M H Ritchie1, J E Oakes, R N Lausch. 1. Department of Microbiology and Immunology, College of Medicine, University of South Alabama, Mobile 36688.
Abstract
PURPOSE: To investigate whether passive transfer of antibodies to viral glycoproteins would protect against herpes simplex virus type 2-induced stromal keratitis. METHODS: Balb/c mice were infected on the scarified cornea with herpes simplex virus types 1 or 2 (HSV-1 and HSV-2, respectively), and monoclonal or polyclonal antibodies were administered intraperitoneally 24 hr later. Eyes were monitored for corneal opacity. Flow cytometry was used to examine the expression of glycoproteins on the surface of HSV-infected cells. RESULTS: Passive transfer of monoclonal 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 challenged 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 expression on the membranes of HSV-2 infected corneal epithelial cells isolated from excised corneas was substantially less (P < 0.005) than that detected on HSV-1 infected cells at both 24 and 48 hours postinfection. This antigenic difference was not due to the failure of HSV-2 to replicate in corneal epithelial cells in vivo. CONCLUSIONS: Decreased levels of membrane glycoprotein antigen expression may be one factor contributing to the refractiveness of HSV-2-induced ocular disease to humoral immunotherapy.
PURPOSE: To investigate whether passive transfer of antibodies to viral glycoproteins would protect against herpes simplex virus type 2-induced stromal keratitis. METHODS: Balb/c mice were infected on the scarified cornea with herpes simplex virus types 1 or 2 (HSV-1 and HSV-2, respectively), and monoclonal or polyclonal antibodies were administered intraperitoneally 24 hr later. Eyes were monitored for corneal opacity. Flow cytometry was used to examine the expression of glycoproteins on the surface of HSV-infected cells. RESULTS: Passive transfer of monoclonal 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 challenged 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 expression on the membranes of HSV-2 infected corneal epithelial cells isolated from excised corneas was substantially less (P < 0.005) than that detected on HSV-1 infected cells at both 24 and 48 hours postinfection. This antigenic difference was not due to the failure of HSV-2 to replicate in corneal epithelial cells in vivo. CONCLUSIONS: Decreased levels of membrane glycoprotein antigen expression may be one factor contributing to the refractiveness of HSV-2-induced ocular disease to humoral immunotherapy.