ArticleHepatology international2008
Immune selection during chronic hepadnavirus infection.
Article in Hepatology international, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 26 citations in OpenAlex.
- HCC-derived SNU cell lines as model systems to study HBV life cycle.Journal of virology · 2025Article
- Developmental Changes of Duckling Liver and Isolation of Primary Hepatocytes.Animals : an open access journal from MDPI · 2023Article
- Review
- Hepatitis B Virus DNA Integration and Clonal Expansion of Hepatocytes in the Chronically Infected Liver.Viruses · 2021Review
- Estimating hepatitis B virus cccDNA persistence in chronic infection.Virus evolution · 2021Article
- Relative Abundance of Integrant-Derived Viral RNAs in Infected Tissues Harvested from Chronic Hepatitis B Virus Carriers.Journal of virology · 2018Article
- Short-Sighted Virus Evolution and a Germline Hypothesis for Chronic Viral Infections.Trends in microbiology · 2017Review
- Review
- Infection Patterns Induced in Naive Adult Woodchucks by Virions of Woodchuck Hepatitis Virus Collected during either the Acute or Chronic Phase of Infection.Journal of virology · 2015Article
- Capacity of a natural strain of woodchuck hepatitis virus, WHVNY, to induce acute infection in naive adult woodchucks.Virus research · 2015Article
- Molecular interactions between hepatitis B virus and delta virus.World journal of virology · 2015Article
- Molecular biology of hepatitis B virus infection.Virology · 2015Review
- Antiviral therapies and prospects for a cure of chronic hepatitis B.Cold Spring Harbor perspectives in medicine · 2015Review
- Superinfection with woodchuck hepatitis virus strain WHVNY of livers chronically infected with strain WHV7.Journal of virology · 2015Article
- Envelope proteins derived from naturally integrated hepatitis B virus DNA support assembly and release of infectious hepatitis delta virus particles.Journal of virology · 2014Article
- Hepatitis delta virus infects the cells of hepadnavirus-induced hepatocellular carcinoma in woodchucks.Hepatology (Baltimore, Md.) · 2012Article
- A high level of mutation tolerance in the multifunctional sequence encoding the RNA encapsidation signal of an avian hepatitis B virus and slow evolution rate revealed by in vivo infection.Journal of virology · 2011Article
- Clonal expansion of normal-appearing human hepatocytes during chronic hepatitis B virus infection.Journal of virology · 2010Article
- Detection of clonally expanded hepatocytes in chimpanzees with chronic hepatitis B virus infection.Journal of virology · 2009Article
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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeLate-stage outcomes of chronic hepatitis B virus (HBV) infection, including fibrosis, cirrhosis, and hepatocellular carcinoma (HCC) result from persistent liver injury mediated by HBV antigen specific cytotoxic T lymphocytes (CTLs). Two other outcomes that often accompany chronic infection, the emergence of mutant viruses, including HBe-antigen negative (HBeAg (-)) HBV, and a reduction over time in the fraction of hepatocytes productively infected with HBV, may also result from persistent immune attack by antiviral CTLs. To gain insights into how these latter changes take place, we employed computer simulations of the chronically infected liver.
methodsComputational programs were used to model the emergence of both virus-free hepatocytes and mutant strains of HBV.
resultsThe computer modeling predicted that if cell-to-cell spread of virus is an efficient process during chronic infections, an HBV mutant that replicated significantly more efficiently than the wild type would emerge as the prevalent virus in a few years, much more rapidly than observed, while a mutant that replicated with the same or lower efficiency would fail to emerge. Thus, either cell-to-cell spread is inefficient or mutants do not replicate appreciably more efficiently than wild type. In contrast, with immune selection and a higher rate of killing of hepatocytes infected with wild-type virus, emergence of mutant virus can be explained without the need for a higher replication rate. Immune selection could also explain the emergence of virus-free hepatocytes that are unable to support HBV infection, since they should have a lower turnover rate than infected hepatocytes.
Identifiers
What OpenQuestion holds
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.