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SummaryHerpetic epithelial and stromal keratitis is a sight-threatening ocular infection. To study the role of the epithelium in the innate response to herpes simplex virus 1 (HSV-1) infection of the cornea, we used a telomeraseimmortalized human corneal epithelial cell (HCEC) line, HUCL, and primary HCECs as a model and infected the cells with HSV-1 (KOS strain). HSV-1 infection of HCECs resulted in a two-phase activation of nuclear factor-kappaB (NF-jB), JNK and p38, with the first peak at 1-4 hr and a second peak at 8 hr. Concomitant with the first peak of activation, transcriptional expression of interleukin (IL)-6, IL-8, tumour necrosis factor (TNF)-a and interferon (IFN)-b was rapidly induced in HSV-1-infected cells. HSV-1 infection also induced the production of IL-6, IL-8, and TNF-a in both HUCL cells and primary HCECs. Coincident with the second phase of NF-jB activation in HSV-1-infected HCECs, the expression of Toll-like receptor 7 (TLR7) was induced, whereas the level of TLR3 was greatly down-regulated. Thus, in response to HSV-1 infection, HCECs produce proinflammatory cytokines, leading to infiltration, and IFNs to enhance the antiviral activity in the cornea, probably through sequential activation of TLRs.

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The distribution of the neurotropic alphaherpesvirusesherpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) and varicella zoster virus (VZV)-was determined in autonomic and sensory ganglia of the head and neck obtained from formalin-fixed human cadavers. HSV-1 and VZV DNA were found in 18 of 58 and 16 of 58 trigeminal, 23 of 58 and 11 of 58 pterygopalatine, 25 of 60 and 14 of 60 ciliary, 25 of 48 and 11 of 48 geniculate, 15 of 50 and 8 of 50 otic, 14 of 47 and 4 of 47 submandibular, 18 of 58 and 10 of 58 superior cervical, and 12 of 36 and 1 of 36 nodose ganglia, respectively. HSV-2 was not detected at any site. Viral DNA positivity and location were independently distributed among autonomic and sensory ganglia of the human head and neck.The neurotropic human herpesviruses-herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) and varicella zoster virus (VZV)-infect a large percentage of the world population and remain latent for the lifetime of the host. Virus can reactivate to cause symptoms ranging from vesicular lesions to encephalitis [1]. In the United States, serologic testing has determined the relative rates of prior infection at 57.7% (HSV-1), 17.0% (HSV-2), and 95.8% (VZV) [2,3]. However, the presence of antibodies does not provide information about where the virus is latent. The trigeminal ganglion is the traditional site of latency of HSV-1 and VZV in the head and neck; however, these viruses have been detected in other sensory and autonomic ganglia, including the dorsal root, geniculate, vestibular, spiral, and nodose (inferior vagal), superior cervical, and ciliary ganglia [4]. Although HSV-2 has been postulated to have a preference for infection and latency in the sacral ganglia, HSV-2 has also been implicated in oral-labial infections [5].Previous studies of the alphaherpesviruses in ganglia have usually reported results from a single donor or from a limited region of the body. Few studies have examined the interaction of different alphaherpesviruses with each other (ie, if one virus is present, are others more likely to also be present in the same site?). The goal of the studies described here was to determine the distribution of HSV-1, HSV-2, and VZV DNA in autonomic and sensory ganglia of the head and neck and to determine whether the presence of virus DNA in one site was predictive of the presence of virus DNA at another site in the same individual or of another virus in the same site.Materials and methods. The ganglia used in these studies were collected from whole embalmed bodies that had been donated to the Medical College of Georgia for use in anatomical education and not from pathology specimens or from specimens collected for diagnostic purposes. The collection and study of donated human material was conducted under Medical College of Georgia Human Assurance Committee protocol #02-06-341. The mean ‫ע(‬ standard deviation)age of cadavers used in this study was years (range, 48-96 years). The 80.8 ‫ע‬ 10.3 age, sex, and presumed cause of death for each donor involved in this study are l...