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Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle
Published on: February 1, 2017
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PPIases Par14/Par17 Affect HBV Replication in Multiple Ways
Kyongmin Kim1,2
1Department of Microbiology, Ajou University School of Medicine, Suwon 16499, Republic of Korea.
Viruses
|February 28, 2023
Summary
Human parvulin 14 (Par14) and parvulin 17 (Par17) are enzymes that boost hepatitis B virus (HBV) replication. They interact with viral proteins HBc and HBx, enhancing viral stability and assembly.
Area of Science:
- Hepatology
- Virology
- Molecular Biology
Background:
- Human parvulin 14 (Par14) and parvulin 17 (Par17) are peptidyl-prolyl cis/trans isomerases.
- These enzymes play a role in regulating hepatitis B virus (HBV) replication.
- Their interaction is dependent on the presence of the hepatitis B virus protein X (HBx).
Purpose of the Study:
- To elucidate the mechanism by which Par14 and Par17 upregulate HBV replication.
- To investigate the specific interactions between Par14/Par17, HBc, HBx, and cccDNA.
- To identify the key residues involved in these interactions and their functional consequences.
Main Methods:
- Analysis of protein-protein interactions between Par14/Par17, HBc, and HBx.
- Investigation of the role of specific amino acid residues in Par14/Par17, HBc, and HBx.
- Assessment of the impact on HBV replication, viral protein stability, and cccDNA transcription.
Main Results:
- Par14/Par17 bind to conserved Arg-Pro motifs in HBc and HBx, enhancing viral protein stability and core particle assembly.
- Par14/Par17 interaction with HBx promotes its translocation to the nucleus and mitochondria.
- In the presence of HBx, Par14/Par17 are recruited to cccDNA, promoting transcriptional activation and HBc recruitment via specific residues.
Conclusions:
- Par14 and Par17 significantly upregulate HBV replication through complex interactions involving HBx, HBc, and cccDNA.
- These interactions occur in both the nucleus (cccDNA complex) and cytoplasm (core particles).
- Specific binding residues on Par14/Par17 are crucial for mediating these pro-viral effects.
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