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
Abstract 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 pr...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2022-08-01
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| Series: | Retrovirology |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s12977-022-00598-0 |
| _version_ | 1811188761471483904 |
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| author | Jian Chen Jinqun Li Xinyi Dong Ming Liao Weisheng Cao |
| author_facet | Jian Chen Jinqun Li Xinyi Dong Ming Liao Weisheng Cao |
| author_sort | Jian Chen |
| collection | DOAJ |
| description | Abstract 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. |
| first_indexed | 2024-04-11T14:23:49Z |
| format | Article |
| id | doaj.art-e3a485f12c4e413594db8b901578872d |
| institution | Directory Open Access Journal |
| issn | 1742-4690 |
| language | English |
| last_indexed | 2024-04-11T14:23:49Z |
| publishDate | 2022-08-01 |
| publisher | BMC |
| record_format | Article |
| series | Retrovirology |
| spelling | doaj.art-e3a485f12c4e413594db8b901578872d2022-12-22T04:18:56ZengBMCRetrovirology1742-46902022-08-0119111210.1186/s12977-022-00598-0The 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-AJian Chen0Jinqun Li1Xinyi Dong2Ming Liao3Weisheng Cao4College of Veterinary Medicine, South China Agricultural UniversityCollege of Veterinary Medicine, South China Agricultural UniversityCollege of Veterinary Medicine, South China Agricultural UniversityCollege of Veterinary Medicine, South China Agricultural UniversityCollege of Veterinary Medicine, South China Agricultural UniversityAbstract 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.https://doi.org/10.1186/s12977-022-00598-0Avian leukosis virus K subgroupEnvTva receptorRecombinant chimaerasBinding capacity |
| spellingShingle | Jian Chen Jinqun Li Xinyi Dong Ming Liao Weisheng Cao 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 Retrovirology Avian leukosis virus K subgroup Env Tva receptor Recombinant chimaeras Binding capacity |
| title | 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 |
| title_full | 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 |
| title_fullStr | 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 |
| title_full_unstemmed | 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 |
| title_short | 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 |
| title_sort | 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 |
| topic | Avian leukosis virus K subgroup Env Tva receptor Recombinant chimaeras Binding capacity |
| url | https://doi.org/10.1186/s12977-022-00598-0 |
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