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November 1967

Experimental Stromal Herpes Simplex Keratitis in Rabbits

Author Affiliations

San Francisco
From the Francis I. Proctor Foundation for Research in Ophthalmology, Department of Ophthalmology, University of California School of Medicine, San Francisco.

Arch Ophthalmol. 1967;78(5):654-663. doi:10.1001/archopht.1967.00980030656018

An attempt was made in rabbits to assess the role of systemic hypersensitivity in the production of stromal lesions in herpes simplex keratitis. Suppression of the immune response by total body x-radiation, with the eyes shielded, did not diminish the stromal lesions. It would thus seem improbable that hypersensitivity plays the major role in their production. Endothelial changes were observed that seemed to correlate with the time of appearance and the severity of the deep stromal edema. Although the endothelial damage was nonspecific morphologically, the fact that it was not affected by suppression of the immune response and that virus could be cultivated regularly from the endothelium suggested that the damage is probably due to the presence of virus within the endothelial cells. These findings support the concept, previously proposed by others, that at least with some strains of Herpesvirus hominis direct endothelial damage by living virus is more important than immune mechanisms in producing the stromal edema of "disciform" herpes simplex keratitis.

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