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Published on: November 1, 2011
The protein encoded by the duck plague virus UL14 gene regulates virion morphogenesis and affects viral replication
Jieyu Wan1, Fangjie Li1, Mingshu Wang1
1Institute of Preventive Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu City, Sichuan, 611130, P.R. China; Key Laboratory of Animal Disease and Human Health of Sichuan Province, Sichuan Agricultural University, Wenjiang, Chengdu City, Sichuan, 611130, P.R. China; Avian Disease Research Center, College of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu City, Sichuan, 611130, P.R. China.
Abstract:
To investigate the pivotal roles of the duck plague virus (DPV) tegument protein UL14 in viral replication, we generated 2 mutated viruses of DPV by using the bacterial artifcial chromosome system, the UL14-null mutant virus (CHv-BAC-ΔUL14) and the corresponding revertant virus (CHv-BAC-ΔUL14R). We found that the CHv-BAC-ΔUL14 viruses exhibited impaired virion morphogenesis in transmission electron microscopy (TEM) studies. Furthermore, CHv-BAC-ΔUL14 exhibited a plaque size reduction in duck embryo fibroblasts (DEFs). Finally, CHv-BAC-ΔUL14 exhibited a significant viral growth defect. Taken together, our findings suggest that DPV UL14 protein regulates viral morphogenesis for efficient viral replication.
Insights
Duck plague virus (DPV) tegument protein UL14 is crucial for efficient viral replication. UL14 regulates viral morphogenesis, impacting virion assembly and viral growth.
Area of Science:
- Virology
- Molecular Biology
- Animal Virology
Background:
- Duck plague virus (DPV) is a significant pathogen affecting waterfowl.
- Tegument proteins play critical roles in the replication cycle of many viruses.
- The specific function of DPV tegument protein UL14 in viral replication remains largely uncharacterized.
Purpose of the Study:
- To elucidate the role of the DPV tegument protein UL14 in viral replication.
- To investigate the impact of UL14 on viral morphogenesis and growth.
Main Methods:
- Generation of a UL14-null mutant DPV (CHv-BAC-ΔUL14) and a revertant virus (CHv-BAC-ΔUL14R) using a bacterial artificial chromosome system.
- Transmission electron microscopy (TEM) to assess virion morphogenesis.
- Plaque assays in duck embryo fibroblasts (DEFs) to evaluate viral spread.
- Viral growth assays to quantify replication efficiency.
Main Results:
- The UL14-null mutant virus (CHv-BAC-ΔUL14) displayed impaired virion morphogenesis.
- CHv-BAC-ΔUL14 showed a significant reduction in plaque size in DEFs.
- A substantial viral growth defect was observed for CHv-BAC-ΔUL14 compared to the wild-type and revertant viruses.
Conclusions:
- DPV tegument protein UL14 is essential for efficient viral replication.
- UL14 plays a critical role in regulating viral morphogenesis, which is vital for DPV propagation.
- These findings highlight UL14 as a potential target for antiviral strategies against DPV.
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