Evidence map›Paper›PMID 18199789›Full record

ArticleJournal of clinical microbiology2008

Evaluation of eight different bioinformatics tools to predict viral tropism in different human immunodeficiency virus type 1 subtypes.

Carolina Garrido, Vanessa Roulet, Natalia Chueca, Eva Poveda, Antonio Aguilera, Katharina Skrabal, Natalia Zahonero, Silvia Carlos, Federico García, Jean Louis Faudon and 2 more

Open access · greenAbstract readEvaluation Study
In one paragraph

Article in Journal of clinical microbiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

50 citing papers in PubMed, 114 citations in OpenAlex.

  1. Article
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  5. Molecular Communications in Viral Infections Research: Modeling, Experimental Data, and Future Directions.IEEE transactions on molecular, biological, and multi-scale communications · 2021
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  11. Envelope gene evolution and HIV-1 neuropathogenesis.Journal of neuroinfectious diseases · 2015
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  17. Dependence on the CCR5 coreceptor for viral replication explains the lack of rebound of CXCR4-predicted HIV variants in the Berlin patient.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2014
    Article
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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

12 authors at 4 institutions in 2 countries.

Carolina GarridoHospital Carlos III, Sinesio Delgado 10, 28029 Madrid, Spain.
Vanessa Roulet
Natalia Chueca
Eva Poveda
Antonio Aguilera
Katharina Skrabal
Natalia Zahonero
Silvia Carlos
Federico García
Jean Louis Faudon
Vincent Soriano
Carmen de Mendoza
Hospital Clínico San Carlos · ESEurofins (United States) · USInstituto de Investigación Biosanitaria de Granada · ESHospital Provincial de Conxo · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human immunodeficiency virus type 1 (HIV-1) tropism can be assessed using phenotypic assays, but this is quite laborious, expensive, and time-consuming and can be made only in sophisticated laboratories. More accessible albeit reliable tools for testing of HIV-1 tropism are needed in view of the prompt introduction of CCR5 antagonists in clinical practice. Bioinformatics tools based on V3 sequences might help to predict HIV-1 tropism; however, most of these methods have been designed by taking only genetic information derived from HIV-1 subtype B into consideration. The aim of this study was to evaluate the performances of several genotypic tools to predict HIV-1 tropism in non-B subtypes, as data on this issue are scarce. Plasma samples were tested using a new phenotypic tropism assay (Phenoscript-tropism; Eurofins), and results were compared with estimates of coreceptor usage using eight different genotypic predictor softwares (Support Vector Machine [SVM], C4.5, C4.5 with positions 8 to 12 only, PART, Charge Rule, geno2pheno coreceptor, Position-Specific Scoring Matrix X4R5 [PSSM(X4R5)], and PSSM(sinsi)). A total of 150 samples were tested, with 115 belonging to patients infected with non-B subtypes and 35 drawn from subtype B-infected patients, which were taken as controls. When non-B subtypes were tested, the concordances between the results obtained using the phenotypic assay and distinct genotypic tools were as follows: 78.8% for SVM, 77.5% for C4.5, 82.5% for C4.5 with positions 8 to 12 only, 82.5% for PART, 82.5% for Charge Rule, 82.5% for PSSM(X4R5), 83.8% for PSSM(sinsi), and 71.3% for geno2pheno. When clade B viruses were tested, the best concordances were seen for PSSM(X4R5) (91.4%), PSSM(sinsi) (88.6%), and geno2pheno (88.6%). The sensitivity for detecting X4 variants was lower for non-B than for B viruses, especially in the case of PSSM(sinsi) (38.4% versus 100%, respectively), SVM(wetcat) (46% versus 100%, respectively), and PART (30% versus 90%, respectively). In summary, while inferences of HIV-1 coreceptor usage using genotypic tools seem to be reliable for clade B viruses, their performances are poor for non-B subtypes, in which they particularly fail to detect X4 variants.

Indexed as

AdultCD4 AntigensComputational BiologyFemaleGenotypeHIV-1HIV Envelope Protein gp120HIV InfectionsHumansMaleMiddle AgedPeptide FragmentsPhenotypeReagent Kits, DiagnosticReceptors, CCR5Receptors, CXCR4CD4 AntigensCXCR4 protein, humanHIV Envelope Protein gp120HIV envelope protein gp120 (305-321)Peptide FragmentsReagent Kits, DiagnosticReceptors, CCR5Receptors, CXCR4

Identifiers

PMID18199789
PMCPMC2268339
OpenAlexW2104289712

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.