Bystander killing during avian leukosis virus subgroup B infection requires TVB(S3) signaling.
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.
Diaz-Griffero
Felipe
F
Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Hoschander
Steven A
SA
Brojatsch
Jürgen
J
D000818:Animals; D017209:Apoptosis; D001354:Avian Leukosis Virus / Q000502:physiology*; D024201:Bystander Effect; D002460:Cell Line; D008856:Microscopy, Fluorescence; D011784:Quail; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism*; D015398:Signal Transduction
D018124:Receptors, Tumor Necrosis Factor