A virion protein of herpes simplex virus type 1 (HSV-1) specifically and potently activates transcription of the viral immediate early genes. Appropriate function of this protein, termed VP16, depends on an acidic transcriptional activation domain located within the 78 carboxyl-terminal amino acids of the protein. Mutated forms of the protein lacking this acidic domain lose the ability to activate transcription, and can dominantly interfere with the trans-activation function of native VP16 (ref. 1). We have prepared stably transformed mouse L cells that constitutively express a form of VP16 lacking its acidic activating domain. In this report we show that these cells are selectively impaired in their capacity to support the lytic infectious cycle of HSV-1, and that this impairment results from their inability to support immediate early transcription.
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