Williams M V
Department of Medical Microbiology and Immunology, Ohio State University, Columbus 43210.
Virology. 1988 Sep;166(1):262-4. doi: 10.1016/0042-6822(88)90171-7.
In studies using mutants of HSV-1 (strain 17), which are defective in inducing the HSV-specific dUTPase, Fisher and Preston concluded that since this enzyme was not essential for HSV replication, it would not be useful as a target site for the development of antiviral agents. In this study, we demonstrate that while these mutants do not induce a HSV-specific dUTPase, they do not shut off cellular dUTPase activity in infected cells and that the cellular dUTPase can function in place of the HSV-induced enzyme during the replication process. Data are also presented that demonstrate that the HSV-induced dUTPase can be used as a target site for the development of specific antiviral compounds.
