My research focuses on Rotavirus (RV) - the causative agent of acute infantile diarrhea, that is responsible for more than 200,000 deaths annually. My earlier work explored RV molecular epidemiology and virion assembly mechanisms. This led to the identification of novel group B rotaviruses, which cause adult diarrhea in humans and exhibit pandemic potential. I subsequently characterized molecular mechanisms by which rotaviruses assemble in infected cells - specifically how a viral non-structural protein, NSP5, forms higher-order assembly scaffolds by a calcium-triggered reversible molecular switch.
Since moving to Stanford University, my research in Dr. Harry Greenberg’s laboratory has focused on understanding the role that innate immunity plays in determining rotavirus species barriers, pathogenicity, and shaping the overall immune response to natural and vaccine-related RV infections. Our work defined the pathways leading to RV recognition by the host interferon response and uncovered viral strategies to regulate this process. Single-cell studies have revealed that RV degrades all three major IFN type receptors in infected cells, and remarkably, also confers pleiotropic IFN resistance to RV-bystander cells (which express normal levels of IFN receptors). These viral regulatory mechanisms possibly underlie the unexpected ability of RV infection to prevent lethal endotoxemia, which we reported recently. I have a strong interest in dissecting host antiviral responses to pathogenic and attenuated viruses at the population and single-cell levels using microfluidics qRT-PCR, multi-color cytometry, and novel mass cytometry techniques. In other ongoing research, I am examining differences in cell type-specific innate responses to pathogenic and attenuated influenza viruses in the human nasal mucosa (primarily using clinical and volunteer nasal swab specimens).