Use of monoclonal antibody directed against herpes simplex virus glycoproteins to protect mice against acute virus-induced neurological disease

Publisher Website
Google Scholar
Abstract
Monoclonal antibodies HC1 and HD1, directed against herpes simplex virus type 1 (HSV-1) glycoproteins gC and gD, respectively, were evaluated for their ability to passively immunize mice against acute virus-induced neurological disease after footpad inoculation with HSV-1 or HSV-2. Control virus-infected mice receiving a single i.p. injection of normal serum died 7-10 days after the spread of virus from footpad to spinal cord and brain. A single i.p. injection of either HC1 or HD1 antibody protected mice from neurological illness and death when administered to HSV-1 (strain HTZ)-infected mice at 2 h before virus challenge or at 24 h after virus inoculation. To determine the in vivo specificity of the antibodies, passive transfer studies were performed with mice infected with the MP strain of HSV-1, a mutant of HSV-1 (mP) which is defective in the production of glycoprotein gC. HD1 antibody decreased the incidence of neurological illness in MP- and mP-infected mice; HC1 antibody, which protected mP-infected animals, failed to protect mice infected with the MP strain. When HD1 antibody was administered to HSV-2 (strain G)-infected mice at 2 h before virus challenge or at 6 h (but not 24 h) after virus inoculation, 100% of the infected animals receiving HD1 antibody survived. Of HSV-2 (strain G)-infected animals passively immunized with HC1 antibody, 100% developed neurological illness and died. These results provide in vivo evidence that the HSV-induced glycoprotein gC expresses type-specific antigenic determinants, glycoprotein gD expresses type-common determinants.