Evidence map›Paper›PMID 21731496›Full record

ArticlePLoS pathogens2011

Detection of inferred CCR5- and CXCR4-using HIV-1 variants and evolutionary intermediates using ultra-deep pyrosequencing.

Evelien M Bunnik, Luke C Swenson, Diana Edo-Matas, Wei Huang, Winnie Dong, Arne Frantzell, Christos J Petropoulos, Eoin Coakley, Hanneke Schuitemaker, P Richard Harrigan and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. CXCR4 Is a Potential Target for Anti-HIV Gene Therapy.International journal of molecular sciences · 2024
    Review
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  19. Deep sequencing: becoming a critical tool in clinical virology.Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2014
    Review
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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

11 authors at 3 institutions in 2 countries.

Evelien M BunnikDepartment of Experimental Immunology, Sanquin Research, Landsteiner Laboratory, Center for Infection and Immunity Amsterdam, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Luke C Swenson
Diana Edo-Matas
Wei Huang
Winnie Dong
Arne Frantzell
Christos J Petropoulos
Eoin Coakley
Hanneke Schuitemaker
P Richard Harrigan
Angélique B van 't Wout
Academic Medical Center · NLAIDS Vancouver · CAUniversity of Amsterdam · NL

Funding

NOVEL ASSAYS FOR MEASURING THE INHIBITION OF VIRUS ENTRYR44AI048990 · NIAID · MONOGRAM BIOSCIENCES, INC. · PI PETROPOULOS, CHRISTOS J · 2003 to 2005
$2.6M
CIHRNIAID NIH HHS R44 AI048990
6 · The paper itself

Abstract

The emergence of CXCR4-using human immunodeficiency virus type 1 (HIV-1) variants is associated with accelerated disease progression. CXCR4-using variants are believed to evolve from CCR5-using variants, but due to the extremely low frequency at which transitional intermediate variants are often present, the kinetics and mutational pathways involved in this process have been difficult to study and are therefore poorly understood. Here, we used ultra-deep sequencing of the V3 loop of the viral envelope in combination with the V3-based coreceptor prediction tools PSSM(NSI/SI) and geno2pheno([coreceptor]) to detect HIV-1 variants during the transition from CCR5- to CXCR4-usage. We analyzed PBMC and serum samples obtained from eight HIV-1-infected individuals at three-month intervals up to one year prior to the first phenotypic detection of CXCR4-using variants in the MT-2 assay. Between 3,482 and 10,521 reads were generated from each sample. In all individuals, V3 sequences of predicted CXCR4-using HIV-1 were detected at least three months prior to phenotypic detection of CXCR4-using variants in the MT-2 assay. Subsequent analysis of the genetic relationships of these V3 sequences using minimum spanning trees revealed that the transition in coreceptor usage followed a stepwise mutational pathway involving sequential intermediate variants, which were generally present at relatively low frequencies compared to the major predicted CCR5- and CXCR4-using variants. In addition, we observed differences between individuals with respect to the number of predicted CXCR4-using variants, the diversity among major predicted CCR5-using variants, and the presence or absence of intermediate variants with discordant phenotype predictions. These results provide the first detailed description of the mutational pathways in V3 during the transition from CCR5- to CXCR4-usage in natural HIV-1 infection.

Indexed as

Genetic VariationReceptors, CCR5Receptors, CXCR4Sequence Analysis, RNABiological Evolutionenv Gene Products, Human Immunodeficiency VirusHIV-1HIV InfectionsHumansRNA, ViralTime Factorsenv Gene Products, Human Immunodeficiency VirusReceptors, CCR5Receptors, CXCR4RNA, Viral

Identifiers

PMID21731496
PMCPMC3121885
OpenAlexW2157219992

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.