Abstract
Of 18 mutants containing clustered point mutations within UL24 (an open reading frame that overlaps the herpes simplex virus thymidine kinase gene on the opposite strand), 15 formed small plaques and were substantially impaired for virus growth in cell culture. Mutations conferring the small plaque phenotype disrupt regions of UL24 that share considerable sequence similarity with open reading frames common to herpesviruses of mammals and birds. We infer that UL24 is expressed and important for virus growth in cell culture and suggest that possible effects on UL24 should be considered in studies of thymidine kinase-deficient mutants.
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