THE REGULATION BY LIGHT OF RETINAL NECROSIS AND THE IMMUNE-RESPONSE FOLLOWING ANTERIOR-CHAMBER INOCULATION OF HERPES-SIMPLEX VIRUS TYPE-1

Citation
M. Kahn et al., THE REGULATION BY LIGHT OF RETINAL NECROSIS AND THE IMMUNE-RESPONSE FOLLOWING ANTERIOR-CHAMBER INOCULATION OF HERPES-SIMPLEX VIRUS TYPE-1, Archives of virology, 131(1-2), 1993, pp. 115-126
Citations number
16
Categorie Soggetti
Virology
Journal title
ISSN journal
03048608
Volume
131
Issue
1-2
Year of publication
1993
Pages
115 - 126
Database
ISI
SICI code
0304-8608(1993)131:1-2<115:TRBLOR>2.0.ZU;2-T
Abstract
Following anterior chamber injection of the KOS strain of herpes simpl ex virus type 1 into Balb/c mice a characteristic pathologic response occurs. When examined 10-14 days later there is intense anterior segme nt inflammation of the injected eye, but the retina is spared. In cont rast, the contralateral eye undergoes intense and destructive retiniti s with little or no involvement of the anterior segment. Coincident wi th these observations is the induction of ACAID (for anterior chamber associated immune deviation) which is characterized by a suppressed DT H response, normal antibody titers, and normal cytolytic T-cell respon ses to HSV antigens. Since we have recently demonstrated that ACAID do es 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 injecti on of HSV-1, contralateral retinitis is abolished. Concurrent with the abrogation of retinitis, is the elimination of ACAID to HSV-1 antigen s. In addition, although contralateral retinitis and ACAID do not deve lop in dark-reared mice if they are placed in the light immediately fo llowing injection, both can be re-established in dark-reared animals f ollowing a 2 week period of re-adaptation to light. Our results demons trate that the entrance of light into the eye is not only important fo r ACAID, but also for the development of contralateral HSV-induced ret initis.