Publication Date
2009
Document Type
Thesis
Committee Members
Nancy J. Bigley (Committee Chair), Nancy J. Bigley (Committee Member), Cheryl L. Conley (Committee Member), Barbara E. Hull (Committee Member), Joseph F. Thomas Jr. (Other)
Degree Name
Master of Science (MS)
Abstract
This study reviews the role of interferon-gamma (IFN-gamma) in HSV-1 latency. CD8+ T cells inhibit the reactivation of HSV-1 in trigeminal ganglia (TG) by production of IFN-gamma. Although CD8+ T cells include all the cytotoxic apparatus for cytotoxicity, latently infected neuronal cells are not killed by CD8+ T cells. The CD94-NKG2a molecule on CD8+ T cells, binds to Qa-1b (a MHC class I like molecule) present on neuronal cell to inhibit CD8+ T cells cytotoxicity. Other studies have also determined that the IFN-gamma peptide mimetic 95-132 inhibits HSV-1 replication in the same way as IFN-gamma in infected cells. IFN-gamma mimetic peptide binds to intracellular domain of interferon gamma receptor-1(IFNGR-1) and initiates IFN-gamma signal transduction to the nucleus for gene activation. IFN-gamma mimetic also is more active than IFN-gamma in gamma activated sequences (GAS) promoter. Epithelial cells such as keratinocytes are the major target cell for HSV-1 replication. In a murine keratinocyte cell line (HEL-30), suppressor of cytokine signaling-1 (SOCS-1) prevents the antiviral activity of IFN-gamma by inhibition of the JAK/STAT signaling pathway.
Page Count
50
Department or Program
Department of Biological Sciences
Year Degree Awarded
2009
Copyright
Copyright 2009, all rights reserved. This open access ETD is published by Wright State University and OhioLINK.
