ArticleRetrovirology2022
The key amino acid sites 199-205, 269, 319, 321 and 324 of ALV-K env contribute to the weaker replication capacity of ALV-K than ALV-A.
Article in Retrovirology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 5 citations in OpenAlex.
- Residues Y142, I143, T146, Q206, S215, R228, G267, and M268 in the surface glycoprotein of FGV-like subgroup A avian leukosis virus are the key sites determining Tva receptor binding and infectivity.Veterinary research · 2026Article
- Research note: ELISA kit replacement leads to false negatives in ALV eradication-A case study in Chinese yellow-feathered broilers.Poultry science · 2026Article
- A novel recombinant ALV-K carrying ALV-J-derived LTR, pol, and 3'UTR from Chinese indigenous chicken breeds exhibits enhanced replication and increased hemangioma-associated pathogenicity.BMC veterinary research · 2026Article
- Acetylation-mediated regulation of ALV viral proteins: Implications for retroviral inhibition.PLoS pathogens · 2026Article
- Multi-clade co-evolution and differential replication efficiencies of subgroup A avian leukosis virus in Chinese guinea fowl.BMC veterinary research · 2025Article
- Isolation and molecular characterization of subgroup J avian leukosis virus in native chicken breeds of China during 2022-2025.Frontiers in microbiology · 2025Article
- Avian Leukosis: Will We Be Able to Get Rid of It?Animals : an open access journal from MDPI · 2023Review
- The phylogenetic analysis of the new emerging ALV-K revealing the co-prevailing of multiple clades in chickens and a proposal for the classification of ALV-K.Frontiers in veterinary science · 2023Article
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAvian leukosis virus (ALV) is an infectious retrovirus, that mainly causes various forms of tumours, immunosuppression, a decreased egg production rate and slow weight gain in poultry. ALV consists of 11 subgroups, A-K, among which ALV-K is an emerging subgroup that has become prevalent in the past 10 years. Most ALV-K isolates showed weak replication ability and pathogenicity. In this study, the weak replication ability of ALV-K was explored from the perspective of the interaction between ALV-K gp85 and the Tva receptor.
methodsFourteen soluble recombinant ALV-A/K gp85 chimeric proteins were constructed by substituting the sequence difference regions (hr1, hr2 and vr3) of the ALV-A gp85 protein with the skeleton ALV-K gp85 protein for co-IP and competitive blocking tests.
resultsThe binding capacity of ALV-K gp85 to Tva was significantly weaker than that of ALV-A gp85 (P < 0.05) and the key amino acid sites 199-205, 269, 319, 321 and 324 of ALV-K env contributed to the weaker replication capacity of ALV-K than ALV-A.
conclusionsThis is the first study to reveal the molecular factors of the weak replication ability of ALV-K from the perspective of the interaction of ALV-K gp85 to Tva, providing a basis for further elucidation of the infection mechanism of ALV-K.
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