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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-l) 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,...

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Published in:The Journal of infectious diseases 1979-10, Vol.140 (4), p.534-540
Main Authors: Davis, William B., Taylor, John A., Oakes, John E.
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Taylor, John A.
Oakes, John E.
description The effects of virus-specific antibody on the pathogenesis of infection due to herpes simplex virus type 1 (HSV-l) 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-l 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 antibodymediated 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.
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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-l 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. 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source Oxford University Press Archive; JSTOR Journals and Primary Sources
subjects Animals
Antibodies
Antibodies, Viral - administration & dosage
Antibody Specificity
Antiserum
Brain
Central nervous system
Encephalitis - immunology
Encephalitis - prevention & control
Human herpesvirus 1
Human resources
Immune Sera
Immunization
Immunosuppression
Infections
Inoculation
Keratitis, Dendritic - complications
Major Articles
Mice
Rabbits
Simplexvirus - immunology
Trigeminal ganglion
Virus Replication
Viruses
title Ocular Infection with Herpes Simplex Virus Type 1: Prevention of Acute Herpetic Encephalitis by Systemic Administration of Virus-Specific Antibody
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