Resistance to antiviral inhibitors caused by the mutation S889A in the highly-conserved 885-GDTDS motif of the herpes simplex virus type 1 DNA polymerase.

Virology (1993), Volume 195, Page 831

Abstract:

Most point substitutions in the highly-conserved 885-GDTDS motif of the HSV-1 DNA polymerase inactivate polymerase elongation activity. However, in an assay system based on expression by in vitro transcription-translation, the mutant GDTDA (S889A) possessed wild-type elongation activity which was highly resistant to phosphonoacetic acid and acyclovir triphosphate, but retained sensitivity to aphidicolin.

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