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Journal of Virology, December 2003, p. 12552-12561, Vol. 77, No. 23
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.23.12552-12561.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Bystander Killing during Avian Leukosis Virus Subgroup B Infection Requires TVBS3 Signaling

Felipe Diaz-Griffero, Steven A. Hoschander, and Jürgen Brojatsch*

Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 10461

Received 23 January 2003/ Accepted 2 September 2003

Cell killing by avian leukosis virus subgroup B (ALV-B) in cultures has been extensively studied, but the molecular basis of this process has not been established. Here we show that superinfection, which has been linked to cell killing by ALV-B, plays no crucial role in cell death induction. Instead, we show that signaling by the ALV-B receptor, TVBS3, a member of the tumor necrosis factor receptor family, is essential for ALV-B-mediated cell death. TVBS3 activated caspase-dependent apoptosis during ALV-B infection. Strikingly, apoptosis induction occurred predominantly in uninfected cells, while ALV-B-infected cells were protected against cell death. This bystander killing phenomenon was reproduced in a virus-free system by cocultivating ALV-B Env-expressing cells with TVBS3-expressing cells. Taken together, our results indicated that ALV-B-mediated apoptosis is triggered by ALV-B Env-TVBS3 interactions.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461. Phone: (718) 430-3079. Fax: (718) 430-8711. E-mail: brojatsc{at}aecom.yu.edu.

Journal of Virology, December 2003, p. 12552-12561, Vol. 77, No. 23
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.23.12552-12561.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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