NK CELL MODULATION OF MURINE CYTOMEGALOVIRUS RETINITIS

CMV retinitis, the most common ophthalmic infection of AIDS patients, causes blindness if left untreated. To study the role of NK cells in t he modulation of CMV ocular infection, 9.0 x 10(2) plaque-forming unit s of the Smith strain of murine CMV (MCMV) was injected into the supra ciliary space of the left eyes of BALB/c mice. Lysis of NK-sensitive t arget cells (YAC-1) by effecters from the draining lymph nodes peaked at day 5 postinfection, while the splenic cytolytic response was bipha sic, with peaks at days 2 and 7 postinfection, Flow cytometry showed t hat NK cells (DX-5(+)) increased in spleens and eyes 5 days after supr aciliary infection with MCMV compared with uninfected or mock-infected controls. Eight days after supraciliary injection with 9.0 x 10(2) pl aque forming units of MCMV, 7 of 10 NK-depleted mice developed retinit is compared with only 2 of 10 non-NK-depleted control mice. Poly(I-C) activation of NK cells in T cell-depleted animals protected mice from MCMV retinitis; only 2 of 10 mice in the poly(I-C)-treated group devel oped retinitis compared with 8 of 10 T cell-depleted, non-poly(I-C)-tr eated control mice. These results show the importance of NK cells in p reventing MCMV retinitis and suggest that NK cells may also be involve d in modulation of cytomegalovirus retinitis in human patients.