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Published on: May 1, 2019
Research Note: Duck plague virus pUL48 is a late protein that plays an important role in viral replication
Tong Zhou1, Mingshu Wang1, Peilin Ruan1
1Avian Center of Disease Research, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu City, Sichuan Povince, 611130, China; Institute of Preventive Veterinary Medicine, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu City, Sichuan Povince, 611130, China; Key Laboratory of Animal Disease and Human Health of Sichuan Province, Chengdu City, Sichuan Povince, 611130, China.
Abstract:
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.
Insights
Duck plague virus (DPV) pUL48 protein is crucial for viral replication and infectious virion formation. This study demonstrates its role in DPV cell-to-cell transmission and viral genome transcription.
Area of Science:
- Virology
- Molecular Biology
- Animal Pathology
Background:
- Duck plague virus (DPV) causes significant mortality in waterfowl.
- The DPV pUL48 protein is homologous to herpes simplex virus VP16, known to be essential for viral replication.
- Limited research exists on the specific function of DPV pUL48.
Purpose of the Study:
- To investigate the function of the DPV pUL48 protein in viral replication and pathogenesis.
- To characterize a UL48-deleted DPV mutant and assess the impact of pUL48 deletion.
Main Methods:
- Construction of a UL48-deleted DPV mutant (DPV-BAC-∆UL48) and its revertant (DPV-BAC-∆UL48R) using the 2-step red recombination system.
- Comparative analysis of viral titers, infectious virion production, and plaque sizes between the mutant and parental/revertant viruses.
- Pharmacological inhibition assays to determine the temporal expression of pUL48.
Main Results:
- The UL48-deleted mutant showed a >38.2% reduction in viral titer and significantly reduced infectious virion production compared to controls.
- Plaque size was reduced by approximately 30% in the UL48-deleted mutant, indicating impaired cell-to-cell transmission.
- Pharmacological assays confirmed pUL48 as a late viral protein.
Conclusions:
- The DPV pUL48 protein, a late gene product, is essential for efficient viral replication.
- pUL48 influences infectious virion formation, cell-to-cell transmission, and viral genome transcription.
- Understanding pUL48 function aids in DPV prevention and control strategies.
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