| ARTICLE ABSTRACT | |||||||
| DOI: 10.1099/vir.0.19112-0 | ||||||||
| Online 12 May 2003 | ||||||||
School of Biological Sciences, University of Sussex,
Brighton, East Sussex BN1 9QG, UK
The human gammaherpesviruses Epstein–Barr
virus (EBV) and Kaposi's sarcoma-associated herpesvirus
(KSHV) both infect lymphoid and epithelial cells and both are
implicated in the development of cancer. The two viruses establish
latency in B-lymphoid cells that, once disrupted, leads to a burst
of virus replication during the lytic cycle. A basic leucine zipper
(bZIP) transcription factor encoded by EBV, Zta (also known as
BZLF1 and ZEBRA), is key to the disruption of EBV latency. KSHV
encodes a related protein, K-bZIP (also known as RAP and K8
).
Recent developments in our understanding of the structures and
functions of these two viral bZIP proteins have led to the
conclusion that they are not homologues. Two important features of
Zta are its ability to interact directly with DNA and to induce EBV
replication whereas K-bZIP is not known to interact directly with
DNA or to induce KSHV replication. Despite these differences, the
ability to disrupt cell cycle control is conserved in both Zta and
K-bZIP. The interactions of Zta and K-bZIP with cellular genes will
be reviewed here.
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This article is now available in the August 2003 print issue of JGV (vol. 84, 1941–1949). The complete issue of the journal may be seen in electronic form on JGV Online.
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