Evidence map›Paper›PMID 26807922›Full record

ArticlePloS one2016

Mutations Related to Antiretroviral Resistance Identified by Ultra-Deep Sequencing in HIV-1 Infected Children under Structured Interruptions of HAART.

Jose Manuel Vazquez-Guillen, Gerardo C Palacios-Saucedo, Lydia G Rivera-Morales, Jorge Garcia-Campos, Rocio Ortiz-Lopez, Marc Noguera-Julian, Roger Paredes, Herlinda J Vielma-Ramirez, Teresa J Ramirez, Marcelino Chavez-Garcia and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. 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
0.2field-weighted citation impact, top 41% 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, 4 citations in OpenAlex.

  1. Observational
  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

15 authors at 5 institutions in 3 countries.

Jose Manuel Vazquez-GuillenLaboratorio de Inmunología y Virología, Facultad de Ciencias Biológicas, Universidad Autónoma de Nuevo León, Monterrey, Nuevo León, México.
Gerardo C Palacios-SaucedoDivisión de Investigación, Departamento de Pediatría e Infectología Pediátrica, Unidad Médica de Alta Especialidad, Hospital de Especialidades No. 25, Instituto Mexicano del Seguro Social, Monterrey, Nuevo León, México.
Lydia G Rivera-MoralesLaboratorio de Inmunología y Virología, Facultad de Ciencias Biológicas, Universidad Autónoma de Nuevo León, Monterrey, Nuevo León, México.
Jorge Garcia-CamposDivisión de Investigación, Departamento de Pediatría e Infectología Pediátrica, Unidad Médica de Alta Especialidad, Hospital de Especialidades No. 25, Instituto Mexicano del Seguro Social, Monterrey, Nuevo León, México.
Rocio Ortiz-LopezDepartamento de Bioquímica y Medicina Molecular, Facultad de Medicina and Centro de Investigación y Desarrollo en Ciencias de la Salud, Universidad Autónoma de Nuevo León, Monterrey, Nuevo León, México.
Marc Noguera-JulianInstitut de Recerca de la SIDA, IrsiCaixa, Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de Barcelona, Badalona, España and Cátedra de la SIDA, Universitat de Vic, Vic, España.
Roger ParedesInstitut de Recerca de la SIDA, IrsiCaixa, Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de Barcelona, Badalona, España and Cátedra de la SIDA, Universitat de Vic, Vic, España.
Herlinda J Vielma-RamirezLaboratorio de Inmunología y Virología, Facultad de Ciencias Biológicas, Universidad Autónoma de Nuevo León, Monterrey, Nuevo León, México.
Teresa J RamirezLaboratorio Estatal de Salud Pública del Estado de Nuevo León, Secretaría de Salud, Nuevo León, México.
Marcelino Chavez-GarciaDivisión de Investigación, Departamento de Pediatría e Infectología Pediátrica, Unidad Médica de Alta Especialidad, Hospital de Especialidades No. 25, Instituto Mexicano del Seguro Social, Monterrey, Nuevo León, México.
Paulo Lopez-GuillenUnidad de Infectología "Dr. Juan I. Menchaca", Hospital General Regional No. 45, Instituto Mexicano del Seguro Social, Jalisco, México.
Evangelina Briones-LaraDivisión de Investigación, Departamento de Pediatría e Infectología Pediátrica, Unidad Médica de Alta Especialidad, Hospital de Especialidades No. 25, Instituto Mexicano del Seguro Social, Monterrey, Nuevo León, México.
Luz M Sanchez-SanchezDivisión de Investigación, Departamento de Pediatría e Infectología Pediátrica, Unidad Médica de Alta Especialidad, Hospital de Especialidades No. 25, Instituto Mexicano del Seguro Social, Monterrey, Nuevo León, México.
Carlos A Vazquez-MartinezDivisión de Investigación, Departamento de Pediatría e Infectología Pediátrica, Unidad Médica de Alta Especialidad, Hospital de Especialidades No. 25, Instituto Mexicano del Seguro Social, Monterrey, Nuevo León, México.
Cristina Rodriguez-PadillaLaboratorio de Inmunología y Virología, Facultad de Ciencias Biológicas, Universidad Autónoma de Nuevo León, Monterrey, Nuevo León, México.
Universidad Autónoma de Nuevo León · MXMexican Social Security Institute · MXHospital de Especialidades · MXUniversitat Autònoma de Barcelona · ESSecretaria de Salud · HN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although Structured Treatment Interruptions (STI) are currently not considered an alternative strategy for antiretroviral treatment, their true benefits and limitations have not been fully established. Some studies suggest the possibility of improving the quality of life of patients with this strategy; however, the information that has been obtained corresponds mostly to studies conducted in adults, with a lack of knowledge about its impact on children. Furthermore, mutations associated with antiretroviral resistance could be selected due to sub-therapeutic levels of HAART at each interruption period. Genotyping methods to determine the resistance profiles of the infecting viruses have become increasingly important for the management of patients under STI, thus low-abundance antiretroviral drug-resistant mutations (DRM's) at levels under limit of detection of conventional genotyping (<20% of quasispecies) could increase the risk of virologic failure. In this work, we analyzed the protease and reverse transcriptase regions of the pol gene by ultra-deep sequencing in pediatric patients under STI with the aim of determining the presence of high- and low-abundance DRM's in the viral rebounds generated by the STI. High-abundance mutations in protease and high- and low-abundance mutations in reverse transcriptase were detected but no one of these are directly associated with resistance to antiretroviral drugs. The results could suggest that the evaluated STI program is virologically safe, but strict and carefully planned studies, with greater numbers of patients and interruption/restart cycles, are still needed to evaluate the selection of DRM's during STI.

Indexed as

Antiretroviral Therapy, Highly ActiveMutationAdolescentAnti-HIV AgentsDrug Resistance, ViralFemaleGenotypeHigh-Throughput Nucleotide SequencingHIV InfectionsHumansMaleViral LoadAnti-HIV Agents

Identifiers

PMID26807922
PMCPMC4725846
OpenAlexW2278470909

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.