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Structural Basis for Apoptosis Inhibition by Epstein-Barr Virus BHRF1
Author(s) -
Marc Kvansakul,
Andrew H. Wei,
Jamie I. Fletcher,
Simon N. Willis,
Lin Chen,
Andrew W. Roberts,
David C.S. Huang,
Peter M. Colman
Publication year - 2010
Publication title -
plos pathogens
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.719
H-Index - 206
eISSN - 1553-7374
pISSN - 1553-7366
DOI - 10.1371/journal.ppat.1001236
Subject(s) - puma , lymphoma , virus , cytotoxic t cell , epstein–barr virus , apoptosis , cancer research , biology , virology , immunology , in vitro , genetics
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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