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Review article |
School of Biological Sciences, University of Sussex, Brighton, East Sussex BN1 9QG, UK
Correspondence
Alison Sinclair
A.J.Sinclair{at}Sussex.ac.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.
Published ahead of print on 12 May 2003 as DOI 10.1099/vir.0.19112-0.
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