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. 1997 Apr;71(4):3319-22.
doi: 10.1128/JVI.71.4.3319-3322.1997.

Epstein-Barr virus BHRF1 protein protects intestine 407 epithelial cells from apoptosis induced by tumor necrosis factor alpha and anti-Fas antibody

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Epstein-Barr virus BHRF1 protein protects intestine 407 epithelial cells from apoptosis induced by tumor necrosis factor alpha and anti-Fas antibody

M Kawanishi. J Virol. 1997 Apr.

Abstract

Tumor necrosis factor (TNF) and cytotoxic T lymphocytes, which utilize Fas to induce apoptosis in target cells, are known to play a critical role in the host defense against viral infection. In this study, the Epstein-Barr virus BHRF1 protein was stably expressed in intestine 407 cells which were susceptible to cell death mediated through both the TNF receptor and Fas. WST-1 conversion assays and acridine orange staining showed that vector-transfected control cells were killed by TNF-alpha or anti-Fas antibody in a dose-dependent manner, whereas BHRF1-expressing cells were resistant to apoptosis induced by these mediators. DNA fragmentation, a characteristic of apoptosis induced by TNF-alpha and the anti-Fas antibody, was suppressed in BHRF1-expressing cells. These results indicate that the BHRF1 protein protects cells from apoptosis mediated by the TNF receptor and Fas. The role of BHRF1 as an inhibitor of cytokine-induced apoptosis during the Epstein-Barr virus lytic cycle in vivo is discussed.

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References

    1. Nature. 1984 Jul 19-25;310(5974):207-11 - PubMed
    1. Science. 1995 Mar 10;267(5203):1449-56 - PubMed
    1. J Virol. 1987 Sep;61(9):2902-9 - PubMed
    1. Virology. 1987 Sep;160(1):151-61 - PubMed
    1. Mol Cell Biol. 1988 May;8(5):2159-65 - PubMed

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