Structural Basis for Apoptosis Inhibition by Epstein-Barr Virus BHRF1

被引:95
作者
Kvansakul, Marc [1 ]
Wei, Andrew H. [1 ]
Fletcher, Jamie I. [1 ]
Willis, Simon N. [1 ,2 ]
Chen, Lin [1 ,2 ]
Roberts, Andrew W. [1 ,2 ]
Huang, David C. S. [1 ,2 ]
Colman, Peter M. [1 ,2 ]
机构
[1] Walter & Eliza Hall Inst Med Res, Parkville, Vic, Australia
[2] Univ Melbourne, Dept Med Biol, Parkville, Vic 3052, Australia
基金
澳大利亚国家健康与医学研究理事会;
关键词
PROGRAMMED CELL-DEATH; PROSURVIVAL BCL-2 PROTEINS; BH3; DOMAINS; TRANSGENIC MICE; BAX; HOMOLOG; FAMILY; MYC; BIM; LIGANDS;
D O I
10.1371/journal.ppat.1001236
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Epstein-Barr virus (EBV) is associated with human malignancies, especially those affecting the B cell compartment such as Burkitt lymphoma. The virally encoded homolog of the mammalian pro-survival protein Bcl-2, BHRF1 contributes to viral infectivity and lymphomagenesis. In addition to the pro-apoptotic BH3-only protein Bim, its key target in lymphoid cells, BHRF1 also binds a selective sub-set of pro-apoptotic proteins (Bid, Puma, Bak) expressed by host cells. A consequence of BHRF1 expression is marked resistance to a range of cytotoxic agents and in particular, we show that its expression renders a mouse model of Burkitt lymphoma untreatable. As current small organic antagonists of Bcl-2 do not target BHRF1, the structures of it in complex with Bim or Bak shown here will be useful to guide efforts to target BHRF1 in EBV-associated malignancies, which are usually associated with poor clinical outcomes.
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页数:10
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