Evidence map›Paper›PMID 25341640›Full record

ArticleScientific reports2014

Fetal exposure to HIV-1 alters chemokine receptor expression by CD4+T cells and increases susceptibility to HIV-1.

Madeleine J Bunders, John L van Hamme, Machiel H Jansen, Kees Boer, Neeltje A Kootstra, Taco W Kuijpers

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In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

39 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. Observational
  4. Joining the dots: maternal cytomegalovirus, HIV and the placenta.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
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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

6 authors at 2 institutions in 1 country.

Madeleine J Bunders1] Department of Pediatric Hematology, Immunology and Infectious Diseases, Emma Children's Hospital, Academic Medical Centre (AMC), University of Amsterdam (UvA), Amsterdam, The Netherlands [2] Department of Experimental Immunology, AMC, UvA, Amsterdam, The Netherlands.
John L van Hamme1] Department of Pediatric Hematology, Immunology and Infectious Diseases, Emma Children's Hospital, Academic Medical Centre (AMC), University of Amsterdam (UvA), Amsterdam, The Netherlands [2] Department of Experimental Immunology, AMC, UvA, Amsterdam, The Netherlands.
Machiel H Jansen1] Department of Pediatric Hematology, Immunology and Infectious Diseases, Emma Children's Hospital, Academic Medical Centre (AMC), University of Amsterdam (UvA), Amsterdam, The Netherlands [2] Department of Experimental Immunology, AMC, UvA, Amsterdam, The Netherlands.
Kees BoerDepartment of Obstetrics, AMC, UvA, Amsterdam, The Netherlands.
Neeltje A KootstraDepartment of Experimental Immunology, AMC, UvA, Amsterdam, The Netherlands.
Taco W Kuijpers1] Department of Pediatric Hematology, Immunology and Infectious Diseases, Emma Children's Hospital, Academic Medical Centre (AMC), University of Amsterdam (UvA), Amsterdam, The Netherlands [2] Department of Experimental Immunology, AMC, UvA, Amsterdam, The Netherlands.
Emma Kinderziekenhuis · NLUniversity of Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Absolute numbers of lymphocytes are decreased in uninfected infants born to HIV-1-infected women (HIV-1-exposed). Although the exact mechanism is unknown, fetal exposure to maternal HIV-1-infection could prime the immune system and affect T cell trafficking. We compared the expression of chemokine receptors on cord blood CD4(+) T cells from HIV-1-exposed children and healthy controls. At baseline CD4(+) T cells had a largely naïve phenotype. However, stimulation with cytokines resulted in an upregulation of inflammatory response-related chemokine receptors on CD4(+) T cells, with HIV-1-exposed infants having a significantly higher frequency of CD4(+) T cells expressing, in particularly Th2 associated chemokine receptors (CCR3 p < 0.01, CCR8 p = 0.03). Numbers of naive CCR7(+) CD4(+) T cells were reduced (p = 0.01) in HIV-1-exposed infants. We further assessed whether the inflammatory phenotype was associated with susceptibility to HIV-1 and detected higher levels of p24 upon in in vitro infection of stimulated CD4(+) T cells of HIV-1-exposed infants. In summary, fetal exposure to HIV-1 primes the immune system in the infant leading to an enhanced immune activation and altered T cell homing, with potential ramifications regarding T cell responses and the acquisition of HIV-1 as an infant.

Indexed as

Gene ExpressionGenetic Predisposition to DiseaseHIV-1Case-Control StudiesCD4 Lymphocyte CountCD4-Positive T-LymphocytesCluster AnalysisFemaleFetal BloodGene Expression ProfilingHIV InfectionsHumansImmunophenotypingInfantInfant, NewbornPhenotypeReceptors, Chemokine

Identifiers

PMID25341640
PMCPMC4208038
OpenAlexW2022459783

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.