Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- Part I Introduction: definition and classification of the human herpesviruses
- Part II Basic virology and viral gene effects on host cell functions: alphaherpesviruses
- Part II Basic virology and viral gene effects on host cell functions: betaherpesviruses
- Part II Basic virology and viral gene effects on host cell functions: gammaherpesviruses
- 22 Introduction to the human γ-herpesviruses
- 23 Gammaherpesviruses entry and early events during infection
- 24 Gammaherpesvirus maintenance and replication during latency
- 25 Reactivation and lytic replication of EBV
- 26 Reactivation and lytic replication of KSHV
- 27 EBV gene expression and regulation
- 28 KSHV gene expression and regulation
- 29 Effects on apoptosis, cell cycle and transformation, and comparative aspects of EBV with other DNA tumor viruses
- 30 KSHV manipulation of the cell cycle and programmed cell death pathways
- 31 Human gammaherpesvirus immune evasion strategies
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HSV-1 and HSV-2
- Part III Pathogenesis, clinical disease, host response, and epidemiology: VZU
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HCMV
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HHV- 6A, 6B, and 7
- Part III Pathogenesis, clinical disease, host response, and epidemiology: gammaherpesviruses
- Part IV Non-human primate herpesviruses
- Part V Subversion of adaptive immunity
- Part VI Antiviral therapy
- Part VII Vaccines and immunothgerapy
- Part VIII Herpes as therapeutic agents
- Index
- Plate section
- References
24 - Gammaherpesvirus maintenance and replication during latency
from Part II - Basic virology and viral gene effects on host cell functions: gammaherpesviruses
Published online by Cambridge University Press: 24 December 2009
Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- Part I Introduction: definition and classification of the human herpesviruses
- Part II Basic virology and viral gene effects on host cell functions: alphaherpesviruses
- Part II Basic virology and viral gene effects on host cell functions: betaherpesviruses
- Part II Basic virology and viral gene effects on host cell functions: gammaherpesviruses
- 22 Introduction to the human γ-herpesviruses
- 23 Gammaherpesviruses entry and early events during infection
- 24 Gammaherpesvirus maintenance and replication during latency
- 25 Reactivation and lytic replication of EBV
- 26 Reactivation and lytic replication of KSHV
- 27 EBV gene expression and regulation
- 28 KSHV gene expression and regulation
- 29 Effects on apoptosis, cell cycle and transformation, and comparative aspects of EBV with other DNA tumor viruses
- 30 KSHV manipulation of the cell cycle and programmed cell death pathways
- 31 Human gammaherpesvirus immune evasion strategies
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HSV-1 and HSV-2
- Part III Pathogenesis, clinical disease, host response, and epidemiology: VZU
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HCMV
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HHV- 6A, 6B, and 7
- Part III Pathogenesis, clinical disease, host response, and epidemiology: gammaherpesviruses
- Part IV Non-human primate herpesviruses
- Part V Subversion of adaptive immunity
- Part VI Antiviral therapy
- Part VII Vaccines and immunothgerapy
- Part VIII Herpes as therapeutic agents
- Index
- Plate section
- References
Summary
Introduction
The human gammaherpesviruses Epstein–Barr Virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) are associated with a variety of malignancies involving cells of various lineages.
After primary infection and initial viral propagation in epithelial and lymphoid cells, both viruses establish latency in a subset of CD 19 positive B-cells. In this often lifelong asymptomatic stage, in which EBV genomes are detectable primarily in resting memory B-cells, the number of infected cells is extremely low and virus load is tightly controlled by the host cellular and humoral immune response.
Loss of this balance leads to an increase in viral load, which often precedes the onset of malignant diseases. Both tissue involvement and histopathology are highly variable between EBV - and KSHV -associated malignancies and involve either lymphoid (Burkitt's lymphoma and primary effusion lymphoma), epithelial (nasopharyngeal carcinoma), or endothelial (Kaposi's sarcoma) tissues.
However, common to all gammaherpesvirus-associated tumors is that the majority of tumor cells are latently infected, and harbor extrachromosomal circularized viral genomes called episomes that are replicated and segregated by the host cellular replication machinery indefinitely. This ability to maintain long-term latent infection in quiescent and proliferating cells may be a defining property shared by both the lymphocryptoviruses (LCV, represented by EBV) and the rhadinoviruses (RDV, represented by KSHV).
This chapter aims to summarize our current understanding of the underlying mechanisms by which EBV and KSHV achieve long-term episomal maintenance in latently infected cells, which conceptually can be viewed as a two step process: replication of the viral genome and faithful segregation to daughter cells (Fig. 24.1).
- Type
- Chapter
- Information
- Human HerpesvirusesBiology, Therapy, and Immunoprophylaxis, pp. 379 - 402Publisher: Cambridge University PressPrint publication year: 2007
References
(1987). Replication of latent Epstein–Barr virus genomes in Raji cells. J. Virol., 61(5): 1743–1746.Google ScholarPubMed
and (1975). Epstein–Barr virus genomes with properties of circular DNA molecules in carrier cells. Proc. Natl Acad. Sci. USA, 72(4): 1477–1481.CrossRefGoogle ScholarPubMed
, , , and (1988). Epstein–Barr virus (EBV) infection of murine L cells expressing recombinant human EBV /C3d receptor. Proc. Natl Acad. Sci. USA, 85(23), 9307–9311.CrossRefGoogle ScholarPubMed
, , , and (2001). Human herpesvirus 8 envelope-associated glycoprotein B interacts with heparan sulfate-like moieties. Virology, 284(2), 235–249.CrossRefGoogle ScholarPubMed
, , et al. (2002). Integrin alpha3beta1 (CD 49c/29) is a cellular receptor for Kaposi's sarcoma-associated herpesvirus (KSHV/HHV-8) entry into the target cells. Cell, 108(3), 407–419.CrossRefGoogle ScholarPubMed
, , , , and (2003). Differential hyperacetylation of histones H3 and H4 upon promoter-specific recruitment of EBNA 2 in Epstein-Barr virus chromatin. J. Virol., 77(14), 8166–8172.CrossRefGoogle ScholarPubMed
, , , , , and (2000). The primary sequence of rhesus monkey rhadinovirus isolate 26–95: sequence similarities to Kaposi's sarcoma-associated herpesvirus and rhesus monkey rhadinovirus isolate 17577. J. Virol., 74, 3388–3398.CrossRefGoogle ScholarPubMed
, , and (1991). Early events in Epstein-Barr virus infection of human B lymphocytes. Virology, 181(2), 595–608.CrossRefGoogle ScholarPubMed
, , , and (1990). CpG methylation of viral DNA in EBV -associated tumours. Int. J. Cancer, 45(6), 1125–1130.CrossRefGoogle ScholarPubMed
, , et al. (1990). Oligonucleotides for polymerase chain reaction amplification and hybridization detection of Epstein–Barr virus DNA in clinical specimens. Mol. Cell Probes, 4(5), 397–407.CrossRefGoogle ScholarPubMed
, , , , and (1991). Functional domains of Epstein–Barr virus nuclear antigen EBNA -1. J. Virol., 65(3), 1466–1478.Google ScholarPubMed
, , and (1999). DNA methylation and the Epstein–Barr virus. Semin. Cancer Biol., 9(5), 369–375.CrossRefGoogle ScholarPubMed
, , , , , and (2005). The latency-associated nuclear antigen of Kaposi's sarcoma-asociated herpesvirus modulates cellular gene expression and protects lymphoid cells from p16 INK 4A-induced cell cycle arrest. J. Biol. Chem., 280, 3862–3874.CrossRefGoogle Scholar
Andersson- and (1978). Integrated viral DNA sequences in Epstein–Barr virus-converted human lymphoma lines. J. Virol., 25(3), 710–718.Google Scholar
, , and (1984). Evidence for integrated EBV genomes in Raji cellular DNA. Nucl. Acids Res., 12(2), 1149–1161.CrossRefGoogle ScholarPubMed
, , , , and , (2006). ORC binding to TRF 2 stimulates OriP relplication. EMBO Rep., 7, 716–721.CrossRefGoogle Scholar
Avolio-, , and (2001). Epstein–Barr nuclear antigen 1 binds and destabilizes nucleosomes at the viral origin of latent DNA replication. Nucl. Acids Res., 29(17), 3520–3528.CrossRefGoogle Scholar
(2001). Kaposi's sarcoma associated herpesvirus latency assoiciated nuclear antigen 1 mediates episome persistence through cis-acting terminal repeat (tr) sequence and specifically binds DNA. J. Virol., 75, 3250–3258.CrossRefGoogle Scholar
, , and (1999). Efficient persistence of extrachromosomal KSHV DNA mediated by latency-associated nuclear antigen. Science, 284(5414), 641–644.CrossRefGoogle ScholarPubMed
, , Kelley-et al. (2006). The nucleosomal surface as a docking station for Kaposi's sarcoma herpesvirus LANA. Science, 311, 856–861.CrossRefGoogle ScholarPubMed
and (2001). OriP of Epstein–Barr virus requires exact spacing of two bound dimers of EBNA 1 which bend DNA. J. Virol., 75, 10603–10611.CrossRefGoogle ScholarPubMed
and (2002). DNA replication in eukaryotic cells. Annu. Rev. Biochem., 71, 333–374.CrossRefGoogle ScholarPubMed
Ben- and (1981). Activation of the Epstein–Barr virus genome by 5-aza-cytidine in latently infected human lymphoid lines. Int. J. Cancer, 28, 131–135.CrossRefGoogle Scholar
(1986). CpG-rich islands and the function of DNA methylation. Nature, 321, 209–213.CrossRefGoogle ScholarPubMed
, , et al. (1997). Human CD 8+ T cell responses to EBV EBNA 1: HLA class I presentation of the (Gly–Ala)-containing protein requires exogenous processing. Immunity, 7(6), 791–802.CrossRefGoogle Scholar
, , , , , and (1995). Crystal structure of the DNA binding domain of the Epstein-Barr virus origin binding protein EBNA -1. Cell, 83, 39–46.CrossRefGoogle ScholarPubMed
, , , , and (1996). Crystal structure of the DNA -binding domain of the Epstein–Barr virus origin-binding protein, EBNA 1, bound to DNA. Cell, 84, 791–800.CrossRefGoogle Scholar
, , , and (1998). The 2.2 A structure of a permanganate-sensitive DNA site bound by the Epstein-Barr virus origin binding protein, EBNA 1. J. Mol. Biol., 284(5), 1273–1278.CrossRefGoogle Scholar
and (2002). AIDS-related malignancies. Nature Reviews. Cancer, 2(5), 373–382.CrossRefGoogle ScholarPubMed
and (1994). Conserved structures and diversity of functions of RNA -binding proteins. Science, 265(5172), 615–621.CrossRefGoogle ScholarPubMed
, , , , , and (2005). Kaposi's sarcoma-associated herpesvirus expresses an array of viral microRNAs in latently infected cells. Proc. Natl Acad. Sci. USA, 102, 5570–5575.CrossRefGoogle ScholarPubMed
, , et al. (2000). A new primary effusion lymphoma-derived cell line yields a highly infectious Kaposi's sarcoma herpesvirus-containing supernatant. J. Virol., 74, 10187–10193.CrossRefGoogle ScholarPubMed
and (2000). Functional analyses of the EBNA 1 origin DNA binding protein of Epstein–Barr virus. J. Virol., 74, 4939–4948.CrossRefGoogle Scholar
, , , , , and (1995). In vitro establishment and characterization of two acquired immunodeficiency syndrome-related lymphoma cell lines (BC-1 and BC -2) containing Kaposi's sarcoma-associated herpesvirus (KSHV) DNA sequences. Blood, 86, 2708–2714.Google ScholarPubMed
, , and (2002). Chromosomal integration of Epstein–Barr virus genomes in nasopharyngeal carcinoma cells. Head Neck, 24(2), 143–150.CrossRefGoogle ScholarPubMed
, , et al. (1994). Identification of herpesvirus-like DNA sequences in AIDS -associated kaposis sarcoma. Science, 266(5192), 1865–1869.CrossRefGoogle Scholar
, , , , and (2001). Human DNA replication initiation factors, ORC and MCM, associate with OriP of Epstein–Barr virus. Proc. Natl Acad. Sci. USA, 98, 10085–10089.CrossRefGoogle ScholarPubMed
, , et al. (2001). Activation of latent Kaposi's sarcoma-associated herpesvirus by demethylation of the promoter of the lytic transactivator. Proc. Natl Acad. Sci. USA, 98, 4119–4124.CrossRefGoogle ScholarPubMed
, , and (1993). Separation of the complex DNA binding domain of EBNA -1 into DNA recognition and dimerization subdomains of novel structure. J. Virol., 67(8), 4875–4885.Google ScholarPubMed
, , and (1994). Delineation of a 16 amino acid sequence that forms a core DNA recognition motif in the Epstein–Barr virus EBNA -1 protein. Virology, 205(2), 486–495.CrossRefGoogle ScholarPubMed
