James Bliska Genomics of host-pathogen evolution
We are using functional evolutionary genomic approaches to understand the evolution of virulence in the genus Yersinia. Through these studies we hope to understand how allelic variation of virulence factor genes contributed to the process by which a enteric bacterium of low pathogenicity (Y. pseudotuberculosis) evolved into a bacterium with extremely high pathogenicity (Y. pestis, the agent of plague). Additionally, we are investigating the epidemiology of endemic plague in Madagascar through genomic analysis of the main host reservoir, the black rat.
Laurie Krug Molecular determinants of chronic gammaherpesvirus infection
Our research interests lie in understanding the molecular determinants of virus-host interactions during chronic gammaherpesvirus infections. We seek to dissect this complex virus and host interplay using a model pathogen system. Host signaling pathways can determine whether a gammaherpesvirus establishes a latent infection or undergoes productive replication. We are evaluating the consequence of upstream signaling events and the downstream activation of NF-κB and STAT3 transcription factors on the regulation of viral and host genes. We seek to identify genome-wide occupancy of these host and other viral transcription factors during infection. By coupling these studies with transcriptome profiling and epigenetic landscapes, we aim to understand how the virus co-opts host factors to control the virus and host gene expression program that ultimately determines a latent versus lytic outcome of infection.
Erich Mackow Viral Pathogenesis and Innate Immunity
We use molecular approaches to study hantavirus and dengue virus pathogenesis. We study viral interactions with endothelial cells and the role of viral proteins in altering normal endothelial cell signaling pathways and responses that control vascular integrity and result in lethal vascular permeability.
