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Journal of Virology, April 2002, p. 3605-3614, Vol. 76, No. 8
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.8.3605-3614.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Replication Fidelity of the supF Gene Integrated in the Thymidine Kinase Locus of Herpes Simplex Virus Type 1

Ying T. Hwang, Bu-Yuan Liu,,{dagger} and Charles B. C. Hwang*

Department of Microbiology and Immunology, SUNY Upstate Medical University, Syracuse, New York 13210

Received 20 September 2001/ Accepted 7 January 2002

Recombinant viruses were constructed to have an Escherichia coli replicon containing a mutagenesis marker, the supF gene, integrated within the thymidine kinase locus (tk) of herpes simplex virus type 1. These viruses expressed either wild-type or mutant DNA polymerase (Pol) and were tested in a mutagenesis assay for the fidelity of their replication of the supF gene. A mutation frequency of approximately 10-4 was observed for wild-type strain KOS-derived recombinants in their replication of the supF gene. However, recombinants derived from the PAAr5 Pol mutant, which has been demonstrated to have an antimutator phenotype in replicating the tk gene, had three- to fourfold increases in supF mutation frequency (P < 0.01), a result similar to that exhibited when the supF gene was induced to replicate as episomal DNA (Y. T. Hwang, B.-Y. Liu, C.-Y. Hong, E. J. Shillitoe, and C. B. C. Hwang, J. Virol. 73:5326-5332, 1999). Thus, the PAAr5 Pol mutant had an antimutator function in replicating the tk gene and was less accurate in replicating the supF gene than was the wild-type strain. The spectra of mutations and distributions of substituted bases within the supF genes that replicated as genomic DNA were different from those in the genes that replicated as episomal DNA. Therefore, the differences in sequence contents between the two target genes influenced the accuracy of the Pol during viral replication. Furthermore, the replication mode of the target gene also affected the mutational spectrum.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, SUNY Upstate Medical University, 750 East Adams St., Syracuse, NY 13210. Phone: (315) 464-8739. Fax: (315) 464-7680. E-mail: hwangc{at}mail.upstate.edu.

{dagger} Present address: School of Dentistry, National Taiwan University, Taipei, Taiwan.

Journal of Virology, April 2002, p. 3605-3614, Vol. 76, No. 8
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.8.3605-3614.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Hwang, Y. T., Zuccola, H. J., Lu, Q., Hwang, C. B. C. (2004). A Point Mutation within Conserved Region VI of Herpes Simplex Virus Type 1 DNA Polymerase Confers Altered Drug Sensitivity and Enhances Replication Fidelity. J. Virol. 78: 650-657 [Abstract] [Full Text]  
  • Hwang, Y. T., Hwang, C. B. C. (2003). Exonuclease-Deficient Polymerase Mutant of Herpes Simplex Virus Type 1 Induces Altered Spectra of Mutations. J. Virol. 77: 2946-2955 [Abstract] [Full Text]  
  • Lu, Q., Hwang, Y. T., Hwang, C. B. C. (2002). Mutation Spectra of Herpes Simplex Virus Type 1 Thymidine Kinase Mutants. J. Virol. 76: 5822-5828 [Abstract] [Full Text]  


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