ArticleCPT: pharmacometrics & systems pharmacology2026
A Quantitative Systems Pharmacology (QSP) Model of Acute Hepatitis B Virus Infection: Mechanistic Insights and Foundations for Future Extensions.
Article in CPT: pharmacometrics & systems pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- A Quantitative Systems Pharmacology (QSP) Model of Acute Hepatitis B Virus Infection: Mechanistic Insights and Foundations for Future Extensions.CPT: pharmacometrics & systems pharmacology · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic hepatitis B virus (HBV) infection remains a significant global health challenge. While the dynamic interplay between viral replication and host immune responses determines infection outcomes, the mechanisms driving the resolution of acute infection versus the emergence of chronicity remain incompletely understood. To address this challenge, we developed a detailed quantitative systems pharmacology (QSP) model of acute HBV infection capturing several key host immune and viral mechanisms absent in previous models. The model was parameterized using publicly available data and calibrated against clinical time-course datasets from multiple acute HBV case studies. Perturbation and local sensitivity analyses identified key drivers of biomarker dynamics, particularly hepatitis B virus DNA (HBV DNA), hepatitis B surface antigen (HBsAg), and alanine aminotransferase (ALT). These dynamics were most sensitive to parameters governing viral replication (e.g., HBV entry via the sodium taurocholate cotransporting polypeptide [NTCP] receptor, covalently closed circular DNA [cccDNA] formation, and hepatocyte turnover) and adaptive immune responses (e.g., CD8
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