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Structural Basis for Apoptosis Inhibition by Epstein-Barr Virus BHRF1
被引:92
|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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