Evidence map›Paper›PMID 22351942›Full record

ArticleThe Journal of infectious diseases2012

Genetically associated CD16(+)56(-) natural killer cell interferon (IFN)-αR expression regulates signaling and is implicated in IFN-α-induced hepatitis C virus decline.

Sara J Conry, Qinglai Meng, Gareth Hardy, Nicole L Yonkers, Julia M Sugalski, Amy Hirsch, Perica Davitkov, Anita Compan, Yngve Falck-Ytter, Ronald E Blanton and 3 more

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

Article in The Journal of infectious diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

8 citing papers in PubMed, 8 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Article
  6. Natural killer cells in hepatitis C: Current progress.World journal of gastroenterology · 2016
    Review
  7. Article
  8. 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

13 authors at 5 institutions in 1 country.

Sara J ConryDepartment of Medicine, Division of Infectious Diseases, University Hospital Case Medical Center, Case Western Reserve University, Cleveland, Ohio 44106, USA.
Qinglai Meng
Gareth Hardy
Nicole L Yonkers
Julia M Sugalski
Amy Hirsch
Perica Davitkov
Anita Compan
Yngve Falck-Ytter
Ronald E Blanton
Benigno Rodriguez
Clifford V Harding
Donald D Anthony
University Hospitals Cleveland Medical Center · USUnited States Department of Veterans Affairs · USCenter for Global Health · USInfectious Disease Consultants · USUniversity Hospitals of Cleveland · US

Funding

Host Genetic Contribution to HCV OutcomesR01AI073963 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI BLANTON, RONALD E · 2008 to 2011
$2.1M
Recurrent treatment: Effect on rural and urban S. mansoni population structureR01AI069195 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI BLANTON, RONALD E · 2007 to 2011
$1.8M
Role of immature DC in host defense against HCVR01DK068361 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI ANTHONY, DONALD D · 2006 to 2010
$1.3M
NIAID NIH HHS R01 AI069195NIAID NIH HHS R01 AI073963NIDDK NIH HHS R01 DK068361
6 · The paper itself

Abstract

backgroundNatural killer (NK) cells likely contribute to outcome of acute hepatitis C virus (HCV) infection and interferon (IFN)-induced control of chronic HCV infection. We previously observed IFN-αR and NKp30 expression associated with IFN-α-dependent NK cell activity.

methodsHere, we examined CD16(+)56(-), CD16(+)56(+), and CD16(-)56(+) NK cell subset IFN-αR and NKp30 expression in relation to magnitude of HCV genotype 1 decrease during pegylated IFN-α plus ribavirin therapy.

resultsWe observed greater baseline IFN-αR and NKp30 expression on CD16(+)56(+) and CD16(-)56(+) NK subsets in HCV-infected patients than in healthy control subjects. Baseline CD16(+)56(-) NK IFN-αR expression was associated with IFN-α-induced pSTAT1, and both were associated with magnitude of HCV decrease during pegylated IFN-α plus ribavirin therapy. Baseline CD16(+)56(-) NK IFN-αR expression was associated with race and interleukin 28B genotype, negatively associated with aspartate aminotransferase-to platelet ratio index, and positively associated with increase in NKp30 expression after in vivo IFN-α exposure. Finally, in vitro IFN-α2a-activated NK cytolysis of HCV-infected target cells was in part dependent on NKp30, and CD16(+)56(-) NK cell IFN-αR expression correlated with cytolytic activity.

conclusionsIFN-αR expression on CD16(+)56(-) NK cells during chronic HCV infