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Journal of Virology, October 1998, p. 8392-8395, Vol. 72, No. 10
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Suppression of c-Myc-Induced Apoptosis by the Epstein-Barr Virus Gene Product BHRF1

Abdallah Fanidi,* David C. Hancock, and Trevor D. Littlewood

Biochemistry of the Cell Nucleus, Imperial Cancer Research Fund Laboratories, London WC2A 3PX, United Kingdom

Received 30 March 1998/Accepted 13 July 1998

Constitutive expression of the c-myc proto-oncogene in growth factor-deprived fibroblasts promotes proliferation and induces apoptosis. In these cells, apoptosis can be inhibited by survival factors such as insulin-like growth factor I or the bcl-2 proto-oncogene product. Deregulated c-Myc expression is a common feature in Epstein-Barr virus-positive Burkitt's lymphoma in which the c-myc gene is reciprocally translocated and placed under the control of one of the immunoglobulin loci. BHRF1 is an Epstein-Barr virus protein expressed early in the lytic cycle. BHRF1 is a member of the Bcl-2 family and has been shown to suppress apoptosis and to increase cell survival in different settings. In the present study, we report that BHRF1 inhibits c-Myc-induced apoptosis which occurs in the absence of survival factors. It does not, however, affect the capacity of c-Myc to promote cell growth. These findings demonstrate that BHRF1 has not only structural but also functional similarities to Bcl-2.

* Corresponding author. Present address: Onyx Pharmaceuticals, 3031 Research Dr., Richmond, CA 94806. Phone: (510) 222 9700. Fax: (510) 222 9758. E-mail: afanidi{at}onyx-pharm.com.

Journal of Virology, October 1998, p. 8392-8395, Vol. 72, No. 10
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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