A role for T lymphocytes in preventing experimental herpes simplex virus type 1-induced retinitis.

We have previously shown that herpes simplex virus Type 1 (HSV-1) inoculated into the anterior chamber (AC) of one eye of BALB/c mice results in retinal destruction in the opposite eye while retinas in virus-injected eyes are preserved. In the present study, immunodeficient mice (athymic BALB/c or normal BALB/c which had received either gamma-irradiation [450 R] or cyclophosphamide [150 mg/kg treatment]), demonstrated bilateral retinal destruction upon unilateral AC inoculation of HSV-1. Reconstitution of these immunodeficient mice with spleen cells obtained from days 10-21 AC-inoculated donor mice, prior to AC inoculation of HSV-1, prevented retinal necrosis in more than 80% of both eyes. In contrast, donor cells from mice inoculated subcutaneously (SC) with HSV-1 preserved only about 30% of recipient retinas, regardless of the cell transfer time after donors received HSV-1. Normal unsensitized syngeneic donor spleen cells failed to prevent bilateral retinal necrosis in either athymic or irradiated BALB/c mice, although they eliminated recipient mortality. T cell depletion of AC- or SC-inoculated donor cells removed their retinal protective effects completely. These studies demonstrate an active role for T lymphocytes in controlling the extent of disease in a murine model of HSV-induced retinitis.