Evidence map›Paper›PMID 22173170›Full record

ArticleJournal of hepatology2012

Quantitative dynamics of hepatitis B basal core promoter and precore mutants before and after HBeAg seroconversion.

Hui Nie, Alison A Evans, W Thomas London, Timothy M Block, Xiangdong David Ren

Abstract read
In one paragraph

Article in Journal of hepatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. The evolution and clinical impact of hepatitis B virus genome diversity.Nature reviews. Gastroenterology & hepatology · 2020
    Review
  5. Article
  6. Viruses · 2020
    Article
  7. Review
  8. Article
  9. Review
  10. Observational
  11. Article
  12. The incidence rate over 10 years of naturally occurring, cancer related mutations in the basal core promoter of hepatitis B virus.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2015
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. SASLT practice guidelines for the management of Hepatitis B virus - An update.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Hui NieDepartment of Microbiology and Immunology, Drexel University College of Medicine, Doylestown, PA, USA.
Alison A Evans
W Thomas London
Timothy M Block
Xiangdong David Ren

Funding

EARLY DETECTION OF LIVER CANCER AND HEPATITISU01CA084951 · NCI · THOMAS JEFFERSON UNIVERSITY · PI BLOCK, TIMOTHY M · 1999 to 2010
$4.5M
Liver Cancer and the Role of Protein Hyper-FucosylationR01CA136607 · NCI · DREXEL UNIVERSITY · PI BLOCK, TIMOTHY M · 2009 to 2013
$2.0M
NCI NIH HHS R01 CA136607NCI NIH HHS U01 CA084951
6 · The paper itself

Abstract

BACKGROUND &

aimsHepatitis B e antigen (HBeAg) seroconversion is an important clinical and virological "landmark" during chronic hepatitis B virus (HBV) infection. Mutant viruses carrying the precore G1896A and/or the basal core promoter (BCP) A1762T/G1764A mutations are associated with HBeAg seroconversion. However, the exact role of these mutants in HBeAg seroconversion remains unclear, partly because the evolution of these mutant viruses before and after seroconversion has not been well studied.

methodsUsing our novel mutant quantification methods, the percentage of the mutant viruses was analyzed both cross-sectionally and longitudinally, before and after seroconversion.

resultsCross-sectional analysis showed that the percentage of both precore and BCP mutants gradually increased with age in the HBeAg-positive population. Follow-up of 18 HBeAg-positive patients revealed that the mutant percentage may stay low and stable for many years, followed by a steady increase in the percentage of G1896A and/or A1762T/G1764A mutants, from <10% to 50-100%, within about 3 years prior to seroconversion. In all cases, increase of mutant percentage was preceded or accompanied by elevated serum alanine aminotransferase. After the seroconversion, the mutant percentage could remain high or decrease significantly, sometimes to below 20%.

conclusionsLevels of G1896A and A1762T/G1764A mutants (of genotypes B and C) in the HBeAg-positive patients may predict the time of HBeAg seroconversion. The dominance of these mutants in the HBeAg-positive phase is more likely the result of immune selection rather than the enhanced replication capability of the mutants. However, anti-HBe antibody may not be a major selection force for these mutants.

Indexed as

AdolescentAdultAlanine TransaminaseChildChild, PreschoolCross-Sectional StudiesDNA, ViralFollow-Up StudiesGenotypeHepatitis B, ChronicHepatitis B e AntigensHepatitis B virusHumansInfantLongitudinal StudiesMiddle AgedAlanine TransaminaseDNA, ViralHepatitis B e AntigensViral Core Proteins

Identifiers

PMID22173170
PMCPMC3307917

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Registered trials

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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.