February 17 @ 4:00 – 5:00 pm
Speaker: Vijay Sivaraman, PhD
Presented from NCCU
Broadcast Link: Seminar
The pathogenesis of many organisms requires complex interactions with the host immune response to cause resulting diseases. Human Immunodeficiency Virus (HIV)-1 and Yersinia pestis infection is significant for their severity, and the pathogen/host interactions that lead to disease are incompletely characterized for both. Increasing evidence suggests that both HIV-1 and Y. pestis employ multiple levels of innate immune evasion and activation, to create a finely tuned disease state. In this study, we aim to investigate the contribution of early innate immune activation to the downstream pathogenesis of two organisms. Using data obtained from in vitro, ex vivo and in vivo systems, I will present scenarios where highly lethal organisms aberrantly utilize the host immune response to contribute to disease.
Vijay Sivaraman, PhD is an assistant professor in the department of Biological and Biomedical Science at North Carolina Central University. His long-term research interests involve elucidating immunological interactions between the host-pathogen interfaces that contribute to disease. Currently his work focuses primarily on interaction between the microbial pathogen Y. pestis and immune cells within the lungs. He hopes to broaden his inquiry to include other infectious microbes. His work could generate a more global picture regarding mediators of inflammation that could lead to novel targets for diagnostic, therapeutic and drug development. He has published several articles on pathogen-host interaction, and currently teaches courses on medical microbiology and immunology. He received his PhD from UNC-Chapel Hill in 2009 and has been a fellow at the National Institutes of Health (NIH). He studied chemistry and biology as an undergraduate. From 2012-2013, he was chair of the Microbiology and Immunology Postdoctoral Association at UNC-Chapel Hill. He was published about the Yersinia pestis primary pneumonic plague in PLOS Pathogens.