Viral isolation and systemic immune responses after intracameral inoculation of herpes simplex virus type 1 in Igh-1-disparate congenic murine strains.

Igh-1-disparate congenic murine strains differ in their susceptibility to develop contralateral chorioretinitis after intracameral (AC) inoculation with Herpes simplex virus type 1 (HSV-1): 75% of BALB/cByJ (Igh-1a) and 5% of C.B-17 (Igh-1b) develop necrotizing chorioretinitis. To determine the mechanism of influence of host genetics on development of contralateral chorioretinitis, the authors did viral isolation studies in contralateral eyes, determined in vivo and in vitro T-cell responses, and HSV-antibody levels at various times after AC inoculation of BALB/cByJ and C.B-17 mice with HSV-1. Viral isolation was similar in both mouse strains (P less than 0.2). Similarities in systemic immune responses included suppressed delayed-type hypersensitivity responses 5 days, cytotoxic T-lymphocyte and lymphocyte proliferation responses 8 days, and viral neutralizing antibody titers 5 days postinoculation (PI). Differences in systemic immune responses included: (1) delayed-type hypersensitivity responses were not suppressed in C.B-17 mice (P greater than 0.1) and were hyperactive in BALB/cByJ mice (P less than 0.025) 10 days PI and (2) HSV-neutralizing antibody production was higher in C.B-17 mice 10 days PI. These data suggest that the mere presence of HSV-1 in the uninoculated eye is insufficient for the development of chorioretinitis. Virus-specific delayed-type hypersensitivity reactions might be involved in the pathogenesis of retinitis in BALB/cByJ mice; and virus-neutralizing antibodies and suppressed HSV-specific delayed-type hypersensitivity reactions might be instrumental in the protection enjoyed by C.B-17 mice.