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Identifying Inhibitors of the HBx-DDB1 Interaction Using a Split Luciferase Assay System

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Published on: December 21, 2019

Hepatic Steatosis Inhibits Hepatitis B Virus Replication by Promoting miR-122-5p-SOX4.

Guanghui Ren¹, Kaining Jia², Sitong Yi¹

¹Department of Infectious Disease, Liver Disease Center of Integrated Traditional Chinese and Western Medicine, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.

Journal of Viral Hepatitis

|February 20, 2026

Summary

Metabolic dysfunction-associated fatty liver disease (MAFLD) may suppress chronic hepatitis B (CHB) viral activity. A novel miR-122/SOX4 pathway is identified as a key regulator in this interaction, offering potential therapeutic targets for liver disease.

Keywords:

SOX4 chronic hepatitis B metabolic dysfunction‐associated fatty liver disease miR‐122‐5p

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Area of Science:

Hepatology
Virology
Molecular Biology

Background:

Chronic hepatitis B (CHB) and metabolic dysfunction-associated fatty liver disease (MAFLD) frequently coexist.
The specific role of microRNA-122 (miR-122) in CHB-MAFLD comorbidity is not well understood.

Purpose of the Study:

To investigate the role of miR-122 in the clinical interplay between CHB and MAFLD.
To identify downstream targets of miR-122 in this context and elucidate the underlying regulatory mechanisms.

Main Methods:

Serum analysis of HBV markers and miR-122 levels in CHB and CHB-MAFLD patients.
Bioinformatics analysis and molecular assays to identify miR-122 targets.
In vitro studies using an HBV-infected steatotic cell model to assess viral replication and the miR-122/SOX4 axis.

Main Results:

CHB-MAFLD patients showed lower HBV DNA, pgRNA, and HBsAg levels correlating with higher miR-122 expression.
SOX4 was identified as a direct downstream target of miR-122-5p.
The miR-122-5p/SOX4 axis was upregulated in the comorbid state, suppressing HBV replication markers.
Both miR-122-5p and SOX4 demonstrated inhibitory effects on HBV activity; their knockdown enhanced viral replication, while overexpression suppressed it.

Conclusions:

The metabolic environment in CHB-MAFLD may suppress HBV replication via a novel miR-122/SOX4 regulatory axis.
miR-122 emerges as a potential therapeutic target for managing CHB-MAFLD.
This study provides mechanistic insights into altered viral kinetics in patients with coexisting CHB and MAFLD.