Author(s): Jager MJ, Bradley D, Atherton S, Streilein JW
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Abstract Recurrences of herpetic stromal keratitis are believed to be initiated by reactivation of herpes simplex virus infection, probably in the trigeminal ganglion. Genetic features of the virus and the host as well as the immune status of the host influence the outcome of infection. Following infection on the snout with HSV-1, mice with normal corneas usually develop mild anterior segment disease. We studied the induction of herpetic infection in mice that had abnormal corneas, containing center due to trauma or a spontaneous dystrophy. The corneal abnormality led to more frequent herpetic stromal keratitis and more severe anterior chamber reaction. In addition, we found that snout-infected mice with dystrophic corneas had an increased risk of dying from viral infection. Our data suggest that not only the strain of virus and the genetic background of the mouse, but also the state of the cornea itself, can contribute to susceptibility to ocular herpes infection.
This article was published in Exp Eye Res
and referenced in Journal of Clinical & Experimental Ophthalmology