ArticleCell host & microbe2026
Functional immune responses induced by a capsid assembly modulator in chronic hepatitis B virus-infected humanized mice.
Article in Cell host & microbe, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- A New Role of Class A Hepatitis B Virus Capsid Assembly Modulators in Core Protein Dynamics and Covalently Closed Circular DNA Replenishment.Cellular and molecular gastroenterology and hepatology · 2026Article
- Research Progress on Mechanisms of Immune Tolerance Induced by Hepatitis B Surface Antigen in Chronic HBV Infection.Journal of immunology research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
Abstract
Current treatment strategies for hepatitis B virus (HBV) are lifelong and rarely curative. Finite therapeutic strategies aim to restore efficient immune responses in chronically infected patients for functional cures. Here, we investigate the impact of treatment with the capsid assembly modulator (CAM) GLP-26 in an immunocompetent humanized mouse model of chronic HBV. GLP-26 treatment clears viremia and HBV surface antigen (HBsAg), reduces hepatitis, and potentiates anti-HBs antibody (HBsAb) development. Remarkably, after discontinuing GLP-26, either viral control or viral rebound occurs in half the cohort. In particular, the viral controllers display seroconversion (HBsAg-/HBsAb+) and development of neutralizing antibodies. In the liver, cytotoxic natural killer cells and activated memory T cells are enriched, including HBV-specific polyfunctional T cell responses. Thus, finite treatment with a potent antiviral CAM results in viral clearance and antigen depletion, enabling effective adaptive immune responses and viral control off therapy, suggestive of a functional cure.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.