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Rani Bhatia Herpetic Stromal Keratitis (HSK) disease is an inflammatory process of the cornea that results from infection by Herpes Simplex Virus-1 (HSV-1). The pathogenesis of HSK starts with a primary infection, which is the focus of this project. The primary infection is usually subclinical, with most exceptions involving very young or old individuals and those who are immune suppressed. For these individuals, they may display some combination of lid vesicles, diffuse corneal opacity, neovascularization, blepharitis, conjunctivitis, and encephalitis. BALB/c mice carry the normal Fas gene, while BALB-lpr mice have a mutation in this gene that results in the protein not being expressed. Since it is known that protection of the cornea involves the apoptotic control of inflammation by corneal Fas ligand interacting with Fas+ inflammatory cells, it was appropriate to note that BALB-lpr mice (Fas-) displayed significantly worse corneal disease than wild-type BALB/c mice. The purpose of this project is to better characterize the underlying mechanism(s) responsible for differences in clinical disease between BALB/c and BALB-lpr mice following primary infection with HSV-1. In so doing we will evaluate viral shedding and inflammatory responses both in the cornea and the trigeminal ganglia. Thus far, we have collected all samples required for this analysis and are presently in the process of analyzing them.
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