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The UL31 protein of duck plague virus promotes viral replication and interacts with ICP4, ICP22, and VP16 proteins

Hongying Chen1, Anchun Cheng2, Huijun Cao1

  • 1Engineering Research Center of Southwest Animal Disease Prevention and Control Technology for Ministry of Education of the People's Republic of China, International Joint Research Center for Animal Disease Prevention and Control of Sichuan Province, Key Laboratory of Animal Disease and Human Health of Sichuan Province, Research Center of Avian Disease and Institute of Veterinary Medicine and Immunology, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, China.

Veterinary Microbiology
|July 11, 2026
PubMed

Insights

Duck plague virus (DPV) protein pUL31 interacts with host and viral proteins, enhancing viral gene expression and replication. This study reveals new functions for pUL31 beyond nuclear egress in the DPV life cycle.

Area of Science:

  • Virology
  • Molecular Biology
  • Infectious Diseases

Background:

  • Duck plague virus (DPV) causes a severe contagious disease in waterfowl.
  • The viral protein pUL31 is known to facilitate nuclear egress of herpesviruses.
  • The full role of pUL31 in the DPV life cycle remains largely unexplored.

Purpose of the Study:

  • To investigate the functions of DPV pUL31 in the viral life cycle beyond nuclear egress.
  • To identify host and viral protein interactors of pUL31.
  • To understand pUL31's impact on viral gene expression and replication.

Main Methods:

  • Glutathione S-transferase (GST) pull-down assays combined with LC-MS/MS to identify pUL31 interactors.
  • Bioinformatics analysis of identified protein partners.
  • Co-immunoprecipitation (Co-IP) assays and promoter activity assays to validate interactions and functions.

Main Results:

  • Identified 308 host and 36 viral proteins interacting with pUL31.
  • Discovered pUL31 interacts with viral proteins ICP4, ICP22, ICP27, and VP16.
  • Demonstrated pUL31 enhances promoter activities of ICP4, ICP22, and VP16, boosting viral gene expression.

Conclusions:

  • pUL31 plays a crucial role in regulating DPV gene expression by increasing the activity of key viral transcriptional regulators.
  • pUL31 significantly contributes to DPV replication, expanding its known functions in the viral life cycle.
  • Findings offer novel insights into pUL31's multifaceted role in DPV and other herpesviruses.
Keywords:
Duck plague virusPromoter activationProtein–protein interactionUL31 proteinViral transcriptional regulators

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