Ocular infection with herpes simplex virus type 1: prevention of acute herpetic encephalitis by systemic administration of virus-specific antibody.
The effects of virus-specific antibody on the pathogenesis of infection due to herpes simplex virus type 1 (HSV-1) following corneal inoculation of young adult mice were studied. HSV-1 was inoculated onto the corneal surface immediately after trephination with a capillary pipette. After inoculation, virus spread to the trigeminal ganglion and brain within two days and caused acute herpetic encephalitis, which killed infected animals eight to 10 days after infection. Rabbit hyperimmune antisera to HSV-1 were prepared, diluted to contain antibody at a titer of 1:150, and administered intraperitoneally to mice 8 hr after corneal infection. Administration of antisera did not interfere with the spread of HSV-1 from the site of infection to the trigeminal ganglion and brain but did reduce the multiplication of virus within the central nervous system. Reduction in viral replication resulted in complete recovery of the animals that were given antibody to HSV-1. however, the animals were not protected if they were irradiated with 390 rad 24 hr prior to administration of antibody. This observation suggested that antibody-mediated protection was not the result of in vivo neutralization of virus but instead required the presence of antibody as well as one or more radiation-sensitive components.
D000818:Animals; D000914:Antibodies, Viral / Q000008:administration & dosage*; D000918:Antibody Specificity; D004660:Encephalitis / Q000276:immunology / Q000517:prevention & control*; D007106:Immune Sera; D007114:Immunization; D007165:Immunosuppression Therapy; D007635:Keratitis, Dendritic / Q000150:complications*; D051379:Mice; D011817:Rabbits; D018139:Simplexvirus / Q000276:immunology; D014779:Virus Replication
D000914:Antibodies, Viral; D007106:Immune Sera