The regulation by light of retinal necrosis and the immune response following anterior chamber inoculation of herpes simplex virus type-1.

Following anterior chamber injection of the KOS strain of herpes simplex virus type 1 into Balb/c mice a characteristic pathologic response occurs. When examined 10-14 days later there is intense anterior segment inflammation of the injected eye, but the retina is spared. In contrast, the contralateral eye undergoes intense and destructive retinitis with little or no involvement of the anterior segment. Coincident with these observations is the induction of ACAID (for anterior chamber associated immune deviation) which is characterized by a suppressed DTH response, normal antibody titers, and normal cytolytic T-cell responses to HSV antigens. Since we have recently demonstrated that ACAID does not take place in the absence of light (i.e., is light dependent), we have examined the effect of light on the HSV-retinitis model. When Balb/c mice are either dark-reared or dark-adapted prior to AC injection of HSV-1, contralateral retinitis is abolished. Concurrent with the abrogation of retinitis, is the elimination of ACAID to HSV-1 antigens. In addition, although contralateral retinitis and ACAID do not develop in dark-reared mice if they are placed in the light immediately following injection, both can be re-established in dark-reared animals following a 2 week period of re-adaptation to light. Our results demonstrate that the entrance of light into the eye is not only important for ACAID, but also for the development of contralateral HSV-induced retinitis.