EBNA2 and Activated Notch Induce Expression of BATF.
- Resource Type
- Article
- Authors
- Johansen, Lisa M.; Deppmann, Christopher D.; Erickson, Kimberly D.; Coffin III, William F.; Thornton, Tina M.; Humphrey, Sean E.; Martin, Jennifer M.; Taparowsky, Elizabeth J.
- Source
- Journal of Virology. May2003, Vol. 77 Issue 10, p6029. 12p. 1 Color Photograph, 28 Black and White Photographs, 1 Diagram, 7 Graphs.
- Subject
- *HUMAN herpesvirus-6
*EPSTEIN-Barr virus
- Language
- ISSN
- 0022-538X
The immortalization of human B lymphocytes by Epstein-Barr virus (EBV) requires the virus-encoded transactivator EBNA2 and the products of both viral and cellular genes which serve as EBNA2 targets. In this study, we identified BATF as a cellular gene that is up-regulated dramatically within 24 h following the infection of established and primary human B cells with EBV. The transactivation of BATF is mediated by EBNA2 in a B-cell-specific manner and is duplicated in non-EBV-infected B cells by the expression of mammalian Notch proteins. In contrast to other target genes activated by EBNA2, the BATF gene encodes a member of the AP-1 family of transcription factors that functions as a negative regulator of AP-1 activity and as an antagonist of cell growth. A potential role for BATF in promoting EBV latency is supported by studies in which BATF was shown to negatively impact the expression of a BZLF1 reporter gene and to reduce the frequency of lyric replication in latently infected cells. The identification of BATF as a cellular target of EBV provides important new information on how programs of viral and cellular gene expression may be coordinated to promote viral latency and control lyric-cycle entry. [ABSTRACT FROM AUTHOR]