Nucleic Acids Research, 1995, Vol. 23, No. 24 4978-4985
© 1995
Articles |
Transcription factors interacting with herpes simplex virus 
gene promoters in sensory neurons
Institute fuür Molekularbiologie II de Universitaät Zuürich Winterthurerstrasse 190, Ch-8057 Xuürich, Switzerland
*To whom correspondence should be addressed
Received October 4, 1995. Accepted November 6, 1995.
Interference with VP16-mediated activation of herpes virus immediate-early (or 
) genes is thought to be the major cause of establishing viral latency in sensory neurons. This could be brought about by lack of a key activating transcription factors) or active repression. In this study we find that sensory neurons express all important components for VP16-mediated gene induction, such as the POU transcription factor Oct-1, host cell factor (HCF) and GABP/ß. However, Oct-1 and GABP/ß are only present at low levels and the VP16-induced complex (VIC) appears different. We do not find protein expression of the transcription factor Oct-2, implicated by others as an gene repressor. The POU factor N-Oct3 (Brn 2 or POU3F2) is also present in sensory neurons and binds viral TAATGARAT motifs with higher affinity than Oct-1, Indicating that It may be a candidate repressor for competitive binding to TAATGARAT motifs. When transfected into HeLa cells, where Oct-1 and GABP/ß are highly abundant, N-Oct3 represses model promoters with murtimerlzed TAATGARAT motifs, but fails to repress complete gene promoters. Taken together our findings suggest that modulation of gene promoters could contribute to viral latency when low concentrations of the activating transcription factors Oct-1 and GABP/ß prevail. Our data, however, refute the notion that competing Oct factors are able to block gene transcription to achieve viral latency.
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