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Latent major r host im mechanisms by which these alternative states of viral gene expression are regulated are therefore of considerable significance for the development of vaccine and antiviral drug therapies. The activation of latent virus infection in vivo must initially occur as a single activation event occurring in one, or a few cells in response to a cellular stimulus. The measurement of the averaged gene expression in a cell population, may disguise cell heterogeneity and would not permit analysis of the temporal aspects of viral activation in single cells. It is therefore preferable to study the regulation of viral gene expression in single cells. Human immunodeficiency virus (HIV) can establish productive or latent infections in infected mammalian haemopoietic and other cell lineages (e.g. Folks et al., 1988; Rosenberg and Fauci, 1989). The HIV-1 and HIV-2 long terminal repeats (LTRs) have been shown to contain compact enhancer/promoter elements that control the level of viral gene expression and are inducible by many cellular physiological (e.g. l., auf nd , 198 ng e.g. nd , 199 ral gene expression. Herpes viruses also give rise to both productive and latent viral infections. Primary infection with human cytomegalovirus (hCMV) usually results in establishment of latent infection without overt disease (Rapp and Geder, 1987). Although there have been many studies of hCMV latency in vitro (e.g. Bucher et al., 1983) there is a limited understanding of the molecular mechanisms involved. Sodium butyrate, a short-chain carboxylic acid, activates gene expression and replication of a number of human herpes and retroviruses including Epstein Barr virus (Luka et al., 1979; Contreras-Salazar et al., 1990), herpes simplex virus (HSV) (Ash, 1986), type C virus (Long et al., 1980), human cytomegalovirus (hCMV) (Radsak et al., 1989; Tanaka et al., 1991) and HIV (Bohan et al., 1987, 1989; Golub et al., 1991; Laughlin et al., 1993). Little is known of the mechanism of activation of hCMV and HIV by sodium butyrate. It has been shown that sodium butyrate activates HIV gene expression through transcriptional activation of the long terminal repeat 1

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@inproceedings{Alan1995AaAA, title={Aa Aa Aa Aa Aa Aa Aa Aa Aaa Aaa Aaa Aaa Aaa Aaa Aaa Aaa Aaa Aaa Aaa Aaa Aaa Aaa Aaa Aaa}, author={Micha l El Alan and Martin Braddock and E White and Masayuki Masuko and Lorene Amet and Gil . Kingsman and Susan M . Kingsman}, year={1995} }