antibody responses. A primary goal of our current work is to understand how polyomaviruses evolve to evade antibody-mediated neutralization.  This work has opened the door to our ongoing clinical development of virus-like particle vaccines against BKV and JCV.