IMMUNE EFFECTOR CELL (IEC)-MEDIATED PROTECTION FROM HSV-1 RETINITIS OCCURS IN THE BRAIN

Following uniocular anterior chamber inoculation of the ROS strain of HSV-1 into euthymic BALB/c mice, virus spreads from the injected eye t o the brain and from the brain to the optic nerve and retina of the un injected eye resulting in retinitis. Adoptive transfer of HSV-1-specif ic immune effector cells (IEC) within 24 h of anterior chamber inocula tion of virus prevents retinitis. To determine where protection occurs , mice were injected with HSV-1 via the anterior chamber route, and fl uorescently-labeled HSV-1-specific-IEC or ovalbumin-specific lymph nod e cells were adoptively transferred intravenously. The eyes and brains of these mice were sectioned and examined for virus-infected cells an d for fluorescently-labeled adoptively transferred cells. None of the mice in the group receiving an adoptive transfer of virus-specific IEC had evidence of virus infection of the ipsilateral suprachiasmatic nu cleus (SCN), whereas the ipsilateral SCN of all of the mice in the con trol groups were virus-positive by day 5 P.I. Since virus spreads from the ipsilateral SCN to the contralateral optic nerve and retina to ca use retinitis in the uninoculated eye, the results of these studies su ggest IEC-mediated protection from HSV-1 retinitis occurs proximal to the ipsilateral SCN. Furthermore, since only HSV-1-specific IEC confer red protection and only these cells were observed in the brain, protec tion and trafficking of cells after adoptive transfer was virus-specif ic.