Evidence map›Paper›PMID 21346814›Full record

ArticlePloS one2011

KIR-HLA and maternal-infant HIV-1 transmission in sub-Saharan Africa.

Maria Paximadis, Gregory Minevich, Robert Winchester, Diana B Schramm, Glenda E Gray, Gayle G Sherman, Ashraf H Coovadia, Louise Kuhn, Caroline T Tiemessen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. A SYSTEMATIC REVIEW ON THE INFLUENCE OF HLA-B POLYMORPHISMS ON HIV-1 MOTHER-TO-CHILD-TRANSMISSION.The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases
    Pooled it
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  6. The Role of Killer Ig-like Receptors in Diseases from A to Z.International journal of molecular sciences · 2025
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  19. Maternal human leukocyte antigen-G (HLA-G) genetic variants associate with in utero mother-to-child transmission of HIV-1 in Black South Africans.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2015
    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

9 authors at 4 institutions in 2 countries.

Maria PaximadisAIDS Virus Research Unit, National Institute for Communicable Diseases, Johannesburg, South Africa. paxim@nicd.ac.za
Gregory Minevich
Robert Winchester
Diana B Schramm
Glenda E Gray
Gayle G Sherman
Ashraf H Coovadia
Louise Kuhn
Caroline T Tiemessen
Columbia University · USNational Institute for Communicable DiseasesUniversity of the Witwatersrand · ZAChris Hani Baragwanath Hospital · ZA

Funding

HIV Protective Immunity and Perinatal ExposureR01HD042402 · NICHD · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI KUHN, LOUISE · 2002 to 2006
$3.1M
NICHD NIH HHS R01 HD042402PHS HHS NICHD 42402Wellcome TrustWellcome Trust 076352/Z/05/Z
6 · The paper itself

Abstract

Numerous studies have suggested a role for natural killer (NK) cells in attenuation of HIV-1 disease progression via recognition by killer-cell immunoglobulin-like receptors (KIRs) of specific HLA class I molecules. The role of KIR and HLA class I has not been addressed in the context of maternal-infant HIV-1 transmission. KIR and HLA class I B and C genes from 224 HIV-1-infected mothers and 222 infants (72 infected and 150 uninfected) from South Africa were characterized. Although a number of significant associations were determined in both the total group and in the nevirapine (NVP) exposed group, the most significant findings involved KIR2DL2 and KIR2DL3 and HLA-C. KIR2DL2/KIR2DL3 was underrepresented in intrapartum (IP)-transmitting mothers compared to non-transmitting (NT) mothers (P = 0.008) and remained significant (P = 0.036) after correction for maternal viral load (MVL). Homozygosity for KIR2DL3 alone and in combination with HLA-C allotype heterozygosity (C1C2) was elevated in IP-transmitting mothers compared to NT mothers (P = 0.034 and P = 0.01 respectively), and after MVL correction (P = 0.033 and P = 0.027, respectively). In infants, KIR2DL3 in combination with its HLA-C1 ligand (C1) as well as homozygosity for KIR2DL3 with C1C2, were both found to be underrepresented in infected infants compared to exposed uninfected infants in the total group (P = 0.06 and P = 0.038, respectively) and in the sub-group of infants whose mothers received NVP (P = 0.007 and P = 0.03, respectively). These associations were stronger post MVL adjustment (total group: P = 0.02 and P = 0.009, respectively; NVP group: P = 0.004 and P = 0.02, respectively). Upon stratification according to low and high MVL, all significant associations fell within the low MVL group, suggesting that with low viral load, the effects of genotype can be more easily detected. In conclusion this study has identified a number of significant associations that suggest an important role for NK cells in maternal-to-infant HIV-1 transmission.

Indexed as

Infectious Disease Transmission, VerticalAfrica South of the SaharaCohort StudiesFemaleGene FrequencyGenetic Predisposition to DiseaseHaplotypesHIV-1HIV InfectionsHLA AntigensHumansInfantKiller Cells, NaturalLigandsReceptors, KIRHLA AntigensLigandsReceptors, KIR

Identifiers

PMID21346814
PMCPMC3035631
OpenAlexW2074244790

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.