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Bystander killing during avian leukosis virus subgroup B infection requires TVB(S3) signaling.


ABSTRACT: 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, TVB(S3), a member of the tumor necrosis factor receptor family, is essential for ALV-B-mediated cell death. TVB(S3) 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 TVB(S3)-expressing cells. Taken together, our results indicated that ALV-B-mediated apoptosis is triggered by ALV-B Env-TVB(S3) interactions.

SUBMITTER: Diaz-Griffero F 

PROVIDER: S-EPMC262550 | BioStudies | 2003-01-01

SECONDARY ACCESSION(S): 10.1128/JVI.77.23.12552-12561.2003

REPOSITORIES: biostudies

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Bystander killing during avian leukosis virus subgroup B infection requires TVB(S3) signaling.

Diaz-Griffero Felipe F   Hoschander Steven A SA   Brojatsch Jürgen J  

Journal of virology 20031201 23


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, TVB(S3), a member of the tumor necrosis factor receptor family, is essential for ALV-B-mediated cell death. TVB(S3) activated caspase-dependent apoptosi  ...[more]

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