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.
MARTENET A. Herpes Simplex Uveitis: An Experimental Study. Arch Ophthalmol. 1966;76(6):858–865. doi:10.1001/archopht.1966.03850010860014
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