Ace, C. I., McKee, T. A., Ryan, J. M., Cameron, J. M. & Preston, C. M. (1989). Construction and characterization of a herpes simplex virus type 1 mutant unable to transinduce immediate-early gene expression. Journal of Virology63, 2260-2269.
[Google Scholar]
Alvira, M. R., Goins, W. F., Cohen, J. B. & Glorioso, J. G. (1999). Genetic studies exposing the splicing events involved in herpes simplex virus type 1 latency-associated transcript production during lytic and latent infection. Journal of Virology73, 3866-3876.
[Google Scholar]
Arthur, J. L., Everett, R. D., Brierley, I. & Efstathiou, S. (1998). Disruption of the 5′ and 3′ splice sites flanking the major latency-associated transcripts of herpes simplex type 1: evidence for alternate splicing in lytic and latent infections. Journal of General Virology79, 107-116.
[Google Scholar]
Bates, P. A. & DeLuca, N. A. (1998). The polyserine tract of herpes simplex virus ICP4 is required for normal viral gene expression and growth in murine trigeminal ganglia. Journal of Virology72, 7115-7124.
[Google Scholar]
Bohensky, R. A., Papavassiliou, A. G., Gelman, I. H. & Silverstein, S. (1993). Identification of a promoter mapping within the reiterated sequences that flank the herpes simplex virus type 1 UL region. Journal of Virology67, 632-642.
[Google Scholar]
Bohensky, R. A., Lagunoff, M., Roizman, B., Wagner, E. K. & Silverstein, S. (1995). Two overlapping transcription units which extend across the L–S junction of herpes simplex virus type 1. Journal of Virology69, 2889-2897.
[Google Scholar]
Bruni, R. & Roizman, B. (1996). Open reading frame P – a herpes simplex virus gene repressed during productive infection encodes a protein that binds a splicing factor and reduces synthesis of viral proteins made from spliced mRNA. Proceedings of the National Academy of Sciences, USA93, 10423-10427.[CrossRef][Google Scholar]
Cai, W. & Schaffer, P. A. (1989). Herpes simplex virus type 1 ICP0 plays a critical role in the de novo synthesis of infectious virus following transfection of viral DNA. Journal of Virology63, 4579-4589.
[Google Scholar]
Cai, W. & Schaffer, P. A. (1991). A cellular function can enhance gene expression and plating efficiency of a mutant defective in the gene for ICP0, a transactivating protein of herpes simplex virus type 1. Journal of Virology65, 4078-4090.
[Google Scholar]
Cai, W. & Schaffer, P. A. (1992). Herpes simplex virus type 1 ICP0 regulates expression of immediate-early, early and late genes in productively infected cells. Journal of Virology66, 2904-2915.
[Google Scholar]
Cai, W., Astor, T. L., Liptak, L. M., Cho, C., Coen, D. M. & Schaffer, P. A. (1993). The herpes simplex virus type 1 regulatory protein ICP0 enhances viral replication during acute infection and reactivation from latency. Journal of Virology67, 7501-7512.
[Google Scholar]
Carrozza, M. J. & DeLuca, N. A. (1996). Interaction of the viral activator protein ICP4 with TFIID through TAF250. Molecular and Cellular Biology16, 3085-3093.
[Google Scholar]
Chelbi-Alix, M. K. & de The, H. (1999). Herpes virus induced proteasome-dependent degradation of the nuclear bodies-associated PML and Sp100 proteins. Oncogene18, 935-941.[CrossRef][Google Scholar]
Chen, J. & Silverstein, S. (1992). Herpes simplex viruses with mutations in the gene encoding ICP0 are defective in gene expression. Journal of Virology66, 2916-2927.
[Google Scholar]
Chen, X., Schmidt, M. C., Goins, W. F. & Glorioso, J. C. (1995). Two herpes simplex virus type 1 latency-active promoters differ in their contributions to latency-associated transcript expression during lytic and latent infections. Journal of Virology69, 7899-7908.
[Google Scholar]
Chen, S.-H., Kramer, M. F., Schaffer, P. A. & Coen, D. M. (1997). A viral function represses accumulation of transcripts from productive-cycle genes in mouse ganglia latently infected with herpes simplex virus. Journal of Virology71, 5878-5884.
[Google Scholar]
Cheung, P., Panning, B. & Smiley, J. R. (1997). Herpes simplex virus immediate-early proteins ICP0 and ICP4 activate the endogenous human α-globin gene in nonerythroid cells. Journal of Virology71, 1784-1793.
[Google Scholar]
Cleary, M. A., Stern, S., Tanaka, M. & Herr, W. (1993). Differential positive control by Oct-1 and Oct-2 – activation of a transcriptionally silent motif through Oct-1 and VP16 corecruitment. Genes & Development7, 72-83.[CrossRef][Google Scholar]
Clements, G. B. & Stow, N. D. (1989). A herpes simplex virus type 1 mutant containing a deletion within immediate early gene 1 is latency-competent in mice. Journal of General Virology70, 2501-2506.[CrossRef][Google Scholar]
Coen, D. M., Weinheimer, S. P. & McKnight, S. L. (1986). A genetic approach to promoter recognition during trans induction of viral gene expression. Science234, 53-59.[CrossRef][Google Scholar]
Coen, D. M., Kosz-Vnenchak, M., Jacobson, J. G., Leib, D. A., Bogard, C. L., Schaffer, P. A., Tyler, K. L. & Knipe, D. M. (1989). Thymidine kinase-negative herpes simplex virus mutants establish latency in mouse trigeminal ganglia but do not reactivate. Proceedings of the National Academy of Sciences, USA86, 4736-4740.[CrossRef][Google Scholar]
Cook, W. J., Lin, S. M., DeLuca, N. A., Moyinhan, E. B. & Coen, D. M. (1995). Induction of transcription by a viral regulatory protein depends on the relative strengths of functional TATA boxes. Molecular and Cellular Biology15, 4998-5006.
