ArticleJournal of virology2012
Intronic deletions that disrupt mRNA splicing of the tva receptor gene result in decreased susceptibility to infection by avian sarcoma and leukosis virus subgroup A.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Genetic mutations within tva receptor gene confer resistance to ALV-A and ALV-K infection in chickens.Poultry science · 2026Article
- Generation of chimeric chickens resistant to infection by avian leukemia virus subgroups A, B, D, E, and K through primordial germ cells.Poultry science · 2026Article
- Single Amino Acid Residue W33 ofViruses · 2025Article
- Rapid adaptive evolution of avian leukosis virus subgroup J in response to biotechnologically induced host resistance.PLoS pathogens · 2024Article
- Advances on genetic and genomic studies of ALV resistance.Journal of animal science and biotechnology · 2022Review
- A locus conferring tolerance to Theileria infection in African cattle.PLoS genetics · 2022Article
- Avian Leucosis Virus-Host Interaction: The Involvement of Host Factors in Viral Replication.Frontiers in immunology · 2022Review
- Knock-Out of Retrovirus Receptor GeneViruses · 2021Article
- The avian retroviral receptor Tva mediates the uptake of transcobalamin bound vitamin B12 (cobalamin).Journal of virology · 2021Article
- Precise CRISPR/Cas9 editing of the NHE1 gene renders chickens resistant to the J subgroup of avian leukosis virus.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Article
- The Novel Avian Leukosis Virus Subgroup K Shares Its Cellular Receptor with Subgroup A.Journal of virology · 2019Article
- Co-infection of vvMDV with multiple subgroups of avian leukosis viruses in indigenous chicken flocks in China.BMC veterinary research · 2019Article
- Sequential disruption of ALV host receptor genes reveals no sharing of receptors between ALV subgroups A, B, and J.Journal of animal science and biotechnology · 2019Article
- Genetic Resistance to Avian Leukosis Viruses Induced by CRISPR/Cas9 Editing of Specific Receptor Genes in Chicken Cells.Viruses · 2018Article
- Naturally Occurring Frameshift Mutations in theJournal of virology · 2018Article
- A premature stop codon within theOncotarget · 2017Article
- Acquisition of resistance to avian leukosis virus subgroup B through mutations on tvb cysteine-rich domains in DF-1 chicken fibroblasts.Veterinary research · 2017Article
- Identification of New World Quails Susceptible to Infection with Avian Leukosis Virus Subgroup J.Journal of virology · 2017Article
- Genetic Diversity of NHE1, Receptor for Subgroup J Avian Leukosis Virus, in Domestic Chicken and Wild Anseriform Species.PloS one · 2016Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The group of closely related avian sarcoma and leukosis viruses (ASLVs) evolved from a common ancestor into multiple subgroups, A to J, with differential host range among galliform species and chicken lines. These subgroups differ in variable parts of their envelope glycoproteins, the major determinants of virus interaction with specific receptor molecules. Three genetic loci, tva, tvb, and tvc, code for single membrane-spanning receptors from diverse protein families that confer susceptibility to the ASLV subgroups. The host range expansion of the ancestral virus might have been driven by gradual evolution of resistance in host cells, and the resistance alleles in all three receptor loci have been identified. Here, we characterized two alleles of the tva receptor gene with similar intronic deletions comprising the deduced branch-point signal within the first intron and leading to inefficient splicing of tva mRNA. As a result, we observed decreased susceptibility to subgroup A ASLV in vitro and in vivo. These alleles were independently found in a close-bred line of domestic chicken and Indian red jungle fowl (Gallus gallus murghi), suggesting that their prevalence might be much wider in outbred chicken breeds. We identified defective splicing to be a mechanism of resistance to ASLV and conclude that such a type of mutation could play an important role in virus-host coevolution.
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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.