Duck plague virus tegument protein vp22 plays a key role in the secondary envelopment and cell-to-cell spread

Author:

Wu Liping,Wang Mingshu,Cheng AnchunORCID,Tian Bin,Huang Juan,Wu Ying,Yang Qiao,Ou Xumin,Sun Di,Zhang Shaqiu,Zhao Xinxin,Gao Qun,He Yu,Zhu Dekang,Chen Shun,Liu Mafeng,Jia Renyong

Abstract

AbstractDuck plague virus (DPV) is one of the major infectious and fatal diseases of geese, ducks, and other wild waterfowl. The DPV UL49 gene product VP22 is one of the most abundant tegument proteins. However, the role of the DPV VP22 is enigmatic to be clarified. In this study, we found deletion of the UL49 gene resulted in reduced viral growth curve and smaller plaque size in duck embryo fibroblast (DEF) cells, confirming that DPV VP22 is required for efficient viral growth in vitro. In addition, deletion of the UL49 gene inhibited the secondary envelopment of the virus, the release of viral particles, and the spread of viruses between cells. Our study signified the importance of VP22 for DPV secondary envelopment, release, cell-to-cell spread, and accumulation of viral RNA. These findings provide a basis for further study of the function of VP22 in DPV or other herpesviruses.

Publisher

Springer Science and Business Media LLC

Subject

General Veterinary

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