, , , , and (1998). Physical association between the EBV protein EBNA -1 and P32/TAP/hyaluronectin. J. Biomed. Sci., 5(3), 173–179.CrossRefGoogle ScholarPubMed
, , and (1993). Unexpected patterns of Epstein–Barr virus gene expression during early stages of B cell transformation. Int. Immunol., 5(7), 707–716.CrossRefGoogle ScholarPubMed
, , and (1989). Functional limits of OriP, the Epstein–Barr virus plasmid origin of replication. J. Virol., 63, 3016–3025.Google ScholarPubMed
, , , and (2002). The terminal repeats and latency-associated nuclear antigen of herpesvirus saimiri are essential for episomal persistence of the viral genome. J. Gen. Virol., 83(9), 2269–2278.CrossRefGoogle ScholarPubMed
, 2nd and (1999). The latency-associated nuclear antigen tethers the Kaposi's sarcoma-associated herpesvirus genome to host chromosomes in body cavity-based lymphoma cells [In Process Citation]. Virology, 264(2), 254–264.CrossRefGoogle Scholar
, 2nd, , and (2001). The Kaposi's sarcoma-associated herpesvirus latency-associated nuclear antigen binds to specific sequences at the left end of the viral genome through its carboxy-terminus. Virology, 291(2), 241–259.CrossRefGoogle ScholarPubMed
, , , , and (2000). Two domains of the epstein-barr virus origin DNA -binding protein, EBNA 1, orchestrate sequence-specific DNA binding. J. Biol. Chem., 275(29), 22273–22277.CrossRefGoogle Scholar
, , , , , and (2002). Telomeric proteins regulate maintenance of Epstein–Barr Virus origin of plasmid replication. Mol. Cell, 9, 493–503.CrossRefGoogle ScholarPubMed
, , , , and (2003). Telomere repeat binding factors TRF 1, TRF 2, and hRAP1 modulate replication of Epstein–Barr virus OriP. J. Virol., 77(22), 11992–12001.CrossRefGoogle Scholar
and (1996). Control of papillomavirus DNA replication and transcription. Semin. Cancer Biol., 7(6), 339–347.CrossRefGoogle ScholarPubMed
, , et al. (2001). Replication from OriP of Epstein–Barr virus requires human ORC and is inhibited by geminin. Cell, 106, 287–296.CrossRefGoogle ScholarPubMed
and (1983). Epstein–Barr HR -1 virion DNA is very highly methylated. J. Virol., 45(1), 482–483.Google Scholar
, , , , and (1996). Human herpesvirus 8 (Kaposi's sarcoma-associated herpesvirus) DNA in Kaposi's sarcoma lesions, AIDS Kaposi's sarcoma cell lines, endothelial Kaposi's sarcoma simulators, and the skin of immunosuppressed patients. Am. J. Pathol., 148, 2009–2016.Google ScholarPubMed
, , , , , and (1998). A cluster of latently expressed genes in Kaposi's sarcoma-associated herpesvirus. J. Virol., 72(10), 8309–8315.Google ScholarPubMed
, , et al. (1999). Distribution of human herpesvirus-8 latently infected cells in Kaposi's sarcoma, multicentric Castleman's disease, and primary effusion lymphoma. Proc. Natl Acad. Sci. USA, 96(8), 4546–4551.CrossRefGoogle ScholarPubMed
and (1985). Chromatin structure of Esptein-Barr virus. J. Gen. Virol., 66, 1931–1940.CrossRefGoogle Scholar
, , and (1998). Origin DNA -binding proteins. Curr. Opin. Struct. Biol., 8(1), 49–53.CrossRefGoogle ScholarPubMed
, , et al. (1989). The role of methylation in the phenotype-dependent modulation of Epstein-Barr nuclear antigen 2 and latent membrane protein genes in cells latently infected with Epstein–Barr virus. J. Gen. Virol., 70(11), 2989–3002.CrossRefGoogle ScholarPubMed
, , and (1999). The ability of herpes simplex virus type 1 immediate-early protein Vmw110 to bind to a ubiquitin-specific protease contributes to its roles in the activation of gene expression and stimulation of virus replication. J. Virol., 73(1), 417–426.Google Scholar
and (1993). An origin of DNA replication (OriP) in highly methylated episomal Epstein–Barr virus DNA localizes to a 4.5-kb unmethylated region. Virology, 195(2), 608–615.CrossRefGoogle ScholarPubMed
, , , and (1998). Specific methylation patterns in two control regions of Epstein–Barr virus latency: the LMP -1-coding upstream regulatory region and an origin of DNA replication (OriP). J. Virol., 72(4), 2969–2974.Google Scholar
, , and (1994). Stabilization of the EBNA 1 protein on the Epstein–Barr virus latent origin of DNA replication by a DNA looping mechanism. J. Biol. Chem., 269(2), 1057–1062.Google Scholar
, , , and (2000). p53 inhibition by the LANA protein of KSHV protects against cell death. Nature, 402(6764), 889–894.CrossRefGoogle Scholar
, , , and (1995). Identification of a novel human zinc finger protein that specifically interacts with the activation domain of lentiviral Tat proteins. Virology, 209(2), 347–357.CrossRefGoogle ScholarPubMed
and (2003). The latency-associated nuclear antigen of Kaposi's sarcoma-associated herpesvirus manipulates the activity of glycogen synthase kinase-3beta. J. Virol., 77(14), 8019–8030.CrossRefGoogle ScholarPubMed
, , et al. (2003). A novel viral mechanism for dysregulation of beta-catenin in Kaposi's sarcoma-associated herpesvirus latency. Nat. Med., 9(3), 300–306.CrossRefGoogle ScholarPubMed
and (1989). The Epstein–Barr virus origin of plasmid replication, OriP, contains both the initiation and termination sites of DNA replication. Cell, 58, 527–535.CrossRefGoogle ScholarPubMed
and (1995). An EBNA -1-dependent enhancer acts from a distance of 10 kilobase pairs to increase expression of the Esptein-Barr virus LMP Gene. J. Virol., 69, 2633–2636.Google Scholar
(1997). KSHV and Kaposi'2 sarcoma. The end of the beginning?Cell, 91, 157–160.CrossRefGoogle ScholarPubMed
, , et al. (1996). KSHV antibodies among Americans, Italians and Ugandans with and without Kaposi's sarcoma [see comments]. Nat. Med., 2(8), 925–928.CrossRefGoogle Scholar
, , , , , and (1999). Molecular polymorphism of Kaposi's sarcoma-associated herpesvirus (Human herpesvirus 8) latent nuclear antigen: evidence for a large repertoire of viral genotypes and dual infection with different viral genotypes [In Process Citation]. J. Infect. Dis., 180(5), 1466–1476.CrossRefGoogle Scholar
, , , and (2001). DNA binding and modulation of gene expression by the latency-associated nuclear antigen of Kaposi's sarcoma-associated herpesvirus. J. Virol., 75(17), 7882–7892.CrossRefGoogle ScholarPubMed
