Evidence map›Paper›PMID 38970627›Full record

ArticleImmunologic research2024

Association of HLA-G 3'UTR polymorphisms with hepatitis B virus infection in Tunisian population.

Ahmed Baligh Laaribi, Asma Mehri, Hamza Ben Yahia, Houda Chaouch, Wafa Babay, Amel Letaief, Hadda-Imene Ouzari, Naila Hannachi, Jalel Boukadida, Ines Zidi

Abstract read
PubMed Publisher
In one paragraph

Article in Immunologic research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Ahmed Baligh LaaribiLaboratory of Microorganisms and Active Biomolecules (LR03ES03), Sciences Faculty of Tunis, University of Tunis El Manar, Tunis, Tunisia. Laaribi.ahmed.baligh@proton.me.
Asma MehriLaboratory of Microorganisms and Active Biomolecules (LR03ES03), Sciences Faculty of Tunis, University of Tunis El Manar, Tunis, Tunisia.
Hamza Ben YahiaLaboratory of Microorganisms and Active Biomolecules (LR03ES03), Sciences Faculty of Tunis, University of Tunis El Manar, Tunis, Tunisia.
Houda ChaouchDepartment of Internal Medicine and Infectious Diseases, University Hospital Farhat Hached, Sousse, Tunisia.
Wafa BabayLaboratory of Microorganisms and Active Biomolecules (LR03ES03), Sciences Faculty of Tunis, University of Tunis El Manar, Tunis, Tunisia.
Amel LetaiefDepartment of Internal Medicine and Infectious Diseases, University Hospital Farhat Hached, Sousse, Tunisia.
Hadda-Imene OuzariLaboratory of Microorganisms and Active Biomolecules (LR03ES03), Sciences Faculty of Tunis, University of Tunis El Manar, Tunis, Tunisia.
Naila HannachiLaboratory of Microbiology (UR12SP34), Faculty of Medicine, University Hospital Farhat Hached, Sousse, Tunisia.
Jalel BoukadidaLaboratory of Microbiology (UR12SP34), Faculty of Medicine, University Hospital Farhat Hached, Sousse, Tunisia.
Ines ZidiLaboratory of Microorganisms and Active Biomolecules (LR03ES03), Sciences Faculty of Tunis, University of Tunis El Manar, Tunis, Tunisia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) infection is a major public health burden. The mechanisms of immune evasion during chronic HBV (CHB) infection are poorly understood. Human leukocyte antigen (HLA)-G, an immune checkpoint molecule, plays a crucial role in the tolerance mechanisms of various infectious diseases. The 3' untranslated region (3'UTR), including the HLA-G + 3142 C > G polymorphism (rs1063320) and the 14-pb Ins/Del (rs66554220) has been strongly suggested to influence HLA-G expression. This study conducted a case-control analysis to evaluate the potential correlation between the HLA-G + 3142 C > G polymorphism and HBV infection outcome in a Tunisian cohort. The HLA-G + 3142 C > G polymorphism was analysed by PCR-RFLP in 242 patients with chronic HBV infection (116 males and 126 females), 241 healthy controls (116 males and 125 females), and 100 spontaneously resolved subjects (52 males and 48 females). Patients with chronic HBV infection showed a higher frequency of the + 3142G allele compared to healthy controls and spontaneously resolved subjects (p = 0.001 and p = 0.002, respectively). An association between the + 3142G allele and high HBV DNA levels was observed when HBV patients were stratified based on their HBV DNA levels (p = 0.016). Furthermore, the dominant model (GG + GC vs CC) was associated with liver function parameters, including AST, ALT, and high HBV DNA levels (p = 0.04, p < 0.001 and p = 0.002, respectively). However, there was no significant association found between this polymorphism and the fibrosis stage (p = 0.32). The haplotype analysis, using a subset of previously published data on the HLA-G 14-pb Ins/Del polymorphism, revealed an association between the Ins/G haplotype and chronic HBV infection (H1: InsG, p < 0.001). Our findings suggest that the + 3142G allele is a risk factor for the persistence and progression of HBV infection, while the + 3142C allele serves as a protective allele associated with the spontaneous resolution of the infection. Additionally, the HLA-G 3'UTR haplotype Ins/G is associated with chronic HBV infection in the Tunisian population.

Indexed as

3' Untranslated RegionsGene FrequencyGenetic Predisposition to DiseaseHepatitis B, ChronicHepatitis B virusHLA-G AntigensAdultAllelesCase-Control StudiesFemaleGenetic Association StudiesGenotypeHepatitis BHumansMaleMiddle Aged3' Untranslated RegionsHLA-G AntigensHepatitis B infectionHLA-GHLA-G 14-pb Ins/delHLA-G + 3142C > GPolymorphism

Identifiers

What OpenQuestion holds

Textmetadata
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.