Bin He |
 Associate Professor Ph.D., Purdue University, 1993 Room:8035 COMRB, Tel: 312-996-4986 Email: tshuo@uic.edu |
Virus infection and innate immunity Herpes simplex virus infections are the most common cause of genital ulcer disease worldwide and increase the risk of HIV transmission. Furthermore, herpes simplex virus infections cause encephalitis and ocular diseases. Following infection, Herpes simplex viruses establish a latent or lytic infection in which the viruses undergo transcription, replication, assembly and egress. In this process the viruses trigger innate immunity through Toll-like receptor and cytosolic receptor mediated signaling pathways. This activates transcription factors NF-kB, AP-1, and IRF3/7 and subsequently induces the expression of cytokines, including type I interferon. Type I interferon exerts its antiviral activity by inhibition of viral gene expression, protein synthesis, and maturation. Additionally, type I interferon promotes the maturation of dendritic cells, stimulates the cytotoxic activity of natural killer cells, and activates T cells.
Innate immune defenses involve the recognition of pathogen associated molecular patterns. In cells infected with herpes simplex viruses, a number of antiviral mechanisms operate in a cell-type specific and temporal manner. This partly stems from a complex viral life cycle that proceeds in a cascade fashion. As a way to replicate or persist in host cells, the viruses express an array of viral proteins that compromise innate immunity related to cytokine induction, signal transduction, and effector functions. Coordinated actions of these proteins are believed to facilitate viral persistency. Accordingly, the balance between the viral activities and host innate responses dictates the outcome of infection and pathogenesis. Using molecular, genetic, and systems biology approaches, we aim to identify viral elements that induce or inhibit cytokine responses, to investigate viral mechanisms that modulate innate immunity, to characterize cellular factors responsive to virus infection, and to explore the role of cytokines in viral pathogenesis. Our long-term goal is to understand the nature of virus-host interactions, which may lead to the development of preventive and therapeutic measures. |