, , and (2002). Latency-associated nuclear antigen (LANA) cooperatively binds to two sites within the terminal repeat, and both sites contribute to the ability of LANA to suppress transcription and to facilitate DNA replication. J. Biol. Chem., 277(30), 27401–27411.CrossRefGoogle ScholarPubMed
, , , and (1984). Detection of circular and linear herpesvirus DNA molecules in mammalian cells by gel electrophoresis. J. Virol., 50(1), 248–254.Google ScholarPubMed
(2001). Making sense of eukaryotic DNA replication origins. Science, 294(5540), 96–100.CrossRefGoogle ScholarPubMed
, , and (1993). Identification of EBNA 1 amino acid sequences required for the interaction of the functional elements of the Epstein–Barr virus latent origin of DNA replication. J. Virol., 67(6), 3418–3426.Google Scholar
and (1996). EBNA1 and E2: a new paradigm for origin-binding proteins?Trends Microbiol., 4(3), 87–89.CrossRefGoogle ScholarPubMed
, , and (2002). MEF2-mediated recruitment of class III HDAC at the EBV immediate early gene BZLF 1 links latency and chromatin remodeling. EMBO Rep., 3(2), 141–146.CrossRefGoogle Scholar
and (2003). The latency-associated nuclear antigen of Kaposi's sarcoma-associated herpesesvirus permits replication of terminal repeat-containing plasmids. J. Virol., 77(4), 2779–2783.CrossRefGoogle ScholarPubMed
, and (2004). Inefficient establishment of KSHV latency suggests an additional role for continued lytic replication in Kaposi sarcoma pathogenesis. J. Clin. Invest., 113, 124–136.CrossRefGoogle ScholarPubMed
, , , , , and (2002). The Herpesvirus Saimiri open reading frame 73 gene product interacts with the cellular protein p32. J. Virol., 76(22), 11612–11622.CrossRefGoogle ScholarPubMed
, , and (1994). Sequence requirements of the Epstein–Barr virus latent origin of DNA replication. J. Virol., 68(3), 1913–1925.Google ScholarPubMed
, , and (1992). Interaction of Epstein–Barr virus nuclear antigen 1 with the viral latent origin of replication. J. Virol., 66, 694–705.Google ScholarPubMed
, , , and (2003). The spacing between adjacent binding sites in the family of repeats affects the functions of Epstein–Barr nuclear antigen 1 in transcription activation and stable plasmid maintenance. Virology, 311(2), 263–274.CrossRefGoogle ScholarPubMed
and (2001). The biology of Kaposi's sarcoma. Cancer Treat. Res., 104, 89–126.CrossRefGoogle ScholarPubMed
Hirai, K. and Shirakata, M. (2001). OriP Minichromosome. In Epstein–Barr Virus and Human Cancer, ed. . Heidelberg, Springer, 258.CrossRefGoogle Scholar
, , et al. (2003). Protein profiling with Epstein–Barr nuclear antigen-1 reveals an interaction with the herpesvirus-associated ubiquitin-specific protease HAUSP /USP7. J. Biol. Chem., 278(32), 29987–29994.CrossRefGoogle ScholarPubMed
(1999). Evidence that protein binding specifies sites of DNA demethylation. Mol. Cell Biol., 19(1), 46–56.CrossRefGoogle ScholarPubMed
, , and (1993). Constitutive binding of EBNA 1 protein to the Epstein–Barr virus replication origin, OriP, with distortion of DNA structure during latent infection. EMBO J., 12(13), 4933–4944.Google Scholar
, , , , and (1999). CIR, a corepressor linking the DNA binding factor CBF 1 to the histone deacetylase complex. Proc. Natl Acad. Sci. USA, 96(1), 23–28.CrossRefGoogle Scholar
and (2005). Characterization of the minimal replicator of Kaposi's sarcoma-associated herpesvirus latent origin. J. Virol., 79, 2637–2642.CrossRefGoogle ScholarPubMed
, , et al. (1991). Variable expression of latent membrane protein in nasopharyngeal carcinoma can be related to methylation status of the Epstein–Barr virus BNLF -1 5′-flanking region. J. Virol., 65(3), 1558–1567.Google ScholarPubMed
, , and (2002). The latency-associated nuclear antigen of Kaposi's sarcoma-associated herpesvirus supports latent DNA replication in dividing cells. J. Virol., 76(22), 11677–11687.CrossRefGoogle ScholarPubMed
, , , , and (2000). The budding yeast homolog of the human EBNA 1-binding protein 2 (Ebp2p) is an essential nucleolar protein required for pre-rRNA processing. J. Biol. Chem., 275, 28764–28770.CrossRefGoogle Scholar
, , et al. (2003). The EBV nuclear antigen 1 (EBNA1) enhances B cell immortalization several thousandfold. Proc. Natl Acad. Sci. USA, 100(19), 10989–10994.CrossRefGoogle ScholarPubMed
, , and (2001). Maintenance of Epstein–Barr virus (EBV) OriP-based episomes requires EBV -encoded nuclear antigen-1 chromosome-binding domains, which can be replaced by high-mobility group-I or histone H1. Proc. Natl. Acad. Sci. USA, 98, 1865–1870.CrossRefGoogle ScholarPubMed
and Thorley- (1988). B cell activation and the establishment of Epstein–Barr virus latency. J. Exp. Med., 168(6), 2059–2075.CrossRefGoogle ScholarPubMed
, , , 2nd, , and (2001). Latency-associated nuclear antigen encoded by Kaposi's sarcoma-associated herpesvirus interacts with Tat and activates the long terminal repeat of human immunodeficiency virus type 1 in human cells. J. Virol., 75(18), 8761–8771.CrossRefGoogle Scholar
, , et al. (2000). Epstein–Barr virus nuclear antigen-1 binds to nuclear transporter karyopherin alpha1/NPI-1 in addition to karyopherin alpha2/Rch1. Virology, 266(1), 110–119.CrossRefGoogle ScholarPubMed
and (2003). Epstein–Barr virus (EBV) nuclear antigen 1 colocalizes with cellular replication foci in the absence of EBV plasmids. J. Virol., 77(6), 3824–3831.CrossRefGoogle ScholarPubMed
, , , and (1992). A nuclear matrix attachment region organizes the Epstein–Barr viral plasmid in Raji cells into a single DNA domain. EMBO J., 11(3), 1165–1176.Google ScholarPubMed
, , and (2000). Histone acetylation and reactivation of Epstein–Barr virus from latency. J. Virol., 74, 710–720.CrossRefGoogle ScholarPubMed
, , and (2001). Differential regulation of the overlapping Kaposi's sarcoma-associated herpesvirus vGCR (orf74) and LANA (orf73) promoters. J. Virol., 75(4), 1798–1807.CrossRefGoogle ScholarPubMed
and (1999). Relationships between chromatin organization and DNA methylation in determining gene expression. Semin. Cancer Biol., 9(5), 339–347.CrossRefGoogle ScholarPubMed
, , and (2001). Coupling of mitotic chromosome tethering and replication competence in epstein-barr virus-based plasmids. Mol. Cell. Biol., 21, 3576–3588.CrossRefGoogle ScholarPubMed
