A double-edged sword in antiviral defence: ATG7 binding dicer to promote virus replication
Abstract RNA interference (RNAi) and autophagy are two pivotal biological processes that regulate virus replication. This study explored the complex relationship between autophagy and RNAi in controlling influenza virus replication. Initially, we reported that influenza virus (H9N2) infection increa...
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| Format: | Article |
| Language: | English |
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Springer
2025-02-01
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| Series: | Cellular and Molecular Life Sciences |
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| Online Access: | https://doi.org/10.1007/s00018-025-05603-1 |
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| author | Yaotang Wu Yang Wu Chenlu Wang Ningna Xiong Wenxin Ji Mei Fu Junpeng Zhu Zhixin Li Jian Lin Qian Yang |
| author_facet | Yaotang Wu Yang Wu Chenlu Wang Ningna Xiong Wenxin Ji Mei Fu Junpeng Zhu Zhixin Li Jian Lin Qian Yang |
| author_sort | Yaotang Wu |
| collection | DOAJ |
| description | Abstract RNA interference (RNAi) and autophagy are two pivotal biological processes that regulate virus replication. This study explored the complex relationship between autophagy and RNAi in controlling influenza virus replication. Initially, we reported that influenza virus (H9N2) infection increases the viral load and the expression of autophagy markers while inhibiting the RNAi pathway. Subsequent studies employing autophagy enhancer and inhibitor treatments confirmed that avian influenza virus (AIV, H9N2) promotes viral replication by enhancing autophagy pathways. Further analysis revealed that ATG7, an autophagy protein, can interact with dicer to affect its antiviral functions. Finally, we discovered that infection with other avian RNA viruses, including infectious bursal disease virus (IBDV) and infectious bronchitis virus (IBV), induced the upregulation of ATG7, which blocked the RNAi pathway to facilitate virus replication. Our findings suggested that virus infection might trigger the upregulation of autophagy and downregulation of the RNAi pathway, revealing a complex interaction between these two biological processes in the defence against viral replication. |
| format | Article |
| id | doaj-art-2b5cd25c172d43f6990425cc1ccf0e7a |
| institution | Kabale University |
| issn | 1420-9071 |
| language | English |
| publishDate | 2025-02-01 |
| publisher | Springer |
| record_format | Article |
| series | Cellular and Molecular Life Sciences |
| spelling | doaj-art-2b5cd25c172d43f6990425cc1ccf0e7a2025-08-20T03:46:04ZengSpringerCellular and Molecular Life Sciences1420-90712025-02-0182111910.1007/s00018-025-05603-1A double-edged sword in antiviral defence: ATG7 binding dicer to promote virus replicationYaotang Wu0Yang Wu1Chenlu Wang2Ningna Xiong3Wenxin Ji4Mei Fu5Junpeng Zhu6Zhixin Li7Jian Lin8Qian Yang9College of Veterinary Medicine, Nanjing Agricultural UniversityCollege of Life Sciences, Nanjing Agricultural UniversityCollege of Life Sciences, Nanjing Agricultural UniversityCollege of Veterinary Medicine, Nanjing Agricultural UniversityCollege of Veterinary Medicine, Nanjing Agricultural UniversityCollege of Veterinary Medicine, Nanjing Agricultural UniversityCollege of Veterinary Medicine, Nanjing Agricultural UniversityNingxia Animal Disease Prevention and Control CenterCollege of Veterinary Medicine, Nanjing Agricultural UniversityCollege of Veterinary Medicine, Nanjing Agricultural UniversityAbstract RNA interference (RNAi) and autophagy are two pivotal biological processes that regulate virus replication. This study explored the complex relationship between autophagy and RNAi in controlling influenza virus replication. Initially, we reported that influenza virus (H9N2) infection increases the viral load and the expression of autophagy markers while inhibiting the RNAi pathway. Subsequent studies employing autophagy enhancer and inhibitor treatments confirmed that avian influenza virus (AIV, H9N2) promotes viral replication by enhancing autophagy pathways. Further analysis revealed that ATG7, an autophagy protein, can interact with dicer to affect its antiviral functions. Finally, we discovered that infection with other avian RNA viruses, including infectious bursal disease virus (IBDV) and infectious bronchitis virus (IBV), induced the upregulation of ATG7, which blocked the RNAi pathway to facilitate virus replication. Our findings suggested that virus infection might trigger the upregulation of autophagy and downregulation of the RNAi pathway, revealing a complex interaction between these two biological processes in the defence against viral replication.https://doi.org/10.1007/s00018-025-05603-1RNAiDicerAutophagyATG7H9N2 |
| spellingShingle | Yaotang Wu Yang Wu Chenlu Wang Ningna Xiong Wenxin Ji Mei Fu Junpeng Zhu Zhixin Li Jian Lin Qian Yang A double-edged sword in antiviral defence: ATG7 binding dicer to promote virus replication Cellular and Molecular Life Sciences RNAi Dicer Autophagy ATG7 H9N2 |
| title | A double-edged sword in antiviral defence: ATG7 binding dicer to promote virus replication |
| title_full | A double-edged sword in antiviral defence: ATG7 binding dicer to promote virus replication |
| title_fullStr | A double-edged sword in antiviral defence: ATG7 binding dicer to promote virus replication |
| title_full_unstemmed | A double-edged sword in antiviral defence: ATG7 binding dicer to promote virus replication |
| title_short | A double-edged sword in antiviral defence: ATG7 binding dicer to promote virus replication |
| title_sort | double edged sword in antiviral defence atg7 binding dicer to promote virus replication |
| topic | RNAi Dicer Autophagy ATG7 H9N2 |
| url | https://doi.org/10.1007/s00018-025-05603-1 |
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