Abstract
Summary
Two periods of homologous intracerebral resistance to ic challenge with HSV were demonstrated following sc inoculation of HSV. The early protective effect occurred between days 0–6; the late period of resistance occurred about day 21. The early intracerebral resistance was characterized by nonspecificity (resistance to heterologous ic challenge with EMCV) and absence of serum neutralizing antibody to HSV. The late period of intracerebral resistance to ic HSV infection was specific (no resistance to heterologous ic challenge with EMCV) and associated with serum HSV neutralizing antibody. Indirect evidence indicated that the small sc dose of HSV used was capable of replicating in some mice and reaching the brain. However, interferon and virus were not detected in brain homogenates of apparently healthy mice with the small doses of HSV inoculated subcutaneously. The inability to explain the Magrassi phenomenon may be due to the relative insensitivity of the techniques employed. However, the availability of a model system in the mouse may permit further investigations of this phenomenon.
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