| Virus Name | Human herpesvirus 4 (Epstein-Barr virus) |
| Virus Short Name | EBV |
| Order | Herpesvirales |
| Virus Family | Herpesviridae |
| Virus Subfamily | Gammaherpesvirinae |
| Genus | Lymphocryptovirus |
| Species | Human herpesvirus 4 |
| Host | Human, mammals |
| Cell Tropism | B lymphocytes, oral epithelial cells, latency: remains latent in cd19+ b cells |
| Associated Disease | Mononucleosis, associated with environemental diseases: burkitt?s lymphoma nasopharyngeal carcinoma (npc) |
| Mode of Transmission | Contact, saliva |
| VIPR DB link | http://www.viprbrc.org/brc/vipr_allSpecies_search.do?method=SubmitForm&decorator=herpes |
| ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/dsdna-viruses-2011/w/dsdna_viruses/91/herpesviridae |
| Virus Host DB link | http://www.genome.jp/virushostdb/view/?virus_lineage=Herpesviridae |
| Paper Title | Telomere repeat binding factors TRF1, TRF2, and hRAP1 modulate replication of Epstein-Barrvirus OriP |
| Author's Name | Deng Z, Lezina L, Chen C-J, Shtivelband S, So W, Lieberman PM |
| Journal Name | Journal Of Virology |
| Pubmed ID | 23031715 |
| Abstract | Epstein-Barr virus OriP confers cell cycle-dependent DNA replication and stable maintenance on plasmids in EBNA1-positive cells. The dyad symmetry region of OriP contains four EBNA1 binding sites that are punctuated by 9-bp repeats referred to as nonamers. Previous work has shown that the nonamers bind to cellular factors associated with human telomeres and contribute to episomal maintenance of OriP. In this work, we show that substitution mutation of all three nonamer sites reduces both DNA replication and plasmid maintenance of OriP-containing plasmids by 2.5- to 5-fold. The nonamers were required for high-affinity binding of TRF1, TRF2, and hRap1 to the dyad symmetry element but were not essential for the binding of EBNA1 as determined by DNA affinity purification from nuclear extracts. Chromatin immunoprecipitation assays indicated that TRF1, TRF2, and hRap1 bound OriP in vivo. Cell cycle studies indicate that TRF2binding to OriP peaks in G(1)/S while TRF1 binding peaks in G(2)/M. OriP replication was inhibited by transfection of full-length TRF1but not by deletion mutants lacking the myb DNA binding domain. In contrast, OriP replication was not affected by transfection of full-length TRF2 or hRap1 but was potently inhibited by dominant-negative TRF2 or hRap1 amino-terminal truncation mutants. Knockdown experiments with short interfering RNAs (siRNAs) directed against TRF2 and hRap1 severely reduced OriP replication, while TRF1siRNA had a modest stimulatory effect on OriP replication. These results indicate that TRF2 and hRap1 promote, while TRF1antagonizes, OriP-dependent DNA replication and suggest that these telomeric factors contribute to the establishment of replicationcompetence at OriP. |
| Used Model | N.A. |
| DOI | 10.1128/JVI.77.22.11992-12001.2003 |
