Evidence map›Paper›PMID 39879199›Full record

ArticlePloS one2025

HIV-1 resistance mutations and genetic diversity among children failing antiretroviral treatment in five healthcare facilities in Benin, West Africa.

Edwige Hermione Dagba Gbessin, Edmond Tchiakpe, René Kpemahouton Keke, Nicole Vidal, Michel Kiréopori Gomgnimbou, Haziz Sina, Euloge Senan Adjou, Aldric Afangnihoun, Moussa Bachabi, Akadiri Yessoufou and 2 more

Abstract read
In one paragraph

Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–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

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. 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

12 authors.

Edwige Hermione Dagba GbessinNAZI BONI University, Bobo-Dioulasso, Burkina Faso.ORCID 0009-0005-6950-1668
Edmond TchiakpeNational Reference Laboratory of Health Program Fighting Against AIDS in Benin (LNR/PSLS), Health Ministry, Akpakpa, Littoral, Benin.
René Kpemahouton KekeNational Reference Laboratory of Health Program Fighting Against AIDS in Benin (LNR/PSLS), Health Ministry, Akpakpa, Littoral, Benin.
Nicole VidalUMI233 -TransVIHMI, Université de Montpellier, Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de Recherche pour le Développement (IRD), Montpellier, France.
Michel Kiréopori GomgnimbouHigher Institute of Health Sciences (INSSA), Nazi Boni University, Bobo-Dioulasso. Molecular Biology Laboratory, Muraz Center, Bobo-Dioulasso, Burkina Faso.
Haziz SinaFaculty of Sciences and Technology (FAST), Laboratory of Biology and Molecular Typing in Microbiology (LBTMM), University of Abomey-Calavi, Atlantic, Benin.
Euloge Senan AdjouFaculty of Sciences and Technology (FAST) and Institute of Applied Biomedical Sciences (ISBA), Department of Biochemistry and Cellular Biology, Laboratory of Cell Biology and Physiology, University of Abomey-Calavi, Abomey-Calavi, Atlantic, Benin.
Aldric AfangnihounHealth Program Fighting Against AIDS in Benin (PSLS), Health Ministry, Akpakpa, Littoral, Benin.
Moussa BachabiHealth Program Fighting Against AIDS in Benin (PSLS), Health Ministry, Akpakpa, Littoral, Benin.
Akadiri YessoufouFaculty of Sciences and Technology (FAST) and Institute of Applied Biomedical Sciences (ISBA), Department of Biochemistry and Cellular Biology, Laboratory of Cell Biology and Physiology, University of Abomey-Calavi, Abomey-Calavi, Atlantic, Benin.
Abdoul-Salam OuedraogoLaboratory of Emerging and Re-emerging Pathogens (LaPathER), Doctoral School of Health Sciences, Nazi BONI University, Bobo-Dioulasso, Burkina Faso.
Lamine Baba-MoussaFaculty of Sciences and Technology (FAST), Laboratory of Biology and Molecular Typing in Microbiology (LBTMM), University of Abomey-Calavi, Atlantic, Benin.ORCID 0000-0002-8160-5954

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAntiretroviral treatment increases the risk of accumulation of resistance mutations that negatively impact the possibilities of future treatment. This study aimed to present the frequency of HIV-1 antiretroviral resistance mutations and the genetic diversity among children with virological failure in five pediatric care facilities in Benin.

methodsA cross-sectional study was carried out from November 20, 2020, to November 30, 2022, in children under 15 years of age who failed ongoing antiretroviral treatment at five facilities care in Benin (VL > 3log10 on two consecutive realizations three months apart). Viral loads were measured using the m2000 RealTime Abbott platform. Genotyping was carried out with the commercial Viroseq kit. Sequences were read on the ABI 3500 sequencer and then edited with ViroSeqHIVv3.0 software. The HIV drug resistance database at Stanford University was used to identify mutations and viral subtypes were assigned by phylogenetic analyses.

resultsThe HIV-1 pol gene was sequenced in 47 participants with virological failure of antiretroviral treatment. The median age was 120 [Interquartile Range 90-144] months. The prevalent treatment was EFV base regimen (22/47; 46.8%). Median viral load was 4.39 log10 [IQR 3.81-4.86 log10] respectively. Resistance testing was successful among (37/47; 78.72%) children, resistance mutations were detected in (32/37; 86.48%) children, and (29/32; 90.62%) had at least one surveillance drug resistance mutation. Respectively (25/32; 78.12%), (28/32; 87.5%), (4/32; 12.90%), (22/32; 68.75%) had at least one resistance mutation associated with NRTIs, NNRTIs, PIs and NNRTIs+NRTIs. (12/32; 37.5%) of children carried mutations related to TAMs. the most frequently NRTIs identified were M184V (21/62; 33.9%) followed by TAMs (20/62; 32.2%) and T69G/D (2/62; 3.2%)s. Among mutations associated with NNRTIs K103N represented (18/64; 28.1%) followed by P225H (7/64; 10.9%). The I54V (3/6; 50%) mutation is the major PI observed. Genetic diversity is characterized by a preponderance of CRF02_AG (72%, 23/32), followed by unique recombinant forms (URFs) (25%, 8/32) and one subtype G.

conclusionA high rate of mutations has been observed in children. These data underline the importance of implementing routine genotypic testing in the biological monitoring of infected children to anticipate the accumulation of resistance mutations and thus compromise the treatment options available in Benin.

Indexed as

Anti-HIV AgentsDrug Resistance, ViralGenetic VariationHIV-1HIV InfectionsMutationAdolescentBeninChildChild, PreschoolCross-Sectional StudiesFemaleHealth FacilitiesHumansInfantMaleAnti-HIV Agents

Identifiers

PMID39879199
PMCPMC11778783

What OpenQuestion holds

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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.