Schisis contributes to necrosis in experimental HSV-1 retinitis.

Injection of the KOS strain of herpes simplex virus type 1 into the anterior chamber of one eye of a BALB/c mouse produces bilateral retinal inflammation which progresses in the contralateral eye to total retinal necrosis by day 10 post-inoculation. Although both immune and direct viral cytopathic effects have been proposed as causes of the initial infiltration, the precise mechanism(s) of the contralateral retinal necrosis remains uncertain. In this study, histopathological examination of the uninoculated eyes of HSV-1 injected BALB/c mice revealed the presence of vitreous traction against the internal limiting membrane of the retina which was associated with separation of the nerve fiber layer from the underlying ganglion cell layer. This separation resulted in avulsion of Mueller cell footplates and retinal vessels, hemorrhage into the schisis cavity and disruption of the underlying retinal architecture. The schisis began focally on day 8 or 9 post-inoculation, and the entire retina of most animals was involved by day 10 or 11. These results suggest that retinal schisis involving separation of the nerve fiber layer from the ganglion cell layer contributes to necrosis of the retina in the uninoculated contralateral eye.