, , and (2001). Reconstitution of Epstein-Barr virus-based plasmid partitioning in budding yeast. EMBO J., 15, 222–230.CrossRefGoogle Scholar
, , , , , and (1996). The seroepidemiology of human herpesvirus 8 (Kaposi's sarcoma-associated herpesvirus), distribution of infection in KS risk groups and evidence for sexual transmission [see comments] [published erratum appears in Nat. Med. 1996 Sep;2(9),1041]. Nat. Med., 2(8), 918–924.CrossRefGoogle Scholar
, , , and (1997). Identification of the gene encoding the major latency-associated nuclear antigen of the Kaposi's sarcoma-associated herpesvirus. J. Clin. Invest., 100(10), 2606–2610.CrossRefGoogle ScholarPubMed
, , , , , and (1997). Identification of a major latent nuclear antigen, LNA -1, in the human herpesvirus 8 genome. J. Hum. Virol., 1(1), 19–29.Google Scholar
and (2003). EBNA-1, a bifunctional transcriptional activator. Mol. Cell. Biol., 23(19), 6901–6908.CrossRefGoogle ScholarPubMed
, , and (2003). Epstein–Barr virus provides a survival factor to Burkitt's lymphomas. Proc. Natl Acad. Sci. USA, 4.Google Scholar
, , et al. (1997). An imperfect correlation between the DNA replication activity of Epstein–Barr virus nuclear antigen 1 (EBNA1) and the binding to the nuclear import receptor, Rch1/importin alpha. Virology, 239, 340–351.CrossRefGoogle ScholarPubMed
and (1979). The structure of the termini of the DNA of Epstein–Barr virus. Cell, 17(3), 661–671.CrossRefGoogle ScholarPubMed
and (1998). Rep∗: a viral element that can partially replace the origin of plasmid DNA synthesis of Epstein–Barr virus. J. Virol., 72(6), 4657–4666.Google ScholarPubMed
, Cotter, 2, and (2001). The latency-associated nuclear antigen of Kaposi's sarcoma-associated herpesvirus transactivates the telomerase reverse transcriptase promoter. J. Biol. Chem., 276(25), 22971–22978.CrossRefGoogle ScholarPubMed
(1979). Mode of integration of Epstein–Barr virus genome into host DNA in Burkitt lymphoma cells. J. Gen. Virol., 44(2), 573–576.CrossRefGoogle ScholarPubMed
, , and (2001). OriP, is composed of multiple functional elements. J. Virol., 75, 10582–10592.CrossRefGoogle ScholarPubMed
Kripalani- and (1994). Identification of integrated Epstein–Barr virus in nasopharyngeal carcinoma using pulse field gel electrophoresis. Int. J. Cancer, 56(2), 187–192.CrossRefGoogle Scholar
, , , , , and (2004). Concurrent expression of latent and a limited number of lytic genes with immune modulation and antiapoptotic function by Kaposi's sarcoma-associated herpesvirus early during infection of primary endothelial and fibroblast cells and subsequent decline of lytic gene expression. J. Virol., 78, 3601–3620.CrossRefGoogle Scholar
, et al. (2000). Human herpesvirus 8 LANA interacts with proteins of the mSin3 corepressor complex and negatively regulates Epstein–Barr virus gene expression in dually infected PEL cells. J. Virol., 74(20), 9637–9645.CrossRefGoogle ScholarPubMed
, et al. (2002). Protein interactions targeting the latency-associated nuclear antigen of Kaposi's sarcoma-associated herpesvirus to cell chromosomes. J. Virol., 76(22), 11596–11604.CrossRefGoogle ScholarPubMed
and (1991). Replication initiates at multiple locations on an autonomously replicating plasmid in human cells. Mol. Cell. Biol., 11(3), 1464–1472.CrossRefGoogle ScholarPubMed
, , and (1989). Isolation of human sequences that replicate autonomously in human cells. Mol. Cell. Biol., 9, 1026–1033.CrossRefGoogle ScholarPubMed
and (1997). The structure and coding organization of the genomic termini of Kaposi's sarcoma-associated herpesvirus. Virology, 236(1), 147–154.CrossRefGoogle ScholarPubMed
, , et al. (2002). De novo infection and serial transmission of Kaposi's sarcoma-associated herpesvirus in cultured endothelial cells. J. Virol., 76, 2440–2448.CrossRefGoogle ScholarPubMed
, , , and , (2004). Kaposi's sarcoma-associated herpesvirus-encoded latency-associated nuclear antigen inhibits lytic replication by targeting Rta: a protential mechanism for virus-mediated control of latency. J. Virol., 78, 6585–6594.CrossRefGoogle Scholar
, , and (1989). The terminal protein gene 2 of Epstein–Barr virus is transcribed from a bidirectional latent promoter region. J. Gen. Virol., 70(11), 3079–3084.CrossRefGoogle ScholarPubMed
, , and (1988). Sensitive, high-resolution chromatin and chromosome mapping in situ: presence and orientation of two closely integrated copies of EBV in a lymphoma line. Cell, 52(1), 51–61.Google Scholar
, , and (1999). Genetic evidence that EBNA -1 is needed for efficient, stable latent infection by Epstein–Barr virus. J. Virol., 73, 2974–2982.Google ScholarPubMed
and (2000). EBNA-1: a protein pivotal to latent infection by Epstein–Barr virus. Rev. Med. Virol., 10(2), 83–100.3.0.CO;2-T>CrossRefGoogle ScholarPubMed
, , , and (2002). Inhibition of ubiquitin-dependent proteolysis by a synthetic glycine-alanine repeat peptide that mimics an inhibitory viral sequence. FEBS Lett., 522(1–3), 93–98.CrossRefGoogle ScholarPubMed
, , et al. (1995). Inhibition of antigen processing by the internal repeat region of the Epstein–Barr virus nuclear antigen-1. Nature, 375(6533), 685–688.CrossRefGoogle ScholarPubMed
, , , , and (1997). Inhibition of ubiquitin/proteasome-dependent degradation by the Gly-Ala repeat domain of Epstein–Barr virus nuclear antigen 1. Proc. Natl Acad. Sci. USA, 94, 12616–12621.CrossRefGoogle ScholarPubMed
, , et al. (1992). Epstein–Barr virus infection and replication in a human epithelial cell system. Nature, 356(6367), 347–350.CrossRefGoogle Scholar
, , , and (2000). Latency-associated nuclear antigen of Kaposi's sarcoma-associated herpesvirus (human herpesvirus-8) binds ATF 4/CREB2 and inhibits its transcriptional activation activity. J. Gen. Virol., 81(11), 2645–2652.CrossRefGoogle ScholarPubMed
, , , , and (2002). Functional dissection of LANA 1 of Kaposi's sarcoma-associated herpesvirus involved in latent DNA replication and transcription of terminal repeats of the viral geneome. J. Virol., 76, 10320–10331.CrossRefGoogle Scholar
, , , and (2000). Modulation of DNA binding protein affinity directly affects target site demethylation. Mol. Cell. Biol., 20(7), 2343–2349.CrossRefGoogle ScholarPubMed