[Google Scholar]
Deb, S. P., Deb, S. & Brown, D. R. (1994). Cell-type-specific induction of the UL9 gene of HSV-1 by cell signalling pathway. Biochemical and Biophysical Research Communications205, 44-51.[CrossRef][Google Scholar]
DeLuca, N. A. & Schaffer, P. A. (1985). Activation of immediate-early, early and late promoters by temperature-sensitive and wild-type forms of herpes simplex virus type 1 protein ICP4. Molecular and Cellular Biology5, 558-570.
[Google Scholar]
Dent, C. L., Lillycrop, K. A., Estridge, J. K., Thomas, N. S. B. & Latchman, D. S. (1991). The B-cell and neuronal forms of the octamer-binding protein Oct-2 differ in DNA-binding specificity and functional activity. Molecular and Cellular Biology11, 3925-3930.
[Google Scholar]
Deshmane, S. L. & Fraser, N. W. (1989). During latency, herpes simplex virus type 1 DNA is associated with nucleosomes in a chromatin structure. Journal of Virology63, 943-947.
[Google Scholar]
Devi-Rao, G. B., Goodart, S. A., Hecht, L. M., Rochford, R., Rice, M. A. & Wagner, E. K. (1991). Relationship between polyadenylated and nonpolyadenylated herpes simplex virus type 1 latency-associated transcripts. Journal of Virology65, 2179-2190.
[Google Scholar]
Devi-Rao, G. B., Bloom, D. C., Stevens, J. G. & Wagner, E. K. (1994). Herpes simplex virus type 1 DNA replication and gene expression during explant-induced reactivation of latently infected murine sensory ganglia. Journal of Virology68, 1271-1282.
[Google Scholar]
Dobson, A. T., Margolis, T. P., Sedarati, F., Stevens, J. G. & Feldman, L. T. (1990). A latent, nonpathogenic HSV-1-derived vector stably expresses β-galactosidase in mouse neurons. Neuron5, 353-360.[CrossRef][Google Scholar]
Dolan, A., Jamieson, F. E., Cunningham, C., Barnett, B. C. & McGeoch, D. J. (1998). The genome sequence of herpes simplex virus type 2. Journal of Virology72, 2010-2021.
[Google Scholar]
Ecob-Prince, M. S. & Hassan, K. (1994). Reactivation of latent herpes simplex virus from explanted dorsal root ganglia. Journal of General Virology75, 2017-2028.[CrossRef][Google Scholar]
Ecob-Prince, M. S., Preston, C. M., Rixon, F. J., Hassan, K. & Kennedy, P. G. E. (1993a). Neurons containing latency-associated transcripts are numerous and widespread in dorsal root ganglia following footpad inoculation of mice with herpes simplex virus type 1 mutant in1814. Journal of General Virology74, 985-994.[CrossRef][Google Scholar]
Ecob-Prince, M. S., Rixon, F. J., Preston, C. M., Hassan, K. & Kennedy, P. G. E. (1993b). Reactivation in vivo and in vitro of herpes simplex virus from mouse dorsal root ganglia which contain different levels of latency-associated transcripts. Journal of General Virology74, 995-1002.[CrossRef][Google Scholar]
Efstathiou, S., Minson, A. C., Field, H. J., Anderson, J. R. & Wildy, P. (1986). Detection of herpes simplex virus-specific DNA sequences in latently infected mice and humans. Journal of Virology57, 446-455.
[Google Scholar]
Efstathiou, S., Kemp, S., Darby, G. K. & Minson, A. C. (1989). The role of herpes simplex virus type 1 thymidine kinase in pathogenesis. Journal of General Virology70, 869-879.[CrossRef][Google Scholar]
Eissenberg, J. C., Morris, G., Reuter, G. & Harnett, T. (1992). The heterochromatin associated protein HP1 is an essential protein in Drosophila with dosage effects on position effect variegation. Genetics131, 345-352.
[Google Scholar]
Everett, R. D. (1984). Transactivation of transcription by herpes virus products: requirement for two HSV-1 immediate-early polypeptides for maximum activity. EMBO Journal3, 3135-3141.
[Google Scholar]
Everett, R. D. (1985). Activation of cellular promoters during herpes simplex virus infection of biochemically transformed cells. EMBO Journal4, 1973-1980.
[Google Scholar]
Everett, R. D. (1989). Construction and characterization of herpes simplex virus type 1 mutants with defined lesions in immediate early gene 1. Journal of General Virology70, 1185-1202.[CrossRef][Google Scholar]
Everett, R. D. & Maul, G. G. (1994). HSV-1 IE protein Vmw110 causes redistribution of PML. EMBO Journal13, 5062-5069.
[Google Scholar]
Everett, R. D., Freemont, P., Saitoh, H., Orr, A., Kathoria, M. & Parkinson, J. (1998a). The disruption of ND10 during herpes simplex virus infection correlates with the Vmw110 and proteasome-dependent loss of several PML isoforms. Journal of Virology72, 6581-6591.
[Google Scholar]
Everett, R. D., Orr, A. & Preston, C. M. (1998b). A viral activator of gene expression functions via the ubiquitin-proteasome pathway. EMBO Journal17, 7161-7169.[CrossRef][Google Scholar]
Everett, R. D., Earnshaw, W. C., Findlay, J. & Lomonte, P. (1999a). Specific destruction of kinetochore protein CENP-C and disruption of cell division by herpes simplex virus immediate-early protein Vmw110. EMBO Journal18, 1526-1538.[CrossRef][Google Scholar]
Everett, R. D., Earnshaw, W. C., Pluta, A. F., Sternsdorf, T., Ainsztein, A. M., Carmena, M., Ruchaud, S., Hsu, W.-L. & Orr, A. (1999b). A dynamic connection between centromeres and ND10 proteins. Journal of Cell Science112, 3443-3454.
