ArticlePLoS pathogens2025
Antiviral and immune modulatory activities of STING agonists in a mouse model of persistent hepatitis B virus infection.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Roles of the cGAS-STING signaling pathway in viral latency.Journal of virology · 2026Review
- STING1 negatively regulates translation and replication of foot-and-mouth disease virus independently of interferon and is antagonized by the viral proteins 3C and 2B.Virologica Sinica · 2026Article
- Research Progress on Mechanisms of Immune Tolerance Induced by Hepatitis B Surface Antigen in Chronic HBV Infection.Journal of immunology research · 2026Review
- Interferon therapy for chronic hepatitis B in children: an immunological perspective.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Activation of antiviral immune responses against hepatitis B virus (HBV) is essential for the durable control of chronic HBV infection and the functional cure of chronic hepatitis B. As a molecular hub at the interface of innate and adaptive immunity, the stimulator of interferon (IFN) genes (STING) is well suited as a therapeutic target to break the immune tolerance against chronic viral infections and tumors. Using STING knockout and human STING knock-in mouse models, we first demonstrated that STING agonist treatment activated robust innate immune responses in the spleen and liver and efficiently suppressed HBV DNA replication in the livers of AAV-HBV transduced mice in a STING-dependent manner. We further demonstrate that AAV-HBV transduced mice are well tolerated for the long-term treatment of STING agonist diamidobenzimidazole (diABZI) at the optimized dose and dosing schedules. Virological and hepatic bulk and single-cell RNA-seq analyses revealed that diABZI treatment activated immune responses in liver microenvironment and significantly inhibited HBV replication and HBeAg expression. Antibodies against HBV surface antigen (HBsAg), HBs-Ab, became detectable in 1/4 mice after 5 weeks of treatment. In conclusion, our findings imply that diABZI treatment activates a STING-dependent immune response that controls HBV replication in a mouse model of persistent HBV infection and thus establishes a scientific basis for further development of STING agonists as immune therapeutics for the treatment of chronic hepatitis B.
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Registered trials
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