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Article
December 1966

Herpes Simplex UveitisAn Experimental Study

Author Affiliations

San Francisco
From the Department of Ophthalmology and the Francis I. Proctor Foundation for Research in Ophthalmology, University of California School of Medicine, San Francisco Medical Center, San Francisco. Dr. Martenet is now at the University Eye Clinic, Raemistrasse 100, 8006 Zurich, Switzerland.

Arch Ophthalmol. 1966;76(6):858-865. doi:10.1001/archopht.1966.03850010860014
Abstract

To explain herpes simplex virus inflammation of the anterior uveal tract, two mechanisms have been postulated: (1) that the inflammation is the result of direct invasion of the iris and ciliary body by virus, or (2) that it is an antigen-antibody reaction resulting from hypersensitivity to viral antigen (Braley,1 Kimura2). In the latter event, the viral antigen either reacts directly or produces its effect by combining with antibody and then reacting with sensitized cells.

Herpetic iridocyclitis is usually secondary to herpetic corneal inflammation in patients who have previously had a cutaneous or mucosal herpes simplex infection, and many of whom have ample circulating antibody to herpes simplex virus. In such cases the infection remains localized to the skin, mucous membrane, cornea, and uveal tissue. Primary herpes simplex infections, on the other hand, although usually characterized by mouth and skin lesions of a benign type, may become disseminated.

It

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