Transcriptional activation and repression of cellular genes during Herpes simplex virus infection are mediated by distinct viral immediate-early proteins (ICP4 and ICP22, respectively).
May guide antiviral targeting of HSV IE proteins; leaves open translation from animal models to human disease.
Nuclear run-off and pulse-labelling techniques have been used to study the changes in transcription rates of a number of cellular genes during infection with Herpes simplex virus. The majority of these genes show a decrease in transcription rate to about 60% of that observed prior to infection. In contrast, a small number of genes are transcriptionally activated during infection. These effects, which occur at a point in infection after the synthesis of viral proteins but prior to the onset of viral DNA synthesis, are mediated by different immediate-early proteins of the virus. Thus we show that, whilst transcriptional activation requires a functional ICP4 protein, repression is dependent upon the presence of another immediate early protein--ICP22.
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Kemp et al. (1988) studied this question.
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