ACAID requires early replication of HSV-1 in the injected eye.

Abstract

After uniocular anterior chamber inoculation of the KOS strain of HSV-1 in BALB/c mice, acute retinal necrosis develops in the uninoculated eye. These mice exhibit suppression of virus-specific delayed hypersensitivity which is the hallmark of anterior chamber associated immune deviation (ACAID). In contrast, inoculation of C57BL/6 mice with KOS induces vigorous virus-specific DTH, and there is no retinal necrosis in the uninoculated eye. We performed experiments using RH116, a mutant of KOS and SC16, a neurovirulent strain of HSV-1, in BALB/c and C57BL/6 mice to examine whether virus or host factors determine the outcome of anterior chamber inoculation of HSV-1 (ACAID or DTH, retinal necrosis or retinal preservation). We found that high titers of virus (approximately 10(5)) within the first 24 hours in the inoculated eye were linked to the induction of ACAID and that the induction of ACAID following anterior chamber inoculation of HSV-1 is neither an exclusive feature of a strain of virus nor is the ability to develop ACAID a distinguishing characteristic of an individual strain of mice. Taken together, our findings suggest that the interplay of both virus and host factors results ultimately in acute retinal necrosis following anterior chamber inoculation of HSV-1 in the mouse.