ArticleScientific reports2020
The Pivotal Roles of US3 Protein in Cell-to-Cell Spread and Virion Nuclear Egress of Duck Plague Virus.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- ERAD inhibitor Eeyarestatin I (EerI) suppresses duck plague virus by restoring STING-mediated antiviral immunity.Poultry science · 2026Article
- The precise function of alphaherpesvirus tegument proteins and their interactions during the viral life cycle.Frontiers in microbiology · 2024Review
- Characterization of a Unique Novel LORF3 Protein of Duck Plague Virus and Its Potential Pathogenesis.Journal of virology · 2023Article
- Modifications of the PI3K/Akt/mTOR axis during FeHV-1 infection in permissive cells.Frontiers in veterinary science · 2023Article
- Mechanism of herpesvirus UL24 protein regulating viral immune escape and virulence.Frontiers in microbiology · 2023Review
- Deletion of Double Copies of the US1 Gene Reduces the Infectivity of Recombinant Duck Plague VirusMicrobiology spectrum · 2022Article
- Duck Enteritis Virus Protein Kinase US3 Inhibits DNA Sensing Signaling by Phosphorylating Interferon Regulatory Factor 7.Microbiology spectrum · 2022Article
- Regulation of alphaherpesvirus protein via post-translational phosphorylation.Veterinary research · 2022Review
- The protein encoded by the duck plague virus UL14 gene regulates virion morphogenesis and affects viral replication.Poultry science · 2022Article
- Duck plague virus US3 protein kinase phosphorylates UL47 and regulates the subcellular localization of UL47.Frontiers in microbiology · 2022Article
- Evaluation of the Safety and Immunogenicity of Duck-Plague VirusFrontiers in immunology · 2022Article
- Review
- UL11 Protein Is a Key Participant of the Duck Plague Virus in Its Life Cycle.Frontiers in microbiology · 2021Article
Corrections and comments
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Authors and funding
21 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The duck plague virus (DPV) US3 protein, a homolog of the herpes simplex virus-1 (HSV-1) US3 protein that is reported to be critical for viral replication, has been minimally studied. Therefore, to investigate the function of the DPV US3 protein, we used scarless Red recombination technology based on an infectious bacterial artificial chromosome (BAC) containing the DPV Chinese virulent strain (CHv) genome and successfully constructed and rescued a US3-deleted mutant and the corresponding revertant virus (BAC-CHv-ΔUS3 and BAC-CHv-ΔUS3R, respectively). For viral growth characteristics, compared to the parental and revertant viruses, the US3-deleted mutant showed an approximately 100-fold reduction in viral titers but no significant reduction in genome copies, indicating that the US3-deleted mutant exhibited decreased viral replication but not decreased viral DNA generation. In addition, the US3-deleted mutant formed viral plaques that were 33% smaller on average than those formed by the parental and revertant viruses, demonstrating that US3 protein affected the viral cell-to-cell spread of DPV. Finally, the results of electron microscopy showed that the deletion of US3 resulted in a large number of virions accumulating in the nucleus and perinuclear space, thus blocking virion nuclear egress. In this study, we found that the DPV US3 protein played pivotal roles in viral replication by promoting viral cell-to-cell spread and virion nuclear egress, which may provide some references for research on the function of the DPV US3 protein.
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