, , Andersson-, and (1978). Integration of Epstein–Barr virus DNA. IARC Sci. Publ. (24, 1), 113–123.Google ScholarPubMed
and (1995). Initiation of latent DNA replication in the Epstein–Barr virus genome can occur at sites other than the genetically defined origin. Mol. Cell. Biol., 15, 2893–2903.CrossRefGoogle Scholar
, , , , and (1997). Cyclosporin A-sensitive induction of the Epstein–Barr virus lytic switch is mediated via a novel pathway involving a MEF 2 family member. EMBO J., 16, 143–153.CrossRefGoogle Scholar
, , , , , and (2003). Chromatin remodeling of the Kaposi's sarcoma-associated herpesvirus ORF 50 promoter correlates with reactivation from latency. J. Virol., 77(21), 11425–11435.CrossRefGoogle Scholar
, , , and (2006). Acetylation of the latency-associated nuclear antigen regulates repression of Kaposi's sarcoma-associated herpesvirus lytic transcription. J. Virol., 80, 5273–5282.CrossRefGoogle ScholarPubMed
and (1985). Mapping genetic elements of Epstein–Barr virus that facilitate extrachromasomal persistence of Epstein–Barr virus-derived plasmids in human cells. Mol. Cell. Biol., 5, 2533–2542.CrossRefGoogle Scholar
and (1999). The linking regions of EBNA 1 are essential for its support of replication and transcription. Mol. Cell. Biol., 19, 3349–3359.CrossRefGoogle Scholar
, , and (1995). Multiple regions within EBNA 1 can link DNA s. J. Virol., 69, 6199–6208.Google Scholar
, , Chikhi-, , and Coppey- (1999). Mapping EBNA -1 domains involved in binding to metaphase chromosomes. J., Virol., 73, 4385–4392.Google ScholarPubMed
, Contreras-, et al. (1989). 5-Azacytidine up regulates the expression of Epstein–Barr virus nuclear antigen 2 (EBNA-2) through EBNA -6 and latent membrane protein in the Burkitt's lymphoma line real. J. Virol., 63(7), 3135–3141.Google Scholar
and (1998). Adenovirus core protein V interacts with p32–a protein which is associated with both the mitochondria and the nucleus. J. Gen. Virol., 79(7), 1677–1685.CrossRefGoogle ScholarPubMed
, , et al. (2002). Latent nuclear antigen of Kaposi's sarcoma herpesvirus/human herpesvirus-8 induces and relocates RING 3 to nuclear heterochromatin regions. J. Gen. Virol., 83(1), 179–188.CrossRefGoogle Scholar
and (1992). EBNA1 can link the enhancer element to the initiator element of the Epstein–Barr virus plasmid origin of DNA replication. J. Virol., 66(1), 489–495.Google ScholarPubMed
, , , and (1994). An integral membrane protein (LMP2) blocks reactivation of Epstein–Barr virus from latency following surface immunoglobulin crosslinking. Proc. Natl Acad. Sci. USA, 91(2), 772–776.CrossRefGoogle ScholarPubMed
, , Minarorits-, , and (1994). Sequence-specific methylation inhibits the activity of the Epstein–Barr virus LMP 1 and BCR 2 enhancer-promoter regions. Virology, 200(2), 661–667.CrossRefGoogle Scholar
, , , , and (1997). p32 protein, a splicing factor 2-associated protein, is localized in mitochondrial matrix and is functionally important in maintaining oxidative phosphorylation. J. Biol. Chem., 272(39), 24363–24370.CrossRefGoogle ScholarPubMed
, , , , , and (2004). Host gene induction and transcriptional reprogramming in Kaposi's sarcoma-associated herpesvirus (KSHV/HHV-8)-infected endothelial, fibroblast, and B cells: insights into modulation events early during infection. Cancer Res., 64(1), 72–84.CrossRefGoogle Scholar
, , , and (1995). Nucleoprotein complexes and DNA 5-ends at OriP of Epstein–Barr virus. J. Biol. Chem., 270, 12864–12868.CrossRefGoogle ScholarPubMed
, , , and (2001). Promoter-proximal regulatory elements involved in OriP-EBNA1-independent and -dependent activation of the Epstein–Barr virus C promoter in B-lymphoid cell lines. J. Virol., 75(13), 5796–5811.CrossRefGoogle ScholarPubMed
and (1975). Plasmid DNA as a possible state of Epstein–Barr virus genomes in nonproductive cells. Cold Spring Harb. Symp. Quant. Biol., 39(2), 807–810.CrossRefGoogle ScholarPubMed
and (2001). Visualization of DNA replication on individual Epstein–Barr virus episomes. Science, 294(5550), 2361–2364.CrossRefGoogle ScholarPubMed
, , and (2000). Initiation of DNA replication within OriP is dispensable for stable replication of the latent Epstein-Barr virus chromosome after infection of established cell lines. J. Virol., 74, 8563–8574.CrossRefGoogle ScholarPubMed
, , , , and (1998). Integrated and episomal forms of Epstein–Barr virus (EBV) in EBV associated disease. Cancer Lett., 122(1–2), 43–50.CrossRefGoogle Scholar
, , Lagos-et al. (2005). Identification of microRNAs of the herpesvirus family. Nat. Methods, 2, 269–276.CrossRefGoogle ScholarPubMed
, , , , and (2001). Close but distinct regions of human herpesvirus 8 latency-associated nuclear antigen 1 are responsible for nuclear targeting and binding to human mitotic chromosomes. J. Virol., 75(8), 3948–3959.CrossRefGoogle ScholarPubMed
, , , and (1999). Latent nuclear antigen of Kaposi's sarcoma-associated herpesvirus interacts with RING 3, a homolog of the drosophila female sterile homeotic (fsh) gene [In Process Citation]. J. Virol., 73(12), 9789–9795.Google Scholar
, , , , (1993). A Burkitt lymphoma cell line with integrated Epstein–Barr virus at a stable chromosome modification site. Virology, 195(1), 248–251.CrossRefGoogle Scholar
, , and (1996). OriP is essential for EBNA gene promoter activity in Epstein-Barr virus immortalized lymphoblastoid cell lines. J. Virol., 70, 5758–5768.Google ScholarPubMed
, , and (2000). The latent nuclear antigen of Kaposi sarcoma-associated herpesvirus targets the retinoblastoma-E2F pathway and with the oncogene Hras transforms primary rat cells. Nat. Med., 6(10), 1121–1127.CrossRefGoogle ScholarPubMed
, , et al. (1997). The 222- to 234-kilodalton latent nuclear protein (LNA) of Kaposi's sarcoma-associated herpesvirus (human herpesvirus 8) is encoded by orf73 and is a component of the latency-associated nuclear antigen. J. Virol., 71(8), 5915–5921.Google ScholarPubMed
, , , and (1985). Sequence-specific DNA binding of the Epstein–Barr virus nuclear antigen (EBNA-1) to clustered sites in the plamid maintenance region. Cell, 42, 859–868.CrossRefGoogle Scholar
