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The Kinase STK3 Interacts with the Viral Structural Protein VP1 and Inhibits Foot-and-Mouth Disease Virus Replication
Huisheng Liu1, Qiao Xue1, Qiaoying Zeng1
1Laboratory of Veterinary Microbiology, College of Veterinary Medicine, Gansu Agricultural University, Lanzhou, China.
Abstract:
Foot-and-mouth disease virus (FMDV) is the etiological agent of FMD, which affects domestic and wild cloven-hoofed animals. The structural protein VP1 plays an important role in FMDV pathogenesis. However, the interacting partners of VP1 in host cells and the effects of these interactions in FMDV replication remain incompletely elucidated. Here, we identified a porcine cell protein, serine/threonine kinase 3 (STK3), which interacts with FMDV VP1 using the yeast two-hybrid system. The VP1-STK3 interaction was further confirmed by coimmunoprecipitation experiments in human embryonic kidney 293T and porcine kidney 15 (PK-15) cells. The carboxyl-terminal region (amino acids 180-214) of VP1 was essential for its interaction with STK3. The effects of overexpression and underexpressing of STK3 in PK-15 cells were assessed, and the results indicated that STK3 significantly inhibited FMDV replication. Our data expand the role of STK3 during viral infection, provide new information regarding the host cell kinases that are involved in viral replication, and identify potential targets for future antiviral strategies.
Insights
We discovered that serine/threonine kinase 3 (STK3) interacts with foot-and-mouth disease virus (FMDV) protein VP1. STK3 inhibits FMDV replication, offering potential antiviral targets.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Foot-and-mouth disease virus (FMDV) causes significant losses in livestock.
- The FMDV structural protein VP1 is crucial for pathogenesis, but its host interactions are not fully understood.
Purpose of the Study:
- To identify host cell proteins interacting with FMDV VP1.
- To investigate the role of these interactions in FMDV replication.
Main Methods:
- Yeast two-hybrid system to screen for interacting proteins.
- Coimmunoprecipitation assays to confirm VP1-STK3 interaction in cell lines.
- Overexpression and knockdown of STK3 to assess its effect on viral replication.
Main Results:
- Identified serine/threonine kinase 3 (STK3) as a binding partner of FMDV VP1.
- Confirmed the interaction between VP1 and STK3 in human and porcine kidney cells.
- Demonstrated that STK3 significantly inhibits FMDV replication in porcine kidney cells.
Conclusions:
- STK3 plays a role in restricting FMDV replication.
- This study reveals novel host cell kinase involvement in FMDV infection.
- STK3 represents a potential target for developing antiviral strategies against FMDV.
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