PhD, Purdue University
Room: 8053 COMRB
Herpes simplex viruses (HSV) are large DNA viruses which switch between latent and lytic infections. Upon infection, the viruses instigate Toll-like receptors and cytosolic sensors, which mediate the production of interferon, inflammatory cytokines, and chemokines. These soluble factors serve to limit viral replication and regulate immunes cells, including dendritic cells, macrophages, and activate T lymphocytes. Remarkably, several innate immune mechanisms operate in a cell-type specific and temporal manner in response to HSV infection. To replicate or persist in the host, herpes simplex viruses produce an array of proteins that function coordinately. Accordingly, dynamic interplay between viruses and their host dictates the outcomes of HSV infection. The long-term goal of our research is to understand the nature of virus-host interactions, with two major themes: Publications
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(2) Oncolytic HSV in cancer immunotherapyBuilt on systematic analyses, we study genetically edited HSV for cancer therapy. Current efforts are directed towards mechanisms of tumor-specific destruction and immune priming mediated by oncolytic HSV. This integrates viral genetics, cancer biology and immunology approaches. Our objective is to rationally develop next generation oncolytic platforms in immunotherapy.
Publications Search PubMed for Articles