ArticleVeterinary research2023
Duck plague virus tegument protein vp22 plays a key role in the secondary envelopment and cell-to-cell spread.
Article in Veterinary research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Anatid herpesvirus 1 UL51 protein is palmitoylated by DHHC9 and DHHC18 for viral replication and virulence.PLoS pathogens · 2026Article
- The Protein Encoded by the UL3.5 Gene of the Duck Plague Virus Affects Viral Secondary Envelopment, Release, and Cell-to-Cell Spread.Veterinary sciences · 2025Article
- The precise function of alphaherpesvirus tegument proteins and their interactions during the viral life cycle.Frontiers in microbiology · 2024Review
- Multiple functions of the herpesvirus UL14 gene product in viral infection.Frontiers in microbiology · 2024Review
Corrections and comments
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duck 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.
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Registered trials
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