Herpes stromal keratitis (HSK) is the leading infectious cause of blindness in the United States and is a consequence of events following HSV-1 infection of the eye. The pathology of the disease is currently thought to be caused by a destructive, CD4(+) T helper 1 (Th1) type inflammatory immune response within the cornea rather than a cytopathic response elicited by the virus. A large percentage of people can become infected with HSV-1 as children whereas some studies have concluded that many others do not become infected with HSV-1 until much later in life. In this paper we investigate the role of increasing age on ocular HSV-1 infection. Following an ocular infection of mice with HSV-1 we observed greater pathology in the cornea during both early and late time-points in adult mice when compared to young animals. No significant differences in viral titers were observed in either the eyes or trigeminal ganglia from infected mice, regardless of age, suggesting that increased viral load may not be responsible for the ocular pathology in the adult mice. We hypothesize that age-related changes in the immune response may predispose adult animals to HSK disease.