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Restoration of Wild-type Pathogenicity to an Attenuated DNA Polymerase Mutant of Herpes Simplex Virus Type 1

Brendan A. Larder

Graham Darby

Division of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 2QQ, U.K.

The drug-resistant variant, RSC-26, which was derived from the herpes simplex virus type 1 wild-type strain SC16, expresses an altered DNA polymerase and has reduced pathogenicity in animal models. To determine whether the attenuation in pathogenicity was due solely to mutation in the polymerase gene, a fragment of the wild-type gene was cloned, transferred into the genome of RSC-26 and recombinants were isolated. Three recombinants examined had similar properties to wild-type virus with respect to their sensitivity to antiviral drugs, DNA polymerase activities and their pathogenicity for mice. These results strongly suggest that expression of the altered polymerase of RSC-26 results in attenuated pathogenicity.

Keywords: HSV-1, DNA polymerase, pathogenicity

Present address: Department of Biochemical Virology, The Wellcome Research Laboratories, Langley Court, Beckenham, Kent BR3 3BS, U.K.

Received 8 April 1986; accepted 10 July 1986.

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