ArticleJournal of virology2003
Bystander killing during avian leukosis virus subgroup B infection requires TVB(S3) signaling.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Proteasome inhibitors prevent caspase-1-mediated disease in rodents challenged with anthrax lethal toxin.The American journal of pathology · 2010Article
- Reticuloendotheliosis virus strain T induces miR-155, which targets JARID2 and promotes cell survival.Journal of virology · 2009Article
- Bystander macrophage apoptosis after Mycobacterium tuberculosis H37Ra infection.Infection and immunity · 2008Article
- Evolution of broad host range in retroviruses leads to cell death mediated by highly cytopathic variants.Journal of virology · 2006Article
- Anthrax lethal toxin-mediated killing of human and murine dendritic cells impairs the adaptive immune response.PLoS pathogens · 2005Article
- Mutations of a residue within the polyproline-rich region of Env alter the replication rate and level of cytopathic effects in chimeric avian retroviral vectors.Journal of virology · 2005Article
- Avian sarcoma and leukosis virus cytopathic effect in the absence of TVB death domain signaling.Journal of virology · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.