RIOK3-Mediated Akt phosphorylation facilitates synergistic replication of Marek’s disease and reticuloendotheliosis viruses
Co-infection of Marek’s disease virus (MDV) and reticuloendotheliosis virus (REV) synergistically drives disease progression, yet little is known about the mechanism of the synergism. Here, we found that co-infection of REV and MDV increased their replication via the RIOK3-Akt pathway. Initially, we...
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Format: | Article |
Language: | English |
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Taylor & Francis Group
2022-12-01
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Series: | Virulence |
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Online Access: | https://www.tandfonline.com/doi/10.1080/21505594.2022.2096247 |
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author | Xusheng Du Defang Zhou Jing Zhou Jingwen Xue Ziqiang Cheng |
author_facet | Xusheng Du Defang Zhou Jing Zhou Jingwen Xue Ziqiang Cheng |
author_sort | Xusheng Du |
collection | DOAJ |
description | Co-infection of Marek’s disease virus (MDV) and reticuloendotheliosis virus (REV) synergistically drives disease progression, yet little is known about the mechanism of the synergism. Here, we found that co-infection of REV and MDV increased their replication via the RIOK3-Akt pathway. Initially, we noticed that the viral titres of MDV and REV significantly increased in REV and MDV co-infected cells compared with single-infected cells. Furthermore, tandem mass tag peptide labelling coupled with LC/MS analysis showed that Akt was upregulated in REV and MDV co-infected cells. Overexpression of Akt promoted synergistic replication of MDV and REV. Conversely, inhibition of Akt suppressed synergistic replication of MDV and REV. However, PI3K inhibition did not affect synergistic replication of MDV and REV, suggesting that the PI3K/Akt pathway is not involved in the synergism of MDV and REV. In addition, we revealed that RIOK3 was recruited to regulate Akt in REV and MDV co-infected cells. Moreover, wild-type RIOK3, but not kinase-dead RIOK3, mediated Akt phosphorylation and promoted synergistic replication of MDV and REV. Our results illustrate that MDV and REV activated a novel RIOK3-Akt signalling pathway to facilitate their synergistic replication. |
first_indexed | 2024-12-11T16:23:42Z |
format | Article |
id | doaj.art-01095dd784eb495d8163a4e68858c471 |
institution | Directory Open Access Journal |
issn | 2150-5594 2150-5608 |
language | English |
last_indexed | 2024-12-11T16:23:42Z |
publishDate | 2022-12-01 |
publisher | Taylor & Francis Group |
record_format | Article |
series | Virulence |
spelling | doaj.art-01095dd784eb495d8163a4e68858c4712022-12-22T00:58:47ZengTaylor & Francis GroupVirulence2150-55942150-56082022-12-011311184119810.1080/21505594.2022.2096247RIOK3-Mediated Akt phosphorylation facilitates synergistic replication of Marek’s disease and reticuloendotheliosis virusesXusheng Du0Defang Zhou1Jing Zhou2Jingwen Xue3Ziqiang Cheng4College of Veterinary Medicine, Shandong Agricultural University, ChinaCollege of Veterinary Medicine, Shandong Agricultural University, ChinaCollege of Veterinary Medicine, Shandong Agricultural University, ChinaCollege of Veterinary Medicine, Shandong Agricultural University, ChinaCollege of Veterinary Medicine, Shandong Agricultural University, ChinaCo-infection of Marek’s disease virus (MDV) and reticuloendotheliosis virus (REV) synergistically drives disease progression, yet little is known about the mechanism of the synergism. Here, we found that co-infection of REV and MDV increased their replication via the RIOK3-Akt pathway. Initially, we noticed that the viral titres of MDV and REV significantly increased in REV and MDV co-infected cells compared with single-infected cells. Furthermore, tandem mass tag peptide labelling coupled with LC/MS analysis showed that Akt was upregulated in REV and MDV co-infected cells. Overexpression of Akt promoted synergistic replication of MDV and REV. Conversely, inhibition of Akt suppressed synergistic replication of MDV and REV. However, PI3K inhibition did not affect synergistic replication of MDV and REV, suggesting that the PI3K/Akt pathway is not involved in the synergism of MDV and REV. In addition, we revealed that RIOK3 was recruited to regulate Akt in REV and MDV co-infected cells. Moreover, wild-type RIOK3, but not kinase-dead RIOK3, mediated Akt phosphorylation and promoted synergistic replication of MDV and REV. Our results illustrate that MDV and REV activated a novel RIOK3-Akt signalling pathway to facilitate their synergistic replication.https://www.tandfonline.com/doi/10.1080/21505594.2022.2096247MDVREVsynergistic replicationRIOK3Akt |
spellingShingle | Xusheng Du Defang Zhou Jing Zhou Jingwen Xue Ziqiang Cheng RIOK3-Mediated Akt phosphorylation facilitates synergistic replication of Marek’s disease and reticuloendotheliosis viruses Virulence MDV REV synergistic replication RIOK3 Akt |
title | RIOK3-Mediated Akt phosphorylation facilitates synergistic replication of Marek’s disease and reticuloendotheliosis viruses |
title_full | RIOK3-Mediated Akt phosphorylation facilitates synergistic replication of Marek’s disease and reticuloendotheliosis viruses |
title_fullStr | RIOK3-Mediated Akt phosphorylation facilitates synergistic replication of Marek’s disease and reticuloendotheliosis viruses |
title_full_unstemmed | RIOK3-Mediated Akt phosphorylation facilitates synergistic replication of Marek’s disease and reticuloendotheliosis viruses |
title_short | RIOK3-Mediated Akt phosphorylation facilitates synergistic replication of Marek’s disease and reticuloendotheliosis viruses |
title_sort | riok3 mediated akt phosphorylation facilitates synergistic replication of marek s disease and reticuloendotheliosis viruses |
topic | MDV REV synergistic replication RIOK3 Akt |
url | https://www.tandfonline.com/doi/10.1080/21505594.2022.2096247 |
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