Necrotizing chorioretinitis in mice inoculated with herpes simplex virus type 1 with or without glycoprotein C: anterior chamber-associated immune deviation does not persist.

BALB/c mice developed contralateral necrotizing retinitis following intracameral inoculation with herpes simplex virus type 1 (HSV-1). The animals showed a positive delayed-type hypersensitivity (DTH) response at 10 days postinoculation, indicating that the anterior chamber-associated immune deviation was transient after HSV-1 inoculation. Since glycoprotein C (gC) of HSV-1 is a major immunogen, we examined DTH and the antibody response induced by a gC-deficient strain TN-1 and compared them with those induced by the recombinant gC-positive mutants. We found that gC was not required for DTH reaction, and that gC was neither necessary for nor protective against the contralateral retinal necrosis. Serial lymphocyte subset analyses of the draining lymph nodes revealed an absolute increase of B cells, CD4-positive T cells, and CD8-positive T cells. CD4-positive T cells but not CD8-positive T cells increased in the contralateral eyes during the inflammation and necrosis. The coincident emergence of the positive DTH and contralateral retinal necrosis of HSV-1-inoculated mice, together with the presence of CD4-positive cells in the retina, indicated that CD4-positive T cells responsible for DTH induction may participate in the retinal necrosis.