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DDX3X Promotes Rotavirus Infection and Serves as an Antiviral Target.

Pengfei Hao1, Yuchen Liu2, Chunmei Cui3

  • 1State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory of Zoonosis Research, Ministry of Education, College of Basic Medical Science, Jilin University, Changchun, China.

Transboundary and Emerging Diseases
|December 1, 2025
PubMed
Summary

Rotavirus (RV) infection relies on the VP4 protein interacting with DDX3X. Inhibiting DDX3X with RK-33 effectively stops RV replication, offering a potential new treatment for this significant zoonotic pathogen.

Keywords:
DDX3XRK-33VP4interactomerotavirus

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Area of Science:

  • Virology
  • Molecular Biology
  • Drug Discovery

Background:

  • Rotavirus (RV) is a major zoonotic pathogen causing severe diarrhea in humans and animals.
  • The RV outer capsid protein VP4 is critical for viral entry and replication, but its interactions are not fully understood.

Purpose of the Study:

  • To comprehensively analyze the RV VP4 interactome.
  • To investigate the role of DDX3X in RV infection.
  • To identify potential therapeutic inhibitors of RV replication.

Main Methods:

  • VP4 interactome analysis.
  • Gene silencing and overexpression of DDX3X.
  • Enzymatic activity assays.
  • Drug screening for VP4 interactors.

Main Results:

  • DDX3X was identified as a VP4-interacting protein crucial for RV infection.
  • DDX3X enzymatic activity promotes RV replication.
  • The DDX3X inhibitor RK-33 significantly inhibited RV infection.

Conclusions:

  • VP4 interacts with DDX3X, and DDX3X's enzymatic activity is essential for RV replication.
  • RK-33 is a promising candidate drug for inhibiting rotavirus.
  • This study elucidates DDX3X's role in RV pathogenesis and identifies a potential therapeutic strategy.