PASSIVE TRANSFER OF ANTI-HERPES-SIMPLEX VIRUS TYPE-2 MONOCLONAL AND POLYCLONAL ANTIBODIES PROTECT AGAINST HERPES-SIMPLEX VIRUS TYPE-1-INDUCED BUT NOT HERPES-SIMPLEX VIRUS TYPE-2-INDUCED STROMAL KERATITIS

Purpose. To investigate whether passive transfer of antibodies to vira l glycoproteins would protect against herpes simplex virus type 2-indu ced stromal keratitis. Methods. Balb/c mice were infected on the scari fied cornea with herpes simplex virus types I or 2 (HSV-1 and HSV-2, r espectively), and monoclonal or polyclonal antibodies were administere d intraperitoneally 24 hr later. Eyes were monitored for corneal opaci ty. Flow cytometry was used to examine the expression of glycoproteins on the surface of HSV-infected cells. Results. Passive transfer of mo noclonal antibodies to viral glycoproteins gB, gD, or gE or anti-HSV-2 hyperimmune serum were all highly effective (P < 0.005) at preventing blinding disease induced by HSV-1. In contrast, none of the antibody preparations could prevent stromal keratitis when the animals were cha llenged with various HSV-2 strains. However, antibody treatment could prevent the development of fatal encephalitis in the majority of HSV-2 infected hosts. Flow cytometry analysis revealed that gD and gB expre ssion on the membranes of HSV-2 infected corneal epithelial cells isol ated from excised corneas was substantially less (P < 0.005) than that detected on HSV-1 infected cells at both 24 and 48 hours postinfectio n. This antigenic difference was not due to the failure of HSV-2 to re plicate in corneal epithelial cells in vivo. Conclusions. Decreased le vels of membrane glycoprotein antigen expression may be one factor con tributing to the refractiveness of HSV-2-induced ocular disease to hum oral immunotherapy.