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鸭瘟病毒UL3.5基因编码的蛋白质影响病毒的二次包膜化、释放及细胞间传播。

The Protein Encoded by the UL3.5 Gene of the Duck Plague Virus Affects Viral Secondary Envelopment, Release, and Cell-to-Cell Spread.

作者信息

Cao Huanhuan, Tian Bin, Tian Yanming, Cai Dongjie, Wang Mingshu, Jia Renyong, Chen Shun, Cheng Anchun

机构信息

Engineering Research Center of Southwest Animal Disease Prevention and Control Technology, Ministry of Education of the People's Republic of China, Chengdu 611130, China.

Research Center of Avian Disease and Institute of Veterinary Medicine and Immunology, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, China.

出版信息

Vet Sci. 2025 May 23;12(6):510. doi: 10.3390/vetsci12060510.

Abstract

Duck plague (DP), caused by duck plague virus (DPV), is a highly contagious and fatal disease among waterfowl. UL3.5, an unconserved gene belonging to the family, subfamily, and genus, is located downstream of UL3 and exhibits high variability in size and sequence, with an absence in herpes simplex virus (HSV). Currently, there is little understanding of DPV UL3.5. In this study, we determined that DPV pUL3.5 is distributed within the cytoplasm and co-located with multiple organelles. In addition, we investigated the genetic type of DPV UL3.5 and found that it is an early gene encoding an early viral protein. To further explore the function of DPV UL3.5, we constructed DPV-BAC-δUL3.5 and discovered that the deletion of UL3.5 significantly impacts the viral secondary envelopment and release processes. Furthermore, the UL3.5-deleted virus shows defects in cell-to-cell spread. In conclusion, our findings demonstrate, for the first time, that the early viral protein encoded by DPV UL3.5 plays a crucial role in promoting viral replication. This offers fundamental insights for further investigations into the function of DPV UL3.5.

摘要

鸭瘟(DP)是由鸭瘟病毒(DPV)引起的一种在水禽中具有高度传染性和致死性的疾病。UL3.5是一个属于 科、 亚科和 属的非保守基因,位于UL3下游,在大小和序列上表现出高度变异性,在单纯疱疹病毒(HSV)中不存在。目前,对DPV UL3.5的了解很少。在本研究中,我们确定DPV pUL3.5分布在细胞质中,并与多个细胞器共定位。此外,我们研究了DPV UL3.5的基因类型,发现它是一个编码早期病毒蛋白的早期基因。为了进一步探索DPV UL3.5的功能,我们构建了DPV-BAC-δUL3.5,并发现删除UL3.5会显著影响病毒的二次包膜化和释放过程。此外,缺失UL3.5的病毒在细胞间传播方面存在缺陷。总之,我们的研究结果首次表明,DPV UL3.5编码的早期病毒蛋白在促进病毒复制中起关键作用。这为进一步研究DPV UL3.5的功能提供了基础见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a02/12197417/e874bd7aa5d9/vetsci-12-00510-g0A1.jpg

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