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Latency Competence of Thirteen HSV-1 Temperature-sensitive Mutants

¹ Reed Neurological Research Center, UCLA School of Medicine, Los Angeles, California 90024, U.S.A.
² Institute of Virology, University of Glasgow, Glasgow G11 5JR, Scotland

Thirteen temperature-sensitive (ts) mutants of HSV-1 were analysed for their capacity to establish latent infections in the brains of mice. Eleven of the mutants could be classified as latency-positive or -negative; two could not be assigned to either group. Leakiness of mutants in the brain and differences in particle/infectivity ratios were found not to play a role in the results. Ts⁺ revertants of selected latency-negative mutants regained the capacity to establish latent infections, indicating that it was the ts lesion in these agents which was involved in latency. Ultrastructural studies of neuroblastoma cells infected with various mutants and maintained at the restrictive temperature showed that no absolute correlations could be made between capacity to establish latent infection and synthesis of various morphologically identifiable virus products. Finally, from a comparison of latency characteristics with previously established polypeptide phenotypes of the mutants it was concluded that one immediate early and one or more later virus functions are necessary for establishment and/or maintenance of the latent state.

^* Author to whom reprint requests should be addressed.

Received 29 November 1979; accepted 19 February 1980.

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