[Google Scholar]
Farrell, M. J., Dobson, A. T. & Feldman, L. T. (1991). Herpes simplex virus latency-associated transcript is a stable intron. Proceedings of the National Academy of Sciences, USA88, 790-794.[CrossRef][Google Scholar]
Feldman, L. T. (1994). Transcription of the HSV-1 genome in neurons in vivo. Seminars in Virology5, 207-212.[CrossRef][Google Scholar]
Field, H. J. & Wildy, P. W. (1978). The pathogenicity of thymidine kinase-deficient mutants of herpes simplex virus in mice. Journal of Hygiene81, 267-277.[CrossRef][Google Scholar]
Fraser, N. W., Block, T. M. & Spivack, J. G. (1992). The latency-associated transcripts of herpes simplex virus: RNA in search of a function. Virology191, 1-8.[CrossRef][Google Scholar]
Garber, D. A., Schaffer, P. A. & Knipe, D. M. (1997). A LAT-associated function reduces productive-cycle gene expression during acute infection of murine sensory neurons with herpes simplex virus type 1. Journal of Virology71, 5885-5893.
[Google Scholar]
Glorioso, J. C., Goins, W. F. & Fink, D. J. (1992). Herpes simplex virus-based vectors. Seminars in Virology3, 265-276.
[Google Scholar]
Glorioso, J. C., DeLuca, N. A. & Fink, D. J. (1995). Development and application of herpes simplex virus vectors for human gene therapy. Annual Review of Microbiology49, 675-710.[CrossRef][Google Scholar]
Gordon, J. Y., McKnight, J. L., Ostrove, J. M., Romanowski, E. & Araullo-Cruz, T. (1990). Host species and strain differences affect the ability of an HSV-1 ICP0 deletion mutant to establish latency and spontaneously reactivate in vivo. Virology178, 469-477.[CrossRef][Google Scholar]
Gressens, P. & Martin, J. R. (1994). In situ polymerase chain reaction: localization of HSV-2 DNA sequences in infections of the nervous system. Journal of Virological Methods46, 61-83.[CrossRef][Google Scholar]
Hagmann, M., Georgiev, O., Schaffner, W. & Douville, P. (1995). Transcription factors interacting with herpes simplex virus α gene promoters in sensory neurons. Nucleic Acids Research23, 4978-4985.[CrossRef][Google Scholar]
Halford, W. P., Gebhardt, B. M. & Carr, D. J. J. (1996). Mechanisms of herpes simplex virus type 1 reactivation. Journal of Virology70, 5051-5060.
[Google Scholar]
Harris, R. A. & Preston, C. M. (1991). Establishment of latency in vitro by the herpes simplex virus type 1 mutant in1814. Journal of General Virology72, 907-913.[CrossRef][Google Scholar]
He, X., Treacy, M. N., Simmons, D. M., Ingraham, H. A., Swanson, L. S. & Rosenberg, M. G. (1989). Expression of a large family of POU-domain relatory genes in mammalian brain development. Nature340, 35-42.[CrossRef][Google Scholar]
Herr, W. & Cleary, M. A. (1995). The POU domain: versatility in transcriptional regulation by a flexible two-in-one DNA-binding domain. Genes & Development9, 1679-1693.[CrossRef][Google Scholar]
Honess, R. W. & Roizman, B. (1974). Regulation of herpesvirus macromolecular synthesis. I. Cascade regulation of the synthesis of three groups of viral proteins. Journal of Virology14, 8-19.
[Google Scholar]
James, T. C., Eissenberg, J. C., Craig, C., Deitrich, V., Hobson, A. & Elgin, S. C. R. (1989). Distribution patterns of HP1, a heterochromatin-associated nonhistone chromosomal protein of Drosophila. European Journal of Cell Biology50, 170-180.
[Google Scholar]
Jamieson, D. R. S., Robinson, L. H., Daksis, J. I., Nicholl, M. J. & Preston, C. M. (1995). Quiescent viral genomes in human fibroblasts after infection with herpes simplex virus Vmw65 mutants. Journal of General Virology76, 1417-1431.[CrossRef][Google Scholar]
Johnson, P. A., Miyanohara, A., Levine, F., Cahill, T. & Friedmann, T. (1992). Cytotoxicity of a replication defective mutant of herpes simplex virus type 1. Journal of Virology66, 2952-2965.
[Google Scholar]
Johnson, P. A., Wang, M. J. & Friedmann, T. (1994). Improved cell survival by the reduction of immediate-early gene expression in replication-defective mutants of herpes simplex virus type 1 but not by mutation of the virion host shutoff function. Journal of Virology68, 6347-6362.
[Google Scholar]
Jordan, R., Pepe, J. & Schaffer, P. A. (1998). Characterization of a nerve growth factor-inducible cellular activity that enhances herpes simplex virus type 1 gene expression and replication of an ICP0 null mutant in cells of neural lineage. Journal of Virology72, 5373-5382.
[Google Scholar]
Katz, J. P., Bodin, E. T. & Coen, D. M. (1990). Quantitative polymerase chain reaction analysis of herpes simplex virus DNA in ganglia of mice infected with replication-incompetent mutants. Journal of Virology64, 4288-4295.
[Google Scholar]
Kemp, L. M. & Latchman, D. S. (1989). Regulated expression of herpes simplex virus immediate-early genes in neuroblastoma cells. Virology171, 607-610.[CrossRef][Google Scholar]
Kemp, L. M., Dent, C. L. & Latchman, D. S. (1990). Octamer motif mediates transcriptional repression of HSV immediate-early genes and octamer-containing cellular promoters in neuronal cells. Neuron4, 215-222.[CrossRef][Google Scholar]
Kosz-Vnenchak, M., Coen, D. M. & Knipe, D. M. (1990). Restricted expression of herpes simplex virus lytic genes during establishment of latent infection by thymidine kinase-negative mutant viruses. Journal of Virology64, 5396-5402.
[Google Scholar]
Kosz-Vnenchak, M., Jacobsen, J., Coen, D. M. & Knipe, D. M. (1993). Evidence for a novel regulatory pathway for herpes simplex virus gene expression in trigeminal ganglion neurons. Journal of Virology67, 5383-5393.
