The pathogenesis of corneal inflammation due to Herpes simplex virus. I. Corneal hypersensitivity in the rabbit.

Corneal immune rings were produced with purified herpes simplex virus (HSV) antigen in both systemically and locally (intracorneal) HSV-sensitized rabbits. The ringlike corneal opacity consisted of a local accumulation of inflammatory cells, HSV antigen, host-antibody, and complement. A similar linear opacity was produced by injection of purified HSV antigen and anti-HSV antibody simultaneously at opposite sides of a normal rabbit cornea in a nonsensitized rabbit. Immunohistopathologic studies of experimental stromal herpes keratitis in rabbits induced by corneal infection with HSV revealed antigen, host-antibody, complement (C3), and inflammatory cells at the site of the stromal infiltrate. The tissue injury occurring in stromal herpes keratitis appears to result from HSV antigen-HSV antibody interaction; this attracts serum complement and results in the leukotaxis of polymorphonuclear leukocytes which constitute the major corneal infiltrate seen in stromal keratitis.