ArticleHepatology communications2025
HBV-specific T-cell function is nonenhanced by tenofovir-induced decline in HBV viremia or HBsAg titer in chronic hepatitis B.
Article in Hepatology communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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Who cites it
4 citing papers in PubMed.
- Review
- Research Progress on Mechanisms of Immune Tolerance Induced by Hepatitis B Surface Antigen in Chronic HBV Infection.Journal of immunology research · 2026Review
- Immune correlates of outcomes after nucleos(t)ide analogue withdrawal in chronic hepatitis B: direct evidence, mechanistic context, and candidate biomarkers.Frontiers in immunology · 2026Review
- Large-scale screening of HBV epitopes restricted by multiple prevalent HLA-B/C allotypes and routine detection of HBV-specific T cells in CHB patients.Frontiers in immunology · 2025Article
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Authors and funding
12 authors.
Funding
Abstract
backgroundChronic hepatitis B is associated with virus-specific and global T-cell dysfunction. We hypothesized that therapeutic reduction in serum HBV DNA, ALT, and HBsAg would restore HBV-specific T-cell function and modify T-cell regulatory phenotype, with associated posttreatment ALT flare.
methodsHBV-specific T-cell lymphoproliferative responses and global T-cell phenotype were prospectively examined at baseline, weeks 24, 48, 192, 216, and 240 in 34 adults with immune-active chronic hepatitis B treated with 192 weeks of tenofovir alone (n=21) or combined with pegylated interferon (PegIFN) in the first 24 weeks (n=13). HBV-specific T-cell IFNγ responses at weeks 0, 24, and 48 were examined by ELISpot assay ex vivo in 24 patients. Posttreatment flare was defined by serum ALT >5 times the upper limit of normal.
resultsTenofovir therapy did not promote sustained induction of HBV-specific T-cell proliferative responses, regardless of PegIFN therapy or decreased serum HBsAg, HBV DNA, or ALT levels. Instead, HBV-specific T-cell IFNγ responses declined significantly by 48 weeks of therapy (p=0.008). Posttreatment ALT flare was associated with higher baseline %PD1+/CD8 (p=0.019), %PD1+/CD4 (p=0.039), and %CTLA4+/CD4 (p=0.003) T cells compared to non-flares, but without associated HBsAg loss or increased HBV-specific T-cell responsiveness.
conclusionHBV-specific T-cell function was not restored after 192 weeks of tenofovir therapy and did not correlate with HBsAg levels before, during, or after therapy. Baseline global T-cell regulatory phenotype was a predictor for ALT flare post-therapy without associated HBsAg decline. These findings support the need for more novel immune-modulatory approaches to enhance HBV-specific T-cell responsiveness.
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