methods. This disease, known as herpes stromal keratitis, can be prevented by the timely passive transfer of monoclonal antibody specific for viral glycoprotein D (gD). On days 4, 7 and 10, eyes with either recurrent epithelial or stromal disease and appropriate controls were stained to identify immune cells and HSV-1 antigens. At 2-4 months post-inoculation, eyes and trigeminal ganglia were assayed for latent virus. 30.0 μM). LL-37 released from the implants blocked HSV-1 infection of HCECs by interfering with viral binding. Of the 80 plus HSV genes, few have been formally tested for their role in HSV keratitis.
Furthermore, our results indicate that MIP-1alpha plays a major role in herpes stromal keratitis development, whereas MCP-1 does not. When HCEn cells were examined for antigen-presenting function, HSV-1-primed HCEn cells stimulated the proliferation of allogeneic CD4(+) T cells and interleukin 10 (IL-10) secretion. These include mechanisms to suppress inflammatory and immune reactions, and means to suppress ocular vascularization, both enemies of normal vision (1, 2). In the third specific aim we will further characterize ICP27 mediated inhibition of ICP4 and VP16 transcription and test hypotheses about the way in which this is achieved. Corneal endothelial cells transcriptionally initiate inflammatory programs in response to HSV-1 infection related to NF-κB, CRE, and C/EBP and express arrays of inflammatory cytokine induction by TLR9. A short period of viral replication within infected sensory ganglia is concomitant with the establishment of a nonproductive latent infection (22).