Evidence map›Paper›PMID 25506344›Full record

ArticleFrontiers in immunology2014

Progression to AIDS in SIV-Infected Rhesus Macaques is Associated with Distinct KIR and MHC class I Polymorphisms and NK Cell Dysfunction.

Christina Albrecht, Dörthe Malzahn, Markus Brameier, Meike Hermes, Aftab A Ansari, Lutz Walter

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

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  17. Roles of natural killer cells in antiviral immunity.Current opinion in virology · 2016
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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 3 institutions in 2 countries.

Christina AlbrechtPrimate Genetics Laboratory, German Primate Center, Leibniz-Institute for Primate Research , Göttingen , Germany.
Dörthe MalzahnDepartment of Genetic Epidemiology, University Medical Center, Georg-August-University , Göttingen , Germany.
Markus BrameierPrimate Genetics Laboratory, German Primate Center, Leibniz-Institute for Primate Research , Göttingen , Germany.
Meike HermesPrimate Genetics Laboratory, German Primate Center, Leibniz-Institute for Primate Research , Göttingen , Germany.
Aftab A AnsariDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine , Atlanta, GA , USA.
Lutz WalterPrimate Genetics Laboratory, German Primate Center, Leibniz-Institute for Primate Research , Göttingen , Germany.
German Primate Center · DEEmory University · USUniversity of Göttingen · DE

Funding

Yerkes National Primate Research Center Role of type-I IFN in regulating COVID-19 induced inflammation and pathogenesisP51OD011132 · OD · EMORY UNIVERSITY · PI Joon Sup Lee · 2012 to 2026
$167.0M
NIH HHS P51 OD011132
6 · The paper itself

Abstract

Killer cell immunoglobulin-like receptors (KIR) regulate the activity of natural killer (NK) cells and have been shown to be associated with susceptibility to a number of human infectious diseases. Here, we analyzed NK cell function and genetic associations in a cohort of 52 rhesus macaques experimentally infected with SIVmac and subsequently stratified into high viral load (HVL) and low viral load (LVL) plasma viral loads at set point. This stratification coincided with fast (HVL) and slow (LVL) disease progression indicated by the disease course and critical clinical parameters including CD4+ T cell counts. HVL animals revealed sustained proliferation of NK cells but distinct loss of peripheral blood NK cell numbers and lytic function. Genetic analyses revealed that KIR genes 3DL05, 3DS05, and 3DL10 as well as 3DSW08, 3DLW03, and 3DSW09 are correlated, most likely due to underlying haplotypes. SIV-infection outcome associated with presence of transcripts for two inhibitory KIR genes (KIR3DL02, KIR3DL10) and three activating KIR genes (KIR3DSW08, KIR3DS02, KIR3DS05). Presence of KIR3DL02 and KIR3DSW08 was associated with LVL outcome, whereas presence of KIR3DS02 was associated with HVL outcome. Furthermore, we identified epistasis between KIR and MHC class I alleles as the transcript presence of the correlated genes KIR3DL05, KIR3DS05, and KIR3DL10 increased HVL risk when Mamu-B*012 transcripts were also present or when Mamu-A1*001 transcripts were absent. These genetic associations were mirrored by changes in the numbers, the level of proliferation, and lytic capabilities of NK cells as well as overall survival time and gastro-intestinal tissue viral load.

Indexed as

AIDSepistasisgenetic polymorphismkiller cell immunoglobulin-like receptorsMHC class I ligandsrhesus macaque SIV infection modelvirus infection

Identifiers

PMID25506344
PMCPMC4246914
OpenAlexW1994262227

What OpenQuestion holds

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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.