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DTMUV upregulates DDX17 expression to facilitate viral replication.
Yuting Cheng1, Wenjing Xie1, Qingkang Zhou1
1Engineering Technology Research Center for Modern Animal Science and Novel Veterinary Pharmaceutic Development, Jiangsu Key Laboratory of Veterinary Bio-Pharmaceutical High Technology Research, Jiangsu Agri-Animal Husbandry Vocational College, Taizhou, 225300, China.
Veterinary Research
|December 16, 2025
Summary
Duck Tembusu virus (DTMUV) infection increases host cell DEAD-box RNA helicase 17 (DDX17) levels. DDX17 promotes DTMUV replication by interacting with the viral C protein.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Duck Tembusu virus (DTMUV) is a significant poultry pathogen.
- Understanding DTMUV infection mechanisms is crucial for disease control.
Purpose of the Study:
- Investigate the role of DEAD-box RNA helicase 17 (DDX17) in DTMUV infection.
- Elucidate the molecular mechanisms by which DDX17 influences viral replication.
Main Methods:
- In vitro infection models using CRISPR/Cas9 gene knockout, siRNA interference, and overexpression.
- Co-immunoprecipitation and mass spectrometry to identify protein interactions.
- Phylogenetic analysis and tissue distribution assays.
Main Results:
- DTMUV infection upregulates DDX17 mRNA and protein expression.
- DDX17 promotes DTMUV replication via its ATP-binding and hydrolysis domain.
- DDX17 interacts with the DTMUV C protein.
- Duck DDX17 shows high homology with avian orthologs and is highly expressed in spleen and liver.
Conclusions:
- DDX17 plays a replication-promoting role in avian DTMUV infection.
- DDX17's interaction with the viral C protein is key to its function.
- This finding provides a basis for developing host-targeted antiviral strategies against DTMUV.
