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From the Reed Neurological Research Center and Department of Microbiology and Immunology, School of Medicine, University of California, Los Angeles, California 90024
Abstract
The mechanism by which latent herpetic infections are maintained in the neurons of murine spinal ganglia was investigated. Initially, it was found that when latently infected ganglia were transplanted to latently infected syngeneic mice, some circulating factor prevented viral reactivation. A systematic analysis of the system led to the demonstration that this effect could be reproduced when anti-viral IgG was administered to noninfected mice receiving the ganglionic transplant. Thus, IgG inhibited intraneuronal viral DNA and antigen synthesis, therefore restricting the appearance of infectious virus. Although a role for cytotoxic antibody has not been completely ruled out, this result suggests that antiviral IgG plays an important role in maintenance of latent herpetic infections.
Footnotes
1 This investigation was supported by Research Grants AI-06246 and NS-08711 from the National Institutes of Health, United States Public Health Service, Bethesda, Maryland.
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