Evidence map›Paper›PMID 38545116›Full record

ArticleFrontiers in immunology2024

HBsAg level defines different clinical phenotypes of HBeAg(-) chronic HBV infection related to HBV polymerase-specific CD8

Julia Peña-Asensio, Henar Calvo-Sánchez, Joaquín Miquel-Plaza, Eduardo Sanz-de-Villalobos, Alejandro González-Praetorius, Alberto Delgado-Fernandez, Miguel Torralba, Juan-Ramón Larrubia

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Peripheral Blood CD4Journal of clinical and translational hepatology · 2025
    Article
  2. 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

8 authors at 2 institutions in 1 country.

Julia Peña-Asensio *Department of Biology of Systems, University of Alcalá, Alcalá de Henares, Spain.
Henar Calvo-Sánchez *Translational Research Group in Cellular Immunology, Instituto de Investigación Sanitaria de Castilla La-Mancha (IDISCAM), Toledo, Spain.
Joaquín Miquel-PlazaTranslational Research Group in Cellular Immunology, Instituto de Investigación Sanitaria de Castilla La-Mancha (IDISCAM), Toledo, Spain.
Eduardo Sanz-de-VillalobosTranslational Research Group in Cellular Immunology, Instituto de Investigación Sanitaria de Castilla La-Mancha (IDISCAM), Toledo, Spain.
Alejandro González-PraetoriusTranslational Research Group in Cellular Immunology, Instituto de Investigación Sanitaria de Castilla La-Mancha (IDISCAM), Toledo, Spain.
Alberto Delgado-FernandezTranslational Research Group in Cellular Immunology, Instituto de Investigación Sanitaria de Castilla La-Mancha (IDISCAM), Toledo, Spain.
Miguel TorralbaTranslational Research Group in Cellular Immunology, Instituto de Investigación Sanitaria de Castilla La-Mancha (IDISCAM), Toledo, Spain.
Juan-Ramón LarrubiaTranslational Research Group in Cellular Immunology, Instituto de Investigación Sanitaria de Castilla La-Mancha (IDISCAM), Toledo, Spain.
Hospital Universitario de Guadalajara · ESUniversidad de Alcalá · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: HBe-antigen(Ag)-negative chronic hepatitis B virus (HBV) infection is characterized by little liver fibrosis progression and vigorous HBV-multispecific CD8 Aims: To assess whether HBsAg level could discriminate different HBeAg-negative chronic HBV infection subtypes with dissimilar quality of HBV-specific CD8 Methods: We recruited 63 HBeAg-negative chronic HBV infection patients in which indirect markers of liver inflammation/fibrosis, portal pressure, viral load (VL), and HBV-specific CD8 Results: A positive linear trend between HBsAg level and APRI, liver stiffness (LS), liver transaminases, and HBV VL, and a negative correlation with platelet count were observed. Frequency of cases with HBV-specific CD8 Conclusion: HBsAg > 1,000 IU/ml HBeAg-negative chronic HBV infection group shows indirect data of higher degree of inflammation, liver stiffness, and fibrosis progression speed, which are related to an impaired HBV-polymerase-specific CD8

Indexed as

Gene Products, polHepatitis B, ChronicAlanine TransaminaseCD8-Positive T-LymphocytesHepatitis B e AntigensHepatitis B Surface AntigensHepatitis B virusHumansInflammationLiver CirrhosisPhenotypeAlanine TransaminaseGene Products, polHepatitis B e AntigensHepatitis B Surface AntigensP protein, Hepatitis B virusfunctional HBV-specific CD8 + T-cell responseHBsAgHBV eAg(-) infection gray-zoneHBV immune controlHBV inactive carrierliver fibrosis progression

Identifiers

PMID38545116
PMCPMC10966405
OpenAlexW4392761055

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.