Virus Details


VHFID3971

Pathogen Information

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

Publication Information

Paper Title Host factors LR1 and Spl regulate the Fp promoter of Epstein-Barrvirus
Author's Name SILVIA BULFONE-PAUS, LAURIE A. DEMPSEY AND NANCY MAIZELS
Journal Name PNAS
Pubmed ID 7667284
Abstract The Epstein-Barr virus EBNA-1 gene product is essential for latent replication of the virus. In transformed cells characterized by the most restricted patterns of viral latent gene expression, EBNA-1 transcription is driven from the Fp promoter. We have used genetic and biochemical techniques to study the promoter-proximal elements that regulate Fp expression in B cells. We show that a 114-bp fragment of DNA spanning the Fp "TATA" box functions as a remarkably active transcriptional regulatory element in B cells. Two host factors, Sp1 and LR1, regulate Fp transcription from the promoter-proximal region. Sp1 binds a single site just downstream of the TATA box, and LR1 binds two sites just upstream of the TATA box. Transcripts from both the viral genome and the minimal promoter initiate at the same unique site, and one function of LR1 at Fp is to direct initiation to this unique start site. In contrast to Sp1, which is ubiquitous, LR1 is present only in activated B cells and may contribute to cell-type-specific transformation by Epstein-Barr virus.
Used Model BL cells
DOI 10.1073/pnas.92.18.8293