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Host cell-dependent expression of latent Epstein-Barr virus genomes: regulation by DNA methylation.
Adv Cancer Res 2003; 89:133-56AC

Abstract

Epstein-Barr virus (EBV) is a ubiquitous human gammaherpesvirus associated with a wide spectrum of malignant neoplasms. Expression of latent (growth transformation-associated) EBV genes is host cell specific. Transcripts for EBV-encoded nuclear antigens (EBNAs) are initiated at one of the alternative promoters: Wp, Cp (for EBNA1-6), or Qp (for EBNA1 only). Wp is active shortly after EBV infection of human B cells in vitro but is progressively methylated and silenced in established lymphoblastoid cell lines (LCLs). In parallel Cp, an unmethylated, lymphoid-specific promoter is switched on. In contrast, Cp is methylated and silent in Burkitt's lymphoma (BL) cell lines, which keep the phenotype of BL biopsy cells (group I BL lines). These cells use Qp for the initiation of EBNA1 messages. Qp is unmethylated both in group I BLs (Qp on) and in LCLs (Qp off). Thus, DNA methylation does not play a role in silencing Qp. In LCLs and nasopharyngeal carcinoma (NPC) cells, transcripts for latent membrane protein 1 (LMP1) are initiated from LMP1p, a promoter regulated by CpG methylation. LMPlp is silent in group I BL lines but can be activated by demethylating agents. Promoter silencing by CpG methylation involves both direct interference with transcription factor binding (Wp, Cp) and indirect mechanisms involving the recruitment of histone deacetylases (LMPlp). A dyad symmetry sequence(DS) within oriP (the latent origin of EBV replication) and intragenic RNA polymerase III control regions of EBER 1 and 2 transcription units are invariably unmethylated in EBV-carrying cells.

Authors+Show Affiliations

Microbiological Research Group, National Center for Epidemiology, H-1529 Budapest, Hungary.No affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

14587872

Citation

Li, Hul, and Janos Minarovits. "Host Cell-dependent Expression of Latent Epstein-Barr Virus Genomes: Regulation By DNA Methylation." Advances in Cancer Research, vol. 89, 2003, pp. 133-56.
Li H, Minarovits J. Host cell-dependent expression of latent Epstein-Barr virus genomes: regulation by DNA methylation. Adv Cancer Res. 2003;89:133-56.
Li, H., & Minarovits, J. (2003). Host cell-dependent expression of latent Epstein-Barr virus genomes: regulation by DNA methylation. Advances in Cancer Research, 89, pp. 133-56.
Li H, Minarovits J. Host Cell-dependent Expression of Latent Epstein-Barr Virus Genomes: Regulation By DNA Methylation. Adv Cancer Res. 2003;89:133-56. PubMed PMID: 14587872.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Host cell-dependent expression of latent Epstein-Barr virus genomes: regulation by DNA methylation. AU - Li,Hul, AU - Minarovits,Janos, PY - 2003/11/1/pubmed PY - 2003/12/25/medline PY - 2003/11/1/entrez SP - 133 EP - 56 JF - Advances in cancer research JO - Adv. Cancer Res. VL - 89 N2 - Epstein-Barr virus (EBV) is a ubiquitous human gammaherpesvirus associated with a wide spectrum of malignant neoplasms. Expression of latent (growth transformation-associated) EBV genes is host cell specific. Transcripts for EBV-encoded nuclear antigens (EBNAs) are initiated at one of the alternative promoters: Wp, Cp (for EBNA1-6), or Qp (for EBNA1 only). Wp is active shortly after EBV infection of human B cells in vitro but is progressively methylated and silenced in established lymphoblastoid cell lines (LCLs). In parallel Cp, an unmethylated, lymphoid-specific promoter is switched on. In contrast, Cp is methylated and silent in Burkitt's lymphoma (BL) cell lines, which keep the phenotype of BL biopsy cells (group I BL lines). These cells use Qp for the initiation of EBNA1 messages. Qp is unmethylated both in group I BLs (Qp on) and in LCLs (Qp off). Thus, DNA methylation does not play a role in silencing Qp. In LCLs and nasopharyngeal carcinoma (NPC) cells, transcripts for latent membrane protein 1 (LMP1) are initiated from LMP1p, a promoter regulated by CpG methylation. LMPlp is silent in group I BL lines but can be activated by demethylating agents. Promoter silencing by CpG methylation involves both direct interference with transcription factor binding (Wp, Cp) and indirect mechanisms involving the recruitment of histone deacetylases (LMPlp). A dyad symmetry sequence(DS) within oriP (the latent origin of EBV replication) and intragenic RNA polymerase III control regions of EBER 1 and 2 transcription units are invariably unmethylated in EBV-carrying cells. SN - 0065-230X UR - https://www.unboundmedicine.com/medline/citation/14587872/Host_cell_dependent_expression_of_latent_Epstein_Barr_virus_genomes:_regulation_by_DNA_methylation_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0065-230X(03)01004-2 DB - PRIME DP - Unbound Medicine ER -