Lyt-1+ T cells participate in recovery from ocular herpes simplex virus type 1 infection.

Herpes simplex virus type 1 (HSV-1) inoculated on the abrased cornea of 4-week-old irradiated (450 R) SJL/J mice spread to the brain and produced a fatal viral encephalitis by 10-12 days post-infection. Adoptive transfer of 2-3 X 10(7) virus-sensitized non-adherent spleen cells 24 hrs before virus challenge led to recovery from infection. Recovery was due to suppression of HSV-1 replication in the brain rather than prevention of virus spread from the cornea to the central nervous system. If the immune cells were treated with monoclonal anti-Thy 1.2 and complement before transfer the protective effect was lost. Pretreatment of the virus-sensitized spleen cells with monoclonal antibody to the Lyt-1 membrane antigen also significantly reduced or completely abrogated the protective effect. In contrast, depletion of Lyt-2 bearing cells resulted in a less-pronounced and not statistically significant loss of protection. It was further observed that spleen cell reconstituted, virus challenged mice had considerably higher serum antibody titers (greater than 10-fold) than unreconstituted virus challenged controls. The results indicate that lymphocytes with a Thy 1.2+, Lyt-1+, Lyt-23- phenotype play a predominant role in promoting recovery following corneal HSV-1 infection.