[Google Scholar]
Kramer, M. F. & Coen, D. M. (1995). Quantification of transcripts from the ICP4 and thymidine kinase genes in mouse trigeminal ganglia latently infected with herpes simplex virus. Journal of Virology69, 1389-1399.
[Google Scholar]
Kramer, M. F., Chen, S.-H., Knipe, D. M. & Coen, D. M. (1998). Accumulation of viral transcripts and DNA during establishment of latency by herpes simplex virus. Journal of Virology72, 1177-1185.
[Google Scholar]
Kristie, T. M. & Roizman, B. (1988). Differentiation and DNA contact points of the host proteins binding at the cis site for virion-mediated induction of herpes simplex virus 1 α genes. Journal of Virology62, 1145-1157.
[Google Scholar]
Kristie, T. M., Pomerantz, J. L., Twomey, T. C., Parent, S. A. & Sharp, P. A. (1995). The cellular C1 factor of the herpes simplex virus enhancer complex is a family of polypeptides. Journal of Biological Chemistry270, 4387-4394.[CrossRef][Google Scholar]
Kristie, T. M., Vogel, J. L. & Sears, A. E. (1999). Nuclear localization of the C1 factor (host cell factor) in sensory neurons correlates with reactivation of herpes simplex virus from latency. Proceedings of the National Academy of Sciences, USA96, 1229-1233.[CrossRef][Google Scholar]
Kwon, B. S., Gangarosa, L. P., Burch, K. D., Deback, J. & Hill, J. M. (1981). Induction of ocular herpes simplex virus shedding induced by iontophoresis of epinephrine into rabbit cornea. Investigative Ophthalmology & Visual Science21, 442-449.
[Google Scholar]
La Boissière, S., Hughes, T. & O’Hare, P. (1999). HCF-dependent nuclear import of VP16. EMBO Journal18, 480-489.[CrossRef][Google Scholar]
Lachmann, R. H. & Efstathiou, S. (1997). Utilization of the herpes simplex virus type 1 latency-associated regulatory region to drive stable reporter gene expression in the nervous system. Journal of Virology71, 3197-3207.
[Google Scholar]
Lachmann, R. H., Browne, H. C. & Efstathiou, S. (1996). A murine RNA polymerase I promoter inserted into the herpes simplex virus type 1 genome is functional during lytic, but not latent, infection. Journal of General Virology77, 2575-2582.[CrossRef][Google Scholar]
Lachmann, R. H., Sadarangani, M., Atkinson, H. R. & Efstathiou, S. (1999). An analysis of herpes simplex virus gene expression during latency establishment and reactivation. Journal of General Virology80, 1271-1282.
[Google Scholar]
Lagunoff, M. & Roizman, B. (1994). Expression of a herpes simplex virus 1 open reading frame antisense to the γ134.5 gene and transcribed by an RNA 3′ coterminal with the unspliced latency-associated transcript. Journal of Virology68, 6021-6028.
[Google Scholar]
Lagunoff, M. & Roizman, B. (1995). The regulation of synthesis and properties of the protein product of open reading frame P of the herpes simplex virus 1 genome. Journal of Virology69, 3615-3623.
[Google Scholar]
Lagunoff, M., Randall, G. & Roizman, B. (1996). Phenotypic properties of herpes simplex virus 1 containing a derepressed open reading frame P gene. Journal of Virology70, 1810-1817.
[Google Scholar]
Latchman, D. S. (1999). POU family transcription factors in the nervous system. Journal of Cellular Physiology179, 126-133.[CrossRef][Google Scholar]
Lee, L. Y. & Schaffer, P. A. (1998). A virus with a mutation in the ICP4-binding site in the L/ST promoter of herpes simplex virus type 1, but not a virus with a mutation in open reading frame P, exhibits cell-type-specific expression of γ134.5 transcripts and latency-associated transcripts. Journal of Virology72, 4250-4264.
[Google Scholar]
Lehming, N., Le Saux, A., Schuller, J. & Ptashne, M. (1998). Chromatin components as part of a putative transcriptional repressing complex. Proceedings of the National Academy of Sciences, USA95, 7322-7326.[CrossRef][Google Scholar]
Leib, D. A., Coen, D. M., Bogard, C. L., Hicks, K. A., Yager, D. R., Knipe, D. M., Tyler, K. L. & Schaffer, P. A. (1989). Immediate-early regulatory gene mutants define different stages in the establishment and reactivation of herpes simplex virus latency. Journal of Virology63, 759-768.
[Google Scholar]
Leist, T. P., Sandri-Goldin, R. M. & Stevens, J. G. (1989). Latent infections in spinal ganglia with thymidine kinase-deficient herpes simplex virus. Journal of Virology63, 4976-4978.
[Google Scholar]
Lekstrom-Himes, J. A., Pesnicak, L. & Straus, S. E. (1998). The quantity of latent viral DNA correlates with the relative rates at which herpes simplex virus types 1 and 2 cause recurrent genital herpes outbreaks. Journal of Virology72, 2760-2764.
[Google Scholar]
Lillycrop, K. A. & Latchman, D. S. (1992). Alternative splicing of the Oct-2 transcription factor RNA is differentially regulated in neuronal cells and B cells and results in protein isoforms with opposite effects on the activity of octamer/TAATGARAT-containing promoters. Journal of Biological Chemistry267, 24960-24965.
[Google Scholar]
Lillycrop, K. A., Dent, C. L., Wheatley, S. C., Beech, N. M., Ninkina, N. N., Wood, J. N. & Latchman, D. S. (1991). The octamer-binding protein Oct-2 represses HSV immediate-early genes in cell lines derived from latently infectable sensory neurons. Neuron7, 381-390.[CrossRef][Google Scholar]
Lillycrop, K. A., Estridge, J. K. & Latchman, D. S. (1993). The octamer binding protein Oct-2 inhibits transactivation of the herpes simplex virus immediate-early genes by the virion protein Vmw65. Virology196, 888-891.[CrossRef][Google Scholar]
Lillycrop, K. A., Howard, M. K., Estridge, J. K. & Latchman, D. S. (1994). Inhibition of herpes simplex virus infection by ectopic expression of neuronal splice variants of the Oct-2 transcription factor. Nucleic Acids Research22, 815-820.[CrossRef][Google Scholar]
Lokensgard, J. R., Bloom, D. C., Dobson, A. T. & Feldman, L. T. (1994). Long-term promoter activity during herpes simplex virus latency. Journal of Virology68, 7148-7158.
