ArticlePLoS computational biology2025
A multiscale model of the action of a capsid assembly modulator for the treatment of chronic hepatitis B.
Article in PLoS computational biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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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
5 citing papers in PubMed.
- AZD5582 robustly reactivates latently infected cells and clears the majority of those reactivated from the SIV reservoir.bioRxiv : the preprint server for biology · 2026Article
- Dynamics and Sensitivity of the Lifecycle of Hepatitis B Virus.Pathogens (Basel, Switzerland) · 2026Article
- A Nonparametric Approach to Practical Identifiability of Nonlinear Mixed Effects Models.Bulletin of mathematical biology · 2026Article
- INHERITANCE OF INTRACELLULAR VIRAL RNA IN A MULTISCALE MODEL OF HEPATITIS C INFECTION.SIAM journal on applied mathematics · 2026Article
- The dynamic states of hepatitis B virus capsid monomers under the impact of different class of capsid-assembly modulators.Scientific reports · 2025Article
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Authors and funding
4 authors.
Funding
Abstract
Chronic hepatitis B virus (HBV) infection is strongly associated with increased risk of liver cancer and cirrhosis. While existing treatments effectively inhibit the HBV life cycle, viral rebound frequently occurs following treatment interruption. Consequently, functional cure rates of chronic HBV infection remain low and there is increased interest in a novel treatment modality, capsid assembly modulators (CAMs). Here, we develop a multiscale mathematical model of CAM treatment in chronic HBV infection. By fitting the model to participant data from a phase I trial of the first-generation CAM vebicorvir, we estimate the drug's dose-dependent effectiveness and identify the physiological mechanisms that drive the observed biphasic decline in HBV DNA and RNA, and mechanistic differences between HBeAg-positive and negative infection. Finally, we demonstrate analytically and numerically that the relative change of HBV RNA more accurately reflects the antiviral effectiveness of a CAM than the relative change in HBV DNA.
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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.