and (1986). Trans-activation of an Epstein–Barr viral transcriptional enhancer by the Epstein–Barr viral nuclear antigen 1. Mol. Cell. Biol., 5, 3838–3846.CrossRefGoogle Scholar
, , and (1985). A putative origin of replication of plasmids derived from Epstein–Barr virus is composed of two cis-acting components. Mol. Cell. Biol., 5, 1822–1832.CrossRefGoogle ScholarPubMed
, , , and (1996a). The size and conformation of Kaposi's sarcoma-associated herpesvirus (human herpesvirus 8) DNA in infected cells and virions. J. Virol., 70(11), 8151–8154.Google Scholar
, , et al. (1996b). Lytic growth of Kaposi's sarcoma-associated herpesvirus (human herpesvirus 8) in culture. Nat. Med., 2, 342–346.CrossRefGoogle Scholar
, , , , , and (2001). Modulation of cellular and viral transcription by the latency-associated nuclears antigen (LANA/ORF73) of KSHV. J. Virol., 75, 458–468.CrossRefGoogle Scholar
, , and (2002). Complete genomic sequence of an Epstein–Barr virus-related herpesvirus naturally infecting a new world primate: a defining point in the evolution of oncogenic lymphocryptoviruses. J. Virol., 76(23), 12055–12068.CrossRefGoogle ScholarPubMed
(2000). The role of DNA methylation in modulating Epstein–Barr virus gene expression. Curr. Top. Microbiol. Immunol., 249, 21–34.Google ScholarPubMed
and (1997). Methylation of the Epstein–Barr virus genome in normal lymphocytes. Blood, 90(11), 4480–4484.Google ScholarPubMed
, , , , , and (1996). CpG methylation of the major Epstein–Barr virus latency promoter in Burkitt's lymphoma and Hodgkin's disease. Blood, 88(8), 3129–3136.Google ScholarPubMed
, , et al. (1996). Nucleotide sequence of the Kaposi sarcoma-associated herpesvirus (HHV8). Proc. Natl Acad. Sci. USA, 93, 14862–14867.CrossRefGoogle Scholar
, , et al. (1999). A complex translational program generates multiple novel proteins from the latently expressed kaposin (K12) locus of Kaposi's sarcoma-associated herpesvirus. J. Virol., 73(7), 5722–5730.Google ScholarPubMed
and Raab- (1995). Structural analyses of the Epstein–Barr virus BamHI A transcripts. J. Virol., 69(2), 1132–1141.Google ScholarPubMed
, , and (1980). Effect of n-butyrate on cellular and viral DNA synthesis in cells latently infected with Epstein–Barr virus. Virology, 107, 557–561.CrossRefGoogle ScholarPubMed
, , and (1983). Intracellular Epstein–Barr virus DNA is methylated in and around the EcoRI-J fragment in both producer and nonproducer cell lines. Virology, 126(2), 701–706.CrossRefGoogle ScholarPubMed
, , , , , and (2000). De novo DNA methylation at nonrandom founder sites 5′ from an unmethylated minimal origin of DNA replication in latent Epstein–Barr virus genomes. Biol. Chem., 381(2), 95–105.CrossRefGoogle ScholarPubMed
, , et al. (2001). Protein–DNA binding and CpG methylation at nucleotide resolution of latency-associated promoters Qp, Cp, and LMP 1p of Epstein–Barr virus. J. Virol., 75(6), 2584–2596.CrossRefGoogle Scholar
, , , and (2005). Cloning and identification of a microRNA cluster within the latency-associated region of Kaposi's sarcoma-associated herpesvirus. J. Virol., 79, 9301–9305.CrossRefGoogle ScholarPubMed
, , et al. (2005). Structure of the p53 binding domain of HAUSP /USP7 bound to Epstein–Barr nuclear antigen 1 implications for EBV -mediated immortalization. Mol. Cell., 18, 25–36.CrossRefGoogle ScholarPubMed
, , and (1997). Host-cell-determined methylation of specific Epstein–Barr virus promoters regulates the choice between distinct viral latency programs. Mol. Cell. Biol., 17(1), 364–377.CrossRefGoogle ScholarPubMed
, , et al. (2001). Human origin recognition complex binds to the region of the latent origin of DNA replication of Epstein–Barr virus. EMBO J., 20, 4588–4602.CrossRefGoogle ScholarPubMed
(1998). Kaposi's sarcoma-associated herpesvirus (human herpesvirus-8). J. Gen. Virol., 79(7), 1573–1591.CrossRefGoogle Scholar
, , , , and (2000). Carboxy terminus of human herpesvirus 8 latency-associated nuclear antigen mediates dimerization, transcriptional repression, and targeting to nuclear bodies. J. Virol., 74(18), 8532–8540.CrossRefGoogle ScholarPubMed
, , , and (1999). Sequence and genomic analysis of a Rhesus macaque rhadinovirus with similarity to Kaposi's sarcoma-associated herpesvirus/human herpesvirus 8. J. Virol., 73, 3040–3053.Google ScholarPubMed
, , , and (2003). Metaphase chromosome tethering is necessary for the DNA synthesis and maintenance of OriP plasmids but is insufficient for transcription activation by EBNA 1. J. Virol., in press.CrossRefGoogle Scholar
, , , , , and (2004). The amino terminus of Epstein–Barr Virus (EBV) nuclear antigen 1 contains AT hooks that facilitate the replication and partitioning of latent EBV genomes by tethering them to cellular chromosomes. J. Virol., 78, 11487–11505.CrossRefGoogle ScholarPubMed
and (1989). Analysis of the Epstein–Barr virus origin of plasmid replication (OriP) reveals an area of nucleosome sparing that spans the 3′ dyad. J. Virol., 63(12), 5505–5508.Google ScholarPubMed
, , and (1979). Nucleosomal structure of Epstein–Barr virus DNA in transformed cell lines. J. Virol., 29, 657–665.Google ScholarPubMed
, , et al. (2002). Chromosome binding site of latency-associated nuclear antigen of Kaposi's sarcoma-associated herpesvirus is essential for persistent episome maintenance and is functionally replaced by histone H1. J. Virol., 76(24), 12917–12924.CrossRefGoogle ScholarPubMed
, , and (1999). Requirement of replication licensing for the dyad symmetry element-dependent replication of the Epstein–Barr virus OriP minichromosome. Virology, 263(1), 42–54.CrossRefGoogle ScholarPubMed
, , Avolio-, and (1999). EBP2, a human protein that interacts with sequences of the Epstein–Barr virus nuclear antigen 1 important for plasmid maintenance. J. Virol., 73, 2587–2595.Google ScholarPubMed
, , , , and (1994). EBNA-1, the major nuclear antigen of Epstein–Barr virus, resembles “RGG” RNA binding proteins. EMBO J., 13(20), 4840–4847.Google ScholarPubMed
, , and (1997). Reactivation of Epstein–Barr virus: regulation and function of the BZLF 1 gene. Trends Microbiol, 5, 399–405.CrossRefGoogle Scholar
, , , and (2004). ORC, MCM, and histone hyperacetylation at the Kaposi's sarcoma-associated herpesvirus latent replication origin. J. Virol., 78(22), 12566–12575.CrossRefGoogle ScholarPubMed
