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Structural and Functional Analysis of ASFV pI73R Reveals GNB1 Binding and Host Gene Modulation
Katarzyna Magdalena Dolata1, Barbara Bettin1, Richard Küchler1
1Institute of Molecular Virology and Cell Biology, Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health, Südufer 10, 17493 Greifswald-Insel Riems, Germany.
International Journal of Molecular Sciences
|December 30, 2025
Summary
African swine fever virus (ASFV) protein pI73R, crucial for virulence, structurally resembles FOX transcription factors. This study reveals its interaction with host GNB1 and modulation of CRNKL1, offering antiviral targets.
Area of Science:
- Virology
- Molecular Biology
- Structural Biology
Background:
- African swine fever virus (ASFV) causes devastating swine disease, impacting global economies.
- Limited characterization of ASFV proteins and functional redundancies hinders vaccine development.
Purpose of the Study:
- To characterize the ASFV I73R protein (pI73R), a key virulence factor.
- To elucidate pI73R's structural and functional relationship with host factors.
- To identify potential targets for antiviral strategies.
Main Methods:
- Combined experimental and computational analyses.
- Structural similarity assessment with transcription factors.
- CRNKL1 expression analysis upon pI73R overexpression.
- High-resolution mass spectrometry for interactome mapping.
Main Results:
- pI73R shares structural similarity with forkhead box (FOX) proteins.
- pI73R overexpression downregulates spliceosome component CRNKL1.
- Guanine nucleotide-binding protein subunit beta-1 (GNB1) identified as a novel pI73R interactor.
- pI73R shows consistent oligomerization and expression across ASFV genotypes.
Conclusions:
- pI73R plays a critical role in ASFV virulence and host protein synthesis modulation.
- GNB1 may facilitate pI73R nuclear transport.
- pI73R is a conserved and functionally important ASFV protein.
- Findings provide insights for developing novel antiviral strategies against ASFV.
