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

Background Avian 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 i...

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Published in:Retrovirology 2022-08, Vol.19 (1), p.1-19, Article 19
Main Authors: Chen, Jian, Li, Jinqun, Dong, Xinyi, Liao, Ming, Cao, Weisheng
Format: Article
Language:English
Subjects:
Amino acids
Antibodies
Avian leukosis
Avian leukosis virus K subgroup
Binding capacity
Egg production
Eggs
Env
Flow cytometry
Health aspects
Immunosuppression
Immunotherapy
Infrared imaging systems
Leukemia
Leukosis
Lymphocytes
Mutation
Pathogenicity
Plasmids
Proteins
Recombinant chimaeras
Replication
Tumors
Tva receptor
Viruses
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Summary:Background Avian 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. Methods Fourteen 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. Results The 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. Conclusions This 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. Keywords: Avian leukosis virus K subgroup, Env, Tva receptor, Recombinant chimaeras, Binding capacity
ISSN:1742-4690
1742-4690
DOI:10.1186/s12977-022-00598-0