Current Status: M4
Graduate Department: Biochemistry, Cell and Developmental Biology
Other Degrees: B.A. in Biochemical Sciences, Harvard University;
Advisor(s): Kenneth Newell, MD, PhD;
Hometown: Toms River, NJ
Polyomavirus-associated allograft nephropathy (PVAN) is an important cause of allograft dysfunction and rejection in renal transplant patients. It is caused by the reactivation of human BK virus, a ubiquitous human pathogen that persists in the uroepithelium. However, whether PVAN pathogenesis is the consequence of direct viral cytolysis, anti-viral immunity, or an elevated anti-donor immune response is not known. Previously, we developed a model of PVAN utilizing mouse polyomavirus (MPyV) and mouse kidney transplantation. Using this model and the mOVA transplant system, we propose two aims designed to elucidate the mechanism of PVAN pathogenesis. Based on preliminary data, we hypothesize that polyomavirus infection augments the alloreactive T cell response, which is responsible for PVAN-associated rejection of renal allografts. The results of these studies will provide critical insight into the mechanisms of PVAN-associated kidney transplant loss, with important implications for treating BKVN in the kidney transplant population.