Evidence map›Paper›PMID 30520960›Full record

ArticleThe Journal of infectious diseases2019

Impact of HLA Allele-KIR Pairs on HIV Clinical Outcome in South Africa.

Masahiko Mori, Ellen Leitman, Bruce Walker, Thumbi Ndung'u, Mary Carrington, Philip Goulder

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of infectious diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Inflammatory Phenotypes Predict Changes in Arterial Stiffness Following Antiretroviral Therapy Initiation.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2020
    Article
  6. Review
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 4 institutions in 5 countries.

Masahiko MoriDepartment of Paediatrics, University of Oxford.
Ellen LeitmanDepartment of Paediatrics, University of Oxford.
Bruce WalkerRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard, Cambridge.
Thumbi Ndung'uRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard, Cambridge.
Mary CarringtonRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard, Cambridge.
Philip GoulderDepartment of Paediatrics, University of Oxford.
Ragon Institute of MGH, MIT and Harvard · USUniversity of Oxford · GBAfrica Health Research Institute · ZANagasaki University · JP

Funding

Molecular genetics and population studies of the KIR and HLA gene complexesZIABC010792 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI CARRINGTON, MARY N. · 2009 to 2025
$7.8M
Maximising Cure Potential in Paediatric HIV InfectionR01AI133673 · NIAID · UNIVERSITY OF OXFORD · PI GOULDER, PHILIP J · 2017 to 2021
$1.4M
CCR NIH HHS HHSN261200800001CNCI NIH HHS HHSN261200800001ENIAID NIH HHS R01 AI133673Wellcome TrustWellcome Trust 107752/Z/15/ZWellcome Trust WT104748MA
6 · The paper itself

Abstract

backgroundHLA class I contributes to HIV immune control through antigen presentation to cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells. In contrast to investigations of CTL, studies of NK cells in HIV control through HLA-killer immunoglobulin-like receptor (KIR) interactions remain sparse in African cohorts.

methodsTreatment-naive, chronically HIV-infected adults (N = 312) were recruited from South Africa, and the effects of HLA-KIR pairs on clinical outcome were analyzed.

resultsThere was no significant difference in viral load among all subjects with HLA alleles from the HLA-C1 group (P = .1). However, differences in HLA-C type significantly influenced viremia among 247 KIR2DL3 positives (P = .04), suggesting that specific HLA-KIR interactions contribute to immune control. Higher viral load (P = .02) and lower CD4+ T-cell counts (P = .008) were observed in subjects with HLA-C*16:01+KIR2DL3+. Longitudinal analysis showed more rapid progression to AIDS among HLA-C*16:01+KIR2DL3+ subjects (adjusted hazard ratio 1.9, P = .03) than those without this genotype, independent of CD4+ T-cell count and viral load.

conclusionsThese results highlight the existence of unique anti-HIV innate immunity within distinct populations and the contribution of KIR on NK cells and some CTLs to the well-described HLA-mediated impact on HIV disease progression.

Indexed as

Anti-HIV AgentsCD4 Lymphocyte CountChronic DiseaseDisease ProgressionFemaleGene FrequencyGenes, MHC Class IGenotypeHistocompatibility Antigens Class IHIV InfectionsHLA-B AntigensHLA-C AntigensHLA-E AntigensHumansImmunity, InnateLinkage DisequilibriumAnti-HIV AgentsHistocompatibility Antigens Class IHLA-B AntigensHLA-C AntigensHLA-E AntigensKIR2DL1 protein, humanKIR2DL3 protein, humanKLRC1 protein, humanNK Cell Lectin-Like Receptor Subfamily CReceptors, KIR2DL1Receptors, KIR2DL3disease outcomeHIVHLAKIRSouth Africa

Identifiers

PMID30520960
PMCPMC6467198
OpenAlexW2904425338

What OpenQuestion holds

Textmetadata
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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.