, , , and (1991). DNA looping between the origin of replication of Epstein–Barr virus and its enhancer site: stabilization of an origin complex with Epstein–Barr nuclear antigen 1. Proc. Natl Acad. Sci. USA, 88, 10870–10874.CrossRefGoogle ScholarPubMed
and (2001). EBV's plasmid replicon: an enigma in cis and trans. Curr. Top. Microbiol. Immunol., 258, 3–11.Google ScholarPubMed
and (1989). A promoter of Esptein-Barr virus that can function during latent infection can be transactivated by EBNA -1, a viral protein required for viral DNA replication during latent infection. J. Virol., 63, 2644–2649.Google Scholar
, , and (1997). Requirements for Epstein-Barr nuclear antigen 1 (EBNA1)-induced permanganate sensitivity of the epstein–barr virus latent origin of DNA replication. J. Biol. Chem., 272(42), 26434–26440.CrossRefGoogle ScholarPubMed
, , , , and (1994). Reciprocal regulation of the Epstein–Barr virus BamHI-F promoter by EBNA -1 and an E2F transcription factor. Mol. Cell. Biol., 14(11), 7144–7152.CrossRefGoogle ScholarPubMed
, , et al. (1999). Human herpesvirus-8-encoded LNA -1 accumulates in heterochromatin-associated nuclear bodies. J. Gen. Virol., 80(11), 2889–2900.CrossRefGoogle ScholarPubMed
, , , and (1999). Transcriptional analysis of human herpesvirus-8 open reading frames 71, 72, 73, K14, and 74 in a primary effusion lymphoma cell line. Virology, 257(1), 84–94.CrossRefGoogle Scholar
, Fujimoto-, et al. (1996). Kid, a novel kinesin-like DNA binding protein, is localized to chromosomes and the mitotic spindle. EMBO J., 15(3), 457–467.Google ScholarPubMed
, , , and (2000). Human p32: A coactivator for Epstein–Barr virus nuclear antigen-1-mediated transcriptional activation and possible role in viral latent cycle DNA replication. Virology, 275, 145–157.CrossRefGoogle ScholarPubMed
Viejo-, , et al. (2003). A domain in the C-terminal region of latency-associated nuclear antigen 1 of Kaposi's sarcoma-associated Herpesvirus affects transcriptional activation and binding to nuclear heterochromatin. J. Virol., 77(12), 7093–7100.CrossRefGoogle Scholar
, , et al. (1998). Plasmid maintenance assay based on green fluorescent protein and FACS of mammalian cells. BioTechniques, 24, 540–544.Google ScholarPubMed
, , , and (1997). P32/TAP, a cellular protein that interacts with EBNA -1 of Epstein–Barr virus. Virology, 236, 18–29.CrossRefGoogle ScholarPubMed
, , et al. (2003). Kaposi's sarcoma-associated herpesvirus latency-associated nuclear antigen prolongs the life span of primary human umbilical vein endothelial cells. J. Virol., 77(11), 6188–6196.CrossRefGoogle ScholarPubMed
, , , , and (1990). Interaction of Epstein–Barr viral (EBV) origin of replication (OriP) with EBNA -1 and cellular anti-EBNA-1 proteins. Virology, 178(1), 293–296.CrossRefGoogle ScholarPubMed
, , , , , and (2001). Variant chromatin structure of the OriP region of Epstein–Barr virus and regulation of EBER 1 expression by upstream sequences and OriP. J. Virol., 75, 6235–6241.CrossRefGoogle ScholarPubMed
, , and (2000). The DNA segregation mechanism of Epstein–Barr virus nuclear antigen 1. EMBO Rep., 1, 140–144.CrossRefGoogle ScholarPubMed
, , and (2002). Separation of the DNA replication, segregation, and transcriptional activation functions of Epstein–Barr nuclear antigen 1. J. Virol., 76(5), 2480–2490.CrossRefGoogle ScholarPubMed
, , and (1996). Frequency and distribution of chromosomal integration sites of the Epstein–Barr virus genome. J. Formos. Med. Assoc., 95(12), 911–916.Google ScholarPubMed
and (1989). Multiple EBNA 1-binding sites are required to form an EBNA 1-dependent enhancer and to activate a minimal replicative origin within OriP of Epstein–Barr virus. J. Virol., 63(6), 2657–2666.Google Scholar
and (1988). Dissection of DNA replication and enhancer activation funcitons of Epstein–Barr virus nuclear antigen 1. Cancer Cells, 6, 197–205.Google Scholar
, and (1991). Epstein–Barr virus-derived plasmids replicate only once per cell cycle and are not amplified after entry into cells. J. Virol., 65(1), 483–488.Google Scholar
, , , and (1984). cis-acting element from Epstein–Barr viral genome that permits stable replication of recombinant plasmids in latently infected cells. Proc. Natl Acad. Sci. USA, 81, 3806–3810.CrossRefGoogle ScholarPubMed
, , and (1985). Stable replication of plasmids derived from Epstein–Barr virus in various mammalian cells. Nature, 313, 812–815.CrossRefGoogle ScholarPubMed
, , and (2000). The minimal replicator of Epstein–Barr virus OriP. J. Virol., 74, 4512–4522.CrossRefGoogle ScholarPubMed
, , and (2003). Self-inhibition of synthesis and antigen presentation by Epstein–Barr virus-endoded EBNA 1. Science, 301, 1334–1335.CrossRefGoogle Scholar
, , et al. (1995). Molecular cloning and characterization of a cellular protein that interacts with the human immunodeficiency virus type 1 Tat transactivator and encodes a strong transcriptional activation domain. J. Virol., 69(5), 3007–3016.Google ScholarPubMed
Zaldumbide, A., Ossevoort, M., Wiertz, E. J., and Hoeben, R. C. (2006). In cis inhibition of antigen processing by the latency-associated nuclear antigen I of Kaposi sarcoma Herpes virus. Mol Immunol., in press.
, , , , and O' (1998). Human RPA (hSSB) interacts with EBNA 1, the latent origin binding protein of Epstein–Barr virus. Nucl. Acids Res., 26, 631–637.CrossRefGoogle Scholar
and (1994). The cellular proteins that bind specifically to the Epstein–Barr virus origin of plasmid DNA replication belong to a gene family. Proc. Natl Acad. Sci. USA, 91(7), 2843–2847.CrossRefGoogle ScholarPubMed
, , , and (1996). Restricted expression of Kaposi sarcoma-associated herpesvirus (human herpesvirus 8) genes in Kaposi sarcoma. Proc. Natl Acad. Sci. USA, 93(13), 6641–6646.CrossRefGoogle ScholarPubMed
and (1995). Structure and role of the terminal repeats of Epstein–Barr virus in processing and packaging of virion DNA. J. Virol., 69(5), 3147–3155.Google ScholarPubMed
, , et al. (2005). Cell cycle regulation of chromatin at an origin of DNA replication. Embo J., 24, 1406–1417.CrossRefGoogle ScholarPubMed
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