ArticlePLoS pathogens2024
N123I mutation in the ALV-J receptor-binding domain region enhances viral replication ability by increasing the binding affinity with chNHE1.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Mapping the mutational landscape of an avian retrovirus envelope protein across its evolutionary trajectory.PLoS pathogens · 2026Article
- Research Progress on Pathogenesis and Prevention of Avian Leukosis Virus J Subgroup (ALV-J).Veterinary sciences · 2026Review
- Glycosylation of GETV E2 promotes pathogenesis in animal models.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- MARCH2 inhibits avian leukosis virus replication by targeting gp85 for ubiquitination and degradation.Journal of virology · 2025Article
- Multi-clade co-evolution and differential replication efficiencies of subgroup A avian leukosis virus in Chinese guinea fowl.BMC veterinary research · 2025Article
- N6-methyladenosine modification of the subgroup J avian leukosis viral RNAs attenuates host innate immunity via MDA5 signaling.PLoS pathogens · 2025Article
- Autophagy-mediated TET2 degradation by ALV-J Env protein suppresses innate immune activation to promote viral replication.Journal of virology · 2025Article
- Characterization of TCRβ and IGH Repertoires in the Spleen of Two Chicken Lines with Differential ALV-J Susceptibility Under Normal and Infection Conditions.Animals : an open access journal from MDPI · 2025Article
- Isolation and molecular characterization of subgroup J avian leukosis virus in native chicken breeds of China during 2022-2025.Frontiers in microbiology · 2025Article
- RNA-Seq Analysis of Glycolysis Regulation of Avian Leukosis Virus Subgroup J Replication.Animals : an open access journal from MDPI · 2024Article
- Rapid adaptive evolution of avian leukosis virus subgroup J in response to biotechnologically induced host resistance.PLoS pathogens · 2024Article
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
Abstract
The subgroup J avian leukosis virus (ALV-J), a retrovirus, uses its gp85 protein to bind to the receptor, the chicken sodium hydrogen exchanger isoform 1 (chNHE1), facilitating viral invasion. ALV-J is the main epidemic subgroup and shows noteworthy mutations within the receptor-binding domain (RBD) region of gp85, especially in ALV-J layer strains in China. However, the implications of these mutations on viral replication and transmission remain elusive. In this study, the ALV-J layer strain JL08CH3-1 exhibited a more robust replication ability than the prototype strain HPRS103, which is related to variations in the gp85 protein. Notably, the gp85 of JL08CH3-1 demonstrated a heightened binding capacity to chNHE1 compared to HPRS103-gp85 binding. Furthermore, we showed that the specific N123I mutation within gp85 contributed to the enhanced binding capacity of the gp85 protein to chNHE1. Structural analysis indicated that the N123I mutation primarily enhanced the stability of gp85, expanded the interaction interface, and increased the number of hydrogen bonds at the interaction interface to increase the binding capacity between gp85 and chNHE1. We found that the N123I mutation not only improved the viral replication ability of ALV-J but also promoted viral shedding in vivo. These comprehensive data underscore the notion that the N123I mutation increases receptor binding and intensifies viral replication.
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