Abstract
Five temperature-sensitive mutants of herpes simplex virus type I were analyzed for their capacity to establish latent infections in the brains of mice. One established such infections efficiently, three somewhat less efficiently, and one not at all. Mutant “leakiness” is not the explanation for the positive results, and inoculation of three of the mutants into footpads resulted in the same pattern of latent infections in spinal ganglia as was observed in brain tissue. This system is being further developed for study of the morphologic and biochemical basis of herpetic latency.
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