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Research Note: Duck plague virus pUL48 is a late protein that plays an important role in viral replication
Duck plague virus (DPV) pUL48 is a homologous of herpes simplex virus VP16, and some studies have shown that VP16 is essential for viral replication and proliferation, but there are few studies on DPV pUL48. Therefore, in order to study the function of pUL48 protein, we constructed a UL48-deleted mu...
Autores principales: | , , , , , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9723934/ https://www.ncbi.nlm.nih.gov/pubmed/36473386 http://dx.doi.org/10.1016/j.psj.2022.102358 |
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author | Zhou, Tong Wang, Mingshu Ruan, Peilin Fan, Dengjian Cheng, Anchun Zhang, Wei Tian, Bin Yang, Qiao Wu, Ying Zhang, Shaqiu Ou, Xumin Mao, Sai Huang, Juan Gao, Qun Sun, Di Zhao, Xinxin Chen, Shun Liu, Mafeng Zhu, Dekang Jia, Renyong |
author_facet | Zhou, Tong Wang, Mingshu Ruan, Peilin Fan, Dengjian Cheng, Anchun Zhang, Wei Tian, Bin Yang, Qiao Wu, Ying Zhang, Shaqiu Ou, Xumin Mao, Sai Huang, Juan Gao, Qun Sun, Di Zhao, Xinxin Chen, Shun Liu, Mafeng Zhu, Dekang Jia, Renyong |
author_sort | Zhou, Tong |
collection | PubMed |
description | Duck plague virus (DPV) pUL48 is a homologous of herpes simplex virus VP16, and some studies have shown that VP16 is essential for viral replication and proliferation, but there are few studies on DPV pUL48. Therefore, in order to study the function of pUL48 protein, we constructed a UL48-deleted mutant (DPV-BAC-∆UL48) that completely reemoved the UL48 gene from the DPV BAC genome and the revertant virus (DPV-BAC-∆UL48R) by using the 2-step red recombination system. Compared with the parental virus (DPV-BAC) and the revertant virus, the titer of UL48-deleted mutant was reduced by more than 38.2%, and the efficiency of producing infectious virions was significantly reduced. In addition, the average size of plaques produced by UL48-deleted mutant was about 30% smaller than that of the parental and revertant viruses, suggesting that pUL48 protein affected the cell-to-cell transmission of DPV. Finally, pharmacological inhibition assay showed that pUL48 is a late protein of DPV. In this study, we found that UL48, as a late gene, plays an important role in viral replication by affecting the formation of DPV infectious virion, virus cell-to-cell transmission, and viral genome transcription, which may provide some help for the study of the function of DPV pUL48 protein and the prevention and control of DPV. |
format | Online Article Text |
id | pubmed-9723934 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-97239342022-12-07 Research Note: Duck plague virus pUL48 is a late protein that plays an important role in viral replication Zhou, Tong Wang, Mingshu Ruan, Peilin Fan, Dengjian Cheng, Anchun Zhang, Wei Tian, Bin Yang, Qiao Wu, Ying Zhang, Shaqiu Ou, Xumin Mao, Sai Huang, Juan Gao, Qun Sun, Di Zhao, Xinxin Chen, Shun Liu, Mafeng Zhu, Dekang Jia, Renyong Poult Sci IMMUNOLOGY, HEALTH AND DISEASE Duck plague virus (DPV) pUL48 is a homologous of herpes simplex virus VP16, and some studies have shown that VP16 is essential for viral replication and proliferation, but there are few studies on DPV pUL48. Therefore, in order to study the function of pUL48 protein, we constructed a UL48-deleted mutant (DPV-BAC-∆UL48) that completely reemoved the UL48 gene from the DPV BAC genome and the revertant virus (DPV-BAC-∆UL48R) by using the 2-step red recombination system. Compared with the parental virus (DPV-BAC) and the revertant virus, the titer of UL48-deleted mutant was reduced by more than 38.2%, and the efficiency of producing infectious virions was significantly reduced. In addition, the average size of plaques produced by UL48-deleted mutant was about 30% smaller than that of the parental and revertant viruses, suggesting that pUL48 protein affected the cell-to-cell transmission of DPV. Finally, pharmacological inhibition assay showed that pUL48 is a late protein of DPV. In this study, we found that UL48, as a late gene, plays an important role in viral replication by affecting the formation of DPV infectious virion, virus cell-to-cell transmission, and viral genome transcription, which may provide some help for the study of the function of DPV pUL48 protein and the prevention and control of DPV. Elsevier 2022-11-19 /pmc/articles/PMC9723934/ /pubmed/36473386 http://dx.doi.org/10.1016/j.psj.2022.102358 Text en © 2022 The Authors https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | IMMUNOLOGY, HEALTH AND DISEASE Zhou, Tong Wang, Mingshu Ruan, Peilin Fan, Dengjian Cheng, Anchun Zhang, Wei Tian, Bin Yang, Qiao Wu, Ying Zhang, Shaqiu Ou, Xumin Mao, Sai Huang, Juan Gao, Qun Sun, Di Zhao, Xinxin Chen, Shun Liu, Mafeng Zhu, Dekang Jia, Renyong Research Note: Duck plague virus pUL48 is a late protein that plays an important role in viral replication |
title | Research Note: Duck plague virus pUL48 is a late protein that plays an important role in viral replication |
title_full | Research Note: Duck plague virus pUL48 is a late protein that plays an important role in viral replication |
title_fullStr | Research Note: Duck plague virus pUL48 is a late protein that plays an important role in viral replication |
title_full_unstemmed | Research Note: Duck plague virus pUL48 is a late protein that plays an important role in viral replication |
title_short | Research Note: Duck plague virus pUL48 is a late protein that plays an important role in viral replication |
title_sort | research note: duck plague virus pul48 is a late protein that plays an important role in viral replication |
topic | IMMUNOLOGY, HEALTH AND DISEASE |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9723934/ https://www.ncbi.nlm.nih.gov/pubmed/36473386 http://dx.doi.org/10.1016/j.psj.2022.102358 |
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