Majidi, Nasrin. M.S., Department of Biological Sciences, Microbiology and Immunology Program, Wright State University, 2009. A potential strategy to maintain HSV-1 in a latent state: use of immunoregulatory peptide mimetics.
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.