Abstract
Two deletions affecting the 5'' end of the herpes simplex virus thymidine kinase (TK) gene were transferred into the intact viral genome. One, extending from -12 to +189, had no effect on TK mRNA synthesis and only a small effect on TK activity, although the first 27 codons of the TK polypeptide were deleted. The other, extending from -85 to +85, severely impaired TK mRNA synthesis. Evidently, the amino terminus of the TK polypeptide is dispensable for catalytic activity, and expression of TK in viral infections requires some of the same promoter elements used in uninfected cells.