[Google Scholar]
Lokensgard, J. R., Berthomme, H. & Feldman, L. T. (1997). The latency-associated promoter of herpes simplex virus type 1 requires a region downstream of the transcription start site for long-term expression during latency. Journal of Virology71, 6714-6719.
[Google Scholar]
McGeoch, D. J., Dalrymple, M. A., Davison, A. J., Dolan, A., Frame, M. C., McNab, D., Perry, L. J., Scott, J. E. & Taylor, P. (1988). The complete DNA sequence of the long unique region in the genome of herpes simplex virus type 1. Journal of General Virology69, 1531-1574.[CrossRef][Google Scholar]
McLennan, J. L. & Darby, G. (1980). Herpes simplex virus latency: the cellular location of virus in dorsal root ganglia and the fate of the infected cell following virus activation. Journal of General Virology51, 233-243.[CrossRef][Google Scholar]
Mador, N., Goldenberg, D., Cohen, O., Panet, A. & Steiner, I. (1998). Herpes simplex virus type 1 latency-associated transcripts suppress viral replication and reduce immediate-early gene mRNA levels in a neuronal cell line. Journal of Virology72, 5067-5075.
[Google Scholar]
Maggioncalda, J., Mehta, A., Su, Y. H., Fraser, N. W. & Block, T. M. (1996). Correlation between herpes simplex virus type 1 reactivation from latent infection and the number of infected neurons in trigeminal ganglia. Virology225, 72-81.[CrossRef][Google Scholar]
Margolis, T. P., Sedarati, F., Dobson, A. T., Feldman, L. T. & Stevens, J. G. (1992). Pathways of viral gene expression during acute neuronal infection with HSV-1. Virology189, 150-160.[CrossRef][Google Scholar]
Maul, G. G. (1998). Nuclear domain 10, the site of DNA virus transcription and replication. BioEssays20, 660-667.[CrossRef][Google Scholar]
Maul, G. G. & Everett, R. D. (1994). The nuclear location of PML, a cellular member of the C3HC4 zinc-binding domain protein family, is rearranged during herpes simplex virus infection by the C3HC4 viral protein ICP0. Journal of General Virology75, 1223-1233.[CrossRef][Google Scholar]
Maul, G. G., Guldner, H. H. & Spivack, J. G. (1993). Modification of discrete nuclear domains induced by herpes simplex virus type 1 immediate early gene 1 product. Journal of General Virology74, 2679-2690.[CrossRef][Google Scholar]
Maul, G. G., Ishov, A. & Everett, R. D. (1996). Nuclear domain 10 as preexisting potential replication start sites of herpes simplex virus type-1. Virology217, 67-75.[CrossRef][Google Scholar]
Mehta, A., Maggioncalda, J., Bagasra, O., Thikkavarapu, S., Saikumari, P., Valyi-Nagy, T., Fraser, N. W. & Block, T. M. (1995).In situ PCR and RNA hybridization detection of herpes simplex virus sequences in trigeminal ganglia of latently infected mice. Virology206, 633-640.[CrossRef][Google Scholar]
Mellerick, D. M. & Fraser, N. W. (1987). Physical state of the latent herpes simplex virus genome in a mouse model system: evidence suggesting an episomal state. Virology158, 265-275.[CrossRef][Google Scholar]
Moriya, A., Yoshiki, A., Kita, M., Fushiki, S. & Imanishi, J. (1994). Heat shock-induced reactivation of herpes simplex virus type 1 in latently infected mouse trigeminal ganglion cells in dissociated culture. Archives of Virology135, 419-425.[CrossRef][Google Scholar]
Muller, S. & Dejean, A. (1999). Viral immediate-early proteins abrogate the modification by SUMO-1 of PML and Sp100 proteins, correlating with nuclear body disruption. Journal of Virology73, 5137-5143.
[Google Scholar]
Nichol, P. F., Chang, J. Y., Johnson, E. M. & Olivo, P. D. (1996). Herpes simplex virus gene expression in neurons: viral DNA synthesis is a critical regulatory event in the branch point between the lytic and latent pathways. Journal of Virology70, 5476-5486.
[Google Scholar]
O’Hare, P. (1993). The virion transactivator of herpes simplex virus. Seminars in Virology4, 145-155.[CrossRef][Google Scholar]
O’Hare, P. & Hayward, G. S. (1985). Evidence for a direct role for both the 175,000- and 110,000-molecular-weight immediate-early proteins of herpes simplex virus in the transactivation of delayed-early promoters. Journal of Virology53, 751-760.
[Google Scholar]
Openshaw, H., Asher, L. V. S., Wohlenberg, C., Sekizawa, T. & Notkins, A. L. (1979). Acute and latent infection of sensory ganglia with herpes simplex virus: immune control and virus reactivation. Journal of General Virology44, 205-215.[CrossRef][Google Scholar]
Perng, G.-C., Ghiasi, H., Slanina, S., Nesburn, A. B. & Weschler, S. L. (1996). The spontaneous reactivation function of the herpes simplex virus type 1 LAT gene resides completely within the first 1·5 kilobases of the 8·3-kilobase primary transcript. Journal of Virology70, 976-984.
[Google Scholar]
Phelan, A. & Clements, J. B. (1998). Posttranscriptional regulation in herpes simplex virus. Seminars in Virology8, 309-318.[CrossRef][Google Scholar]
Post, L. E. & Roizman, B. (1981). A generalized technique for deletion of specific genes in large genomes: α gene 22 of herpes simplex virus is not essential for growth. Cell25, 227-232.[CrossRef][Google Scholar]
Preston, C. M. (1979). Control of herpes simplex virus type 1 mRNA synthesis in cells infected with wild type virus or the temperature sensitive mutant tsK. Journal of Virology29, 275-284.
