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Associate Professor
Ph.D., Purdue University, 1993
Room:8035 COMRB, Tel: 312-996-4986
Email: tshuo@uic.edu
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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 pathways. This activates a spectrum of transcription factors 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 determines the outcome of infection and pathogenesis. Our main research areas are: (1) Mechanisms utilized by viruses to modulate host innate immunity, (2) the role of cellular factors in host resistance to virus infection, and (3) the function of dendritic cells in antiviral immunity and vaccination. Our long-term goal is to understand the nature of virus-host interactions, which may facilitate the development of preventive and therapeutic measures.
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