My thesis research focuses on understanding how host immune responses regulate JC polyomavirus (JCPyV) infection and reactivation, a process that can lead to the rare but lethal neurodegenerative disease progressive multifocal leukoencephalopathy (PML) in immunocompromised individuals. JCPyV establishes a largely benign infection in the kidney of most healthy adults, but viral reactivation may occur following immune suppression, leading to viral dissemination into the CNS and onset of PML. My work investigates both innate immune cell–virus interactions and host factors that shape antiviral immunity during JCPyV infection. 

A major component of my research examines how human innate immune cells, including monocytes, macrophages, and natural killer (NK) cells, interact with and respond to JCPyV. I have identified myeloid cells as potential targets and carriers of JCPyV, suggesting a mechanism in which peripheral immune cells may facilitate viral trafficking into the central nervous system. Additionally, I investigate how vitamin D (calcitriol) modulates NK cell responses to JCPyV infection, demonstrating that vitamin D can enhance NK cell cytotoxicity and suppress viral replication in JCPyV-infected brain cells. Together, my work aims to define immune mechanisms that both contribute to JCPyV pathogenesis and may be leveraged therapeutically to prevent viral reactivation and PML.