Research Projects

We are the first to demonstrate NK cell’s ability to kill JCV (SVE-delta M1 strain)-infected SVG-A cells. Co culturing with NK cells showed significant decrease of JCV-infected SVG-A cells, as measured by decreased SVG-A cells containing the early protein, T Ag, and the late capsid protein, VP1.

NK cell response to the human polyomavirus JC (JCV)

JCV infects most healthy individuals without causing any disease. In immune compromised patients, JCV can cause the often fatal brain infection – progressive multifocal leukoencephalopathy (PML). There is currently no available treatment for PML. The only option to clinicians is to boost immune response, which is not easily achieved in most cases. We are the first to discover NK cell control of JCV-infected cells, adding another aspect of the immune arsenal to fight JCV. Current studies in lab focus on how to augment and harness NK cells to specifically target JCV.

NK cell response to the human polyomavirus BK (BKV)

Like JCV, BKV also infects most healthy individuals without causing any disease. But in kidney transplant recipients, BKV causes nephropathy and can result in loss of the transplanted graft. There is no treatment for BKV. We are mapping the NK cell response to BKV.

Organoids infection with human polyomaviruses JC and BK– There is no animal model for JCV infection. To improve upon the 2D cell culture model of JCV infection, we are creating human organoids to better study JCV virology and immunology.

We conduct translational research following a prospective renal transplant cohort from prior to transplant (baseline) to 1, 3, 6, and 12 months after transplant. Rise of BKV-specific T cells (CD4+ and CD8+) is closely correlated to BKV reactivation, as detected in urine (viruria) or blood (viremia).

Non human primate model of JCV infection

There is no animal model for JCV infection. In collaboration with University of Wisconsin Primate center, we are infecting rhesus macaques with JCV to create a non human primate model for PML.

Multi plex immunofluorescence staining of brain tissues from SIV-infected rhesus macaques showed microglia (Iba-1) and astrocyte (GFAP) activation.

SIV neuropathogenesis

While HIV is now well controlled by antiretroviral therapy in infected individuals, neuro inflammation and cognitive alterations remain an unsolved problem. Using the SIV infection of rhesus macaques, we are dissecting the intricate viral immune and inflammation pathways in the central nervous system to find treatment for patients.

SARS-CoV-2 Neuropathogenesis

Using the rhesus macaque model, we are studying the neuro immune and inflammatory response to SARS-CoV02.