Evidence map›Paper›PMID 22905181›Full record

ArticlePloS one2012

Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression.

Bouchra Kitab, Abdellah Essaid El Feydi, Rajaa Afifi, Christian Trepo, Mustapha Benazzouz, Wafaa Essamri, Fabien Zoulim, Isabelle Chemin, Hanane Salih Alj, Sayeh Ezzikouri and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.5field-weighted citation impact, top 5% of its field
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

26 citing papers in PubMed, 37 citations in OpenAlex.

  1. TRMT6-Mediated mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  3. [Expert consensus on the clinical application of the markers of hepatitis B virus].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023
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  16. Expression of serum sCD163 in patients with liver diseases and inflammatory disorders.International journal of clinical and experimental pathology · 2015
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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

11 authors at 4 institutions in 2 countries.

Bouchra KitabLaboratoire des Hépatites Virales, Institut Pasteur du Maroc, Casablanca, Morocco.
Abdellah Essaid El Feydi
Rajaa Afifi
Christian Trepo
Mustapha Benazzouz
Wafaa Essamri
Fabien Zoulim
Isabelle Chemin
Hanane Salih Alj
Sayeh Ezzikouri
Soumaya Benjelloun
Centre Hospitalier Ibn Sina · MAInserm · FRInstitut Pasteur du Maroc · MAUniversity of Hassan II Casablanca · MA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatitis B virus (HBV) is one of the most common human pathogens that cause aggressive hepatitis and advanced liver disease (AdLD), including liver cirrhosis and Hepatocellular Carcinoma. The persistence of active HBV replication and liver damage after the loss of hepatitis B e antigen (HBeAg) has been frequently associated with mutations in the pre-core (pre-C) and core promoter (CP) regions of HBV genome that abolish or reduce HBeAg expression. The purpose of this study was to assess the prevalence of pre-C and CP mutations and their impact on the subsequent course of liver disease in Morocco. METHODS/PRINCIPAL

findingsA cohort of 186 patients with HBeAg-negative chronic HBV infection was studied (81 inactive carriers, 69 with active chronic hepatitis, 36 with AdLD). Pre-C and CP mutations were analyzed by PCR-direct sequencing method. The pre-C stop codon G1896A mutation was the most frequent (83.9%) and was associated with a lower risk of AdLD development (OR, 0.4; 95% CI, 0.15-1.04; p = 0.04). HBV-DNA levels in patients with G1896A were not significantly different from the other patients carrying wild-type strains (p = 0.84). CP mutations C1653T, T1753V, A1762T/G1764A, and C1766T/T1768A were associated with higher HBV-DNA level and increased liver disease severity. Multiple logistic regression analysis showed that older age (≥ 40 years), male sex, high viral load (>4.3 log(10) IU/mL) and CP mutations C1653T, T1753V, A1762T/G1764A, and C1766T/T1768A were independent risk factors for AdLD development. Combination of these mutations was significantly associated with AdLD (OR, 7.52; 95% CI, 4.8-8; p<0.0001).

conclusionsThis study shows for the first time the association of HBV viral load and CP mutations with the severity of liver disease in Moroccan HBV chronic carriers. The examination of CP mutations alone or in combination could be helpful for prediction of the clinical outcome.

Indexed as

Genetic VariationPromoter Regions, GeneticAdultAgedAged, 80 and overCohort StudiesDisease ProgressionFemaleGenotypeHepatitis BHepatitis B Core AntigensHumansLiver DiseasesMaleMiddle AgedMoroccoHepatitis B Core Antigens

Identifiers

PMID22905181
PMCPMC3419231
OpenAlexW1979190243

What OpenQuestion holds

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LicenceCC BY
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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.