ArticleViruses2017
The Role of Infected Cell Proliferation in the Clearance of Acute HBV Infection in Humans.
Article in Viruses, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 38 citations in OpenAlex.
- Topological Stability and Transcritical Bifurcations in a Target-Cell-Limited Model of HBV-HDV Viral Interference.Viruses · 2026Article
- Clinical trial simulation of antiviral drugs.Journal of virology · 2026Review
- A Quantitative Systems Pharmacology (QSP) Model of Acute Hepatitis B Virus Infection: Mechanistic Insights and Foundations for Future Extensions.CPT: pharmacometrics & systems pharmacology · 2026Article
- INHERITANCE OF INTRACELLULAR VIRAL RNA IN A MULTISCALE MODEL OF HEPATITIS C INFECTION.SIAM journal on applied mathematics · 2026Article
- Investigation of a Two-Patch Within-Host Model of Hepatitis B Viral Infection.Bulletin of mathematical biology · 2025Article
- Disease Progression Mathematical Modeling With a Case Study on Hepatitis B Virus Infection.CPT: pharmacometrics & systems pharmacology · 2025Review
- How robust are estimates of key parameters in standard viral dynamic models?PLoS computational biology · 2024Article
- [Demographic characteristics and associated influencing factors in treated patients with chronic hepatitis B with hypoviremia : a single-center retrospective cross-sectional study].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023Article
- Mitosis of hepatitis B virus-infected cellsJHEP reports : innovation in hepatology · 2022Article
- Article
- Modeling explains prolonged SARS-CoV-2 nasal shedding relative to lung shedding in remdesivir-treated rhesus macaques.iScience · 2022Article
- [A possible mechanism for low-level viremia occurrence in nucleos(t)ide analog-treated chronic hepatitis B patients].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2021Article
- Low-level viremia in nucleoside analog-treated chronic hepatitis B patients.Chinese medical journal · 2021Review
- A delay model for persistent viral infections in replicating cells.Journal of mathematical biology · 2021Article
- Mechanistic Modeling of SARS-CoV-2 and Other Infectious Diseases and the Effects of Therapeutics.Clinical pharmacology and therapeutics · 2021Review
- Understanding the antiviral effects of RNAi-based therapy in HBeAg-positive chronic hepatitis B infection.Scientific reports · 2021Article
- Estimating hepatitis B virus cccDNA persistence in chronic infection.Virus evolution · 2021Article
- Efficient Methods for Parameter Estimation of Ordinary and Partial Differential Equation Models of Viral Hepatitis Kinetics.Mathematics (Basel, Switzerland) · 2020Article
- Within-host mathematical models of hepatitis B virus infection: Past, present, and future.Current opinion in systems biology · 2019Article
- A dual role for SAMHD1 in regulating HBV cccDNA and RT-dependent particle genesis.Life science alliance · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Around 90-95% of hepatitis B virus (HBV) infected adults do not progress to the chronic phase and, instead, recover naturally. The strengths of the cytolytic and non-cytolytic immune responses are key players that decide the fate of acute HBV infection. In addition, it has been hypothesized that proliferation of infected cells resulting in uninfected progeny and/or cytokine-mediated degradation of covalently closed circular DNA (cccDNA) leading to the cure of infected cells are two major mechanisms assisting the adaptive immune response in the clearance of acute HBV infection in humans. We employed fitting of mathematical models to human acute infection data together with physiological constraints to investigate the role of these hypothesized mechanisms in the clearance of infection. Results suggest that cellular proliferation of infected cells resulting in two uninfected cells is required to minimize the destruction of the liver during the clearance of acute HBV infection. In contrast, we find that a cytokine-mediated cure of infected cells alone is insufficient to clear acute HBV infection. In conclusion, our modeling indicates that HBV clearance without lethal loss of liver mass is associated with the production of two uninfected cells upon proliferation of an infected cell.
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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.