Properties of the cornea such as a lack of blood and lymphatic vessels, a lack of professional antigen-presenting cells, and exposure to immunosuppressive factors in the aqueous humor contribute to a relative state of immune privilege. Ironically, corneal damage and the accompanying visual morbidity following herpes simplex virus type 1 (HSV-1) infection does not results from uncontrolled viral replication, but from an immunoinflammatory process referred to as herpes stromal keratitis (HSK). This review highlights changes in the immune-privileged status of the cornea following HSV-1 infection that contribute to HSK.