[Google Scholar]
Preston, C. M. & Nicholl, M. J. (1997). Repression of gene expression upon infection of cells with herpes simplex virus type 1 mutants impaired for immediate early protein synthesis. Journal of Virology71, 7807-7813.
[Google Scholar]
Preston, C. M., Mabbs, R. & Nicholl, M. J. (1997). Construction and characterization of herpes simplex virus type 1 mutants with conditional defects in immediate early gene expression. Virology229, 228-239.[CrossRef][Google Scholar]
Preston, C. M., Rinaldi, A. & Nicholl, M. J. (1998). Herpes simplex virus type 1 immediate early gene expression is stimulated by inhibition of protein synthesis. Journal of General Virology79, 117-124.
[Google Scholar]
Puga, A., Rosenthal, J. D., Openshaw, H. & Notkins, A. L. (1978). Herpes simplex virus DNA and mRNA sequences in acutely and chronically infected trigeminal ganglia of mice. Virology89, 102-111.[CrossRef][Google Scholar]
Ralph, W. M., Cabatingan, M. S. & Schaffer, P. A. (1994). Induction of herpes simplex virus immediate-early gene expression by a cellular activity expressed in Vero and NB41A3 cells after growth arrest-release. Journal of Virology68, 6871-6882.
[Google Scholar]
Ramakrishnan, R., Fink, D. J., Jiang, G., Desai, P., Glorioso, J. G. & Levine, M. (1994a). Competitive quantitative PCR analysis of herpes simplex virus type 1 DNA and latency-associated transcript RNA in latently infected cells of the rat brain. Journal of Virology68, 1864-1873.
[Google Scholar]
Ramakrishnan, R., Levine, M. & Fink, D. J. (1994b). PCR-based analysis of herpes simplex virus type 1 latency in the rat trigeminal ganglion established with a ribonucleotide reductase-deficient mutant. Journal of Virology68, 7083-7091.
[Google Scholar]
Ramakrishnan, R., Poliani, P. L., Levine, M., Glorioso, J. C. & Fink, D. J. (1996). Detection of herpes simplex virus type 1 latency-associated transcript expression in trigeminal ganglia by in situ reverse transcriptase PCR. Journal of Virology70, 6519-6523.
[Google Scholar]
Randall, G., Lagunoff, M. & Roizman, B. (1997). The product of ORF O located within the domain of herpes simplex virus 1 genome transcribed during latent infection binds to and inhibits in vitro binding of infected cell protein 4 to its cognate DNA site. Proceedings of the National Academy of Sciences, USA94, 10379-10384.[CrossRef][Google Scholar]
Rice, S. A., Long, M. C., Lam, V., Schaffer, P. A. & Spencer, C. A. (1995). Herpes simplex virus immediate-early protein ICP22 is required for viral modification of host RNA polymerase II and establishment of the normal viral transcription program. Journal of Virology69, 5550-5559.
[Google Scholar]
Rock, D. L. & Fraser, N. W. (1983). Detection of HSV-1 genome in central nervous system of latently infected mice. Nature302, 523-525.[CrossRef][Google Scholar]
Rock, D. L. & Fraser, N. W. (1985). Latent herpes simplex virus type 1 DNA contains two copies of the virion DNA joint region. Journal of Virology55, 849-852.
[Google Scholar]
Rodahl, E. & Haarr, L. (1997). Analysis of the 2-kilobase latency-associated transcript expressed in PC12 cells productively infected with herpes simplex virus type 1: evidence for a stable, nonlinear structure. Journal of Virology71, 1703-1707.
[Google Scholar]
Roizman, B. & Sears, A. E. (1987). An inquiry into the mechanisms of herpes simplex virus latency. Annual Review of Microbiology41, 543-571.[CrossRef][Google Scholar]
Ryan, A. K. & Rosenfeld, M. G. (1997). POU domain family values: flexibility, partnerships and developmental codes. Genes & Development11, 1207-1225.[CrossRef][Google Scholar]
Sacks, W. R. & Schaffer, P. A. (1987). Deletion mutants in the gene encoding the herpes simplex virus type 1 immediate-early protein ICP0 exhibit impaired growth in culture. Journal of Virology61, 829-839.
[Google Scholar]
Samaniego, L. A., Webb, A. L. & DeLuca, N. A. (1995). Functional interactions between herpes simplex virus immediate-early proteins during infection: gene expression as a consequence of ICP27 and different domains of ICP4. Journal of Virology69, 5705-5715.
[Google Scholar]
Samaniego, L. A., Wu, N. & DeLuca, N. A. (1997). The herpes simplex virus immediate-early protein ICP0 affects transcription from the viral genome and infected-cell survival in the absence of ICP4 and ICP27. Journal of Virology71, 4614-4625.
[Google Scholar]
Samaniego, L. A., Neiderhiser, L. & DeLuca, N. A. (1998). Persistence and expression of the herpes simplex virus genome in the absence of immediate-early proteins. Journal of Virology72, 3307-3320.
[Google Scholar]
Sawtell, N. M. (1997). Comprehensive quantification of herpes simplex virus latency at the single-cell level. Journal of Virology71, 5423-5431.
[Google Scholar]
Sawtell, N. M. (1998). The probability of in vivo reactivation of herpes simplex virus type 1 latency increases with the number of latently infected neurons in the ganglia. Journal of Virology72, 6888-6892.
[Google Scholar]
Sawtell, N. M. & Thompson, R. L. (1992a). Herpes simplex virus type 1 latency-associated transcription unit promotes anatomical site-dependent establishment and reactivation from latency. Journal of Virology66, 2157-2169.
[Google Scholar]
Sawtell, N. M. & Thompson, R. L. (1992b). Rapid in vivo reactivation of herpes simplex virus in latently infected murine ganglionic neurons after transient hyperthermia. Journal of Virology66, 2150-2156.
[Google Scholar]
Sawtell, N. M., Poon, D. K., Tansky, C. S. & Thompson, R. L. (1998). The latent herpes simplex virus type 1 genome copy number in individual neurons is virus strain specific and correlates with reactivation. Journal of Virology72, 5343-5350.
[Google Scholar]
Sears, A. E., Halliburton, I. W., Meignier, B., Silver, S. & Roizman, B. (1985). Herpes simplex virus 1 mutant deleted in the α22 gene: growth and gene expression in permissive and restrictive cells and establishment of latency in mice. Journal of Virology55, 338-346.
[Google Scholar]
Sears, A. E., Hukkanen, V., Labow, M. A., Levine, A. J. & Roizman, B. (1991). Expression of herpes simplex virus 1 α transinducing factor (VP16) does not induce reactivation of latent virus or prevent the establishment of latency in mice. Journal of Virology65, 2929-2935.
[Google Scholar]
Sedarati, F., Margolis, T. P. & Stevens, J. G. (1993). Latent infection can be established with drastically restricted transcription and replication of the HSV-1 genome. Virology192, 687-691.[CrossRef][Google Scholar]
Seeler, J. S., Marchio, A., Sitterlin, D., Transby, C. & Dejean, A. (1998). Interaction of sp100 with HP1 proteins: a link between the promyelocytic leukaemia-associated nuclear bodies and the chromatin compartment. Proceedings of the National Academy of Sciences, USA95, 7316-7321.[CrossRef][Google Scholar]
Shimeld, C., Hill, T. J., Blyth, W. A. & Easty, D. L. (1990). Reactivation of latent infection and induction of recurrent herpetic eye disease in mice. Journal of General Virology71, 397-404.[CrossRef][Google Scholar]
Simmons, A., Slobedman, B., Speck, P., Arthur, J. & Efstathiou, S. (1992). Two patterns of persistence of herpes simplex virus DNA sequences in the nervous systems of latently infected mice. Journal of General Virology73, 1287-1291.[CrossRef][Google Scholar]
Slobedman, B., Efstathiou, S. & Simmons, A. (1994). Quantitative analysis of herpes simplex virus DNA in ganglia of mice latently infected with wild-type and thymidine kinase-deficient viral strains. Journal of General Virology75, 2469-2474.[CrossRef][Google Scholar]
Smith, R. L., Pizer, L. I., Johnson, E. M. & Wilcox, C. L. (1992). Activation of second messenger pathways reactivates latent herpes simplex virus in neuronal cultures. Virology188, 311-318.[CrossRef][Google Scholar]
Smith, R. L., Escudero, J. M. & Wilcox, C. L. (1994). Regulation of the herpes simplex virus latency-associated transcripts during establishment of latency in sensory neurons in vitro. Virology202, 49-60.[CrossRef][Google Scholar]
Speck, P. G. & Simmons, A. (1991). Divergent molecular pathways of productive and latent infection with a virulent strain of herpes simplex virus type 1. Journal of Virology65, 4001-4005.
[Google Scholar]
Speck, P. G. & Simmons, A. (1992). Synchronous appearance of antigen-positive and latently infected neurons in spinal ganglia of mice infected with a virulent strain of herpes simplex virus. Journal of General Virology73, 1281-1285.[CrossRef][Google Scholar]
Stanberry, L. R., Kern, E. R., Richards, J. T., Abbott, T. M. & Overall, J. C. (1982). Genital herpes in guinea pigs: pathogenesis or the primary infection and description of recurrent disease. Journal of Infectious Diseases146, 397-404.[CrossRef][Google Scholar]
Steiner, I., Spivack, J. G., Deshmane, S. L., Ace, C. I., Preston, C. M. & Fraser, N. W. (1990). A herpes simplex virus type 1 mutant containing a non-transinducing Vmw65 protein establishes latent infection in vivo in the absence of viral replication and reactivates efficiently from explanted trigeminal ganglia. Journal of Virology64, 1630-1638.
[Google Scholar]
Stevens, J. G. (1989). Human herpesviruses: a consideration of the latent state. Microbiological Reviews53, 318-332.
[Google Scholar]
Stevens, J. G. & Cook, M. L. (1971). Latent herpes simplex virus in spinal ganglia of mice. Science173, 843-845.[CrossRef][Google Scholar]
Stevens, J. G., Wagner, E. K., Devi-Rao, G. B., Cook, M. L. & Feldman, L. (1987). RNA complementary to a herpesvirus alpha gene mRNA is predominant in latently infected neurons. Science235, 1056-1059.[CrossRef][Google Scholar]
Stow, N. D. & Stow, E. C. (1986). Isolation and characterization of a herpes simplex virus type 1 mutant containing a deletion within the gene encoding the immediate early polypeptide Vmw110. Journal of General Virology67, 2571-2585.[CrossRef][Google Scholar]
Stow, E. C. & Stow, N. D. (1989). Complementation of a herpes simplex virus type 1 Vmw110 mutant by human cytomegalovirus. Journal of General Virology70, 695-704.[CrossRef][Google Scholar]
Sturm, R. A., Das, G. & Herr, W. (1988). The ubiquitous octamer-binding protein Oct-1 contains a POU domain with a homeo box subdomain. Genes & Development2, 1582-1599.[CrossRef][Google Scholar]
Suzuki, N., Peter, W., Ciesiolka, T., Gruss, P. & Scholer, H. R. (1993). Mouse Oct-1 contains a composite homeodomain of human Oct-1 and Oct-2. Nucleic Acids Research21, 245-252.[CrossRef][Google Scholar]
Tal-Singer, R., Lasner, T. M., Podrzucki, W., Skokotas, A., Leary, J., Berger, J. J. & Fraser, N. W. (1997). Gene expression during reactivation of herpes simplex virus type 1 from latency in the peripheral nervous system is different from that during lytic infection of tissue cultures. Journal of Virology71, 5268-5276.
[Google Scholar]
Tenser, R. B., Hay, K. A. & Edris, W. A. (1989). Latency-associated transcript but not reactivatable virus is present in sensory ganglion neurons after inoculation of thymidine kinase-negative mutants of herpes simplex virus type 1. Journal of Virology63, 2861-2865.
[Google Scholar]
Thompson, R. L. & Sawtell, N. M. (1997). The herpes simplex virus type 1 latency-associated transcript gene regulates the establishment of latency. Journal of Virology71, 5432-5440.
[Google Scholar]
Turner, E. E., Fedtsova, N. & Rosenfeld, M. G. (1996). POU-domain factor expression in the trigeminal ganglion and implications for herpes virus regulation. NeuroReport7, 2829-2832.
[Google Scholar]
Valyi-Nagy, T., Deshmane, S., Dillner, A. & Fraser, N. W. (1991a). Induction of cellular transcription factors in trigeminal ganglia of mice by corneal scarification, herpes simplex virus type 1 infection, and explantation of trigeminal ganglia. Journal of Virology65, 4142-4152.
[Google Scholar]
Valyi-Nagy, T., Deshmane, S. L., Spivack, J. G., Steiner, I., Ace, C. I., Preston, C. M. & Fraser, N. W. (1991b). Investigation of herpes simplex virus type 1 (HSV-1) gene expression and DNA synthesis during the establishment of latent infection by an HSV-1 mutant, in1814, that does not replicate in mouse trigeminal ganglia. Journal of General Virology72, 641-649.[CrossRef][Google Scholar]
Valyi-Nagy, T., Deshmane, S. L., Raengsakulrach, B., Nicosia, M., Gesser, R. M., Wysocka, M., Dillner, A. & Fraser, N. W. (1992). Herpes simples virus type 1 mutant strain in1814 establishes a unique, slowly progressing infection in SCID mice. Journal of Virology66, 7336-7345.
[Google Scholar]
Wagner, E. K & Bloom, D. C. (1997). Experimental investigation of herpes simplex virus latency. Clinical Microbiology Reviews10, 419-443.
[Google Scholar]
Wagner, E. K., Guzowski, J. F. & Singh, J. (1995). Transcription of the herpes simplex virus genome during productive and latent infection. Progress in Nucleic Acid Research and Molecular Biology51, 123-165.
[Google Scholar]
Walz, M. A., Price, R. W. & Notkins, A. L. (1974). Latent ganglionic infection with herpes simplex virus types 1 and 2: viral reactivation in vivo after neurectomy. Science184, 1185-1187.[CrossRef][Google Scholar]
Watson, R. J. & Clements, J. B. (1980). A herpes simplex virus type 1 function required for early and late virus RNA synthesis. Nature285, 329-330.[CrossRef][Google Scholar]
Wheatley, S. C., Kemp, L. M., Wood, J. N. & Latchman, D. S. (1990). Cell lines derived from dorsal root ganglion neurons are nonpermissive for HSV and express only the latency-associated transcript following infection. Experimental Cell Research190, 243-246.[CrossRef][Google Scholar]
Wilcox, C. L. & Johnson, E. M. (1987). Nerve growth factor deprivation results in the reactivation of latent herpes simplex virus in vitro. Journal of Virology61, 2311-2315.
[Google Scholar]
Wilcox, C. L. & Johnson, E. M. (1988). Characterization of nerve growth factor-dependent herpes simplex virus latency in neurons in vitro. Journal of Virology62, 393-399.
[Google Scholar]
Wilcox, C. L., Smith, R. L., Freed, C. R. & Johnson, E. M. (1990). Nerve growth factor-dependence of herpes simplex virus latency in peripheral sympathetic and sensory neurons in vitro. Journal of Neuroscience104, 1268-1275.
[Google Scholar]
Wilcox, C. L., Smith, R. L., Everett, R. D. & Mysofski, D. (1997). The herpes simplex virus type 1 immediate-early protein ICP0 is necessary for the efficient establishment of latent infection. Journal of Virology71, 6777-6785.
[Google Scholar]
Wood, J. N., Lillycrop, K. A., Dent, C. L., Ninkina, N. N., Beech, M. M., Willoughby, J. J., Winter, J. & Latchman, D. S. (1992). Regulation of expression of the neuronal POU protein Oct-2 by nerve growth factor. Journal of Biological Chemistry267, 17787-17791.
[Google Scholar]
Wu, N., Watkins, S. C., Schaffer, P. A. & DeLuca, N. A. (1996a). Prolonged gene expression and cell survival after infection by a herpes simplex virus mutant defective in the immediate-early genes encoding ICP4, ICP27, and ICP22. Journal of Virology70, 6358-6369.
[Google Scholar]
Wu, T.-T., Su, Y.-H., Block, T. M. & Taylor, J. M. (1996b). Evidence that two latency-associated transcripts of herpes simplex virus type 1 are nonlinear. Journal of Virology70, 5962-5967.
[Google Scholar]
Yao, F. & Schaffer, P. A. (1995). An activity specified by the osteosarcoma line U2OS can substitute functionally for ICP0, a major regulatory protein of herpes simplex virus type 1. Journal of Virology69, 6249-6258.
[Google Scholar]
Yeh, L. & Schaffer, P. A. (1993). A novel class of transcripts expressed with late kinetics in the absence of ICP4 spans the junction between the long and short segments of the herpes simplex virus type 1 genome. Journal of Virology67, 7373-7382.
[Google Scholar]
York, I. A., Roop, C., Andrews, D. W., Riddell, S. R., Graham, F. L. & Johnson, D. C. (1994). A cytosolic herpes simplex virus protein inhibits antigen presentation to CD8+ lymphocytes. Cell77, 525-535.[CrossRef][Google Scholar]
Zabolotny, J., Krummenacher, C. & Fraser, N. W. (1997). The herpes simplex virus type 1 2·0-kilobase latency-associated transcript is a stable intron which branches at a guanosine. Journal of Virology71, 4199-4208.
[Google Scholar]