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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]

PMID: 14610178

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Project description:The group of highly related avian leukosis viruses (ALVs) in chickens are thought to have evolved from a common retroviral ancestor into six subgroups, A to E and J. These ALV subgroups use diverse cellular proteins encoded by four genetic loci in chickens as receptors to gain entry into host cells. Hosts exposed to ALVs might be under selective pressure to develop resistance to ALV infection. Indeed, resistance alleles have previously been identified in all four receptor loci in chickens. The tvb gene encodes a receptor, which determines the susceptibility of host cells to ALV subgroup B (ALV-B), ALV-D, and ALV-E. Here we describe the identification of two novel alleles of the tvb receptor gene, which possess independent insertions each within exon 4. The insertions resulted in frameshift mutations that reveal a premature stop codon that causes nonsense-mediated decay of the mutant mRNA and the production of truncated Tvb protein. As a result, we observed that the frameshift mutations in the tvb gene significantly lower the binding affinity of the truncated Tvb receptors for the ALV-B, ALV-D, and ALV-E envelope glycoproteins and significantly reduce susceptibility to infection by ALV-B, ALV-D and ALV-E in vitro and in vivo Taken together, these findings suggest that frameshift mutation can be a molecular mechanism of reducing susceptibility to ALV and enhance our understanding of virus-host coevolution.IMPORTANCE Avian leukosis virus (ALV) once caused devastating economic loss to the U.S. poultry industry prior the current eradication schemes in place, and it continues to cause severe calamity to the poultry industry in China and Southeast Asia, where deployment of a complete eradication scheme remains a challenge. The tvb gene encodes the cellular receptor necessary for subgroup B, D, and E ALV infection. Two tvb allelic variants that resulted from frameshift mutations have been identified in this study, which have been shown to have significantly reduced functionality in mediating subgroup B, D, and E ALV infection. Unlike the control of herpesvirus-induced diseases by vaccination, the control of avian leukosis in chickens has relied totally on virus eradication measures and host genetic resistance. This finding enriches the allelic pool of the tvb gene and expands the potential for genetic improvement of ALV resistance in varied chicken populations by selection.

Dataset Information

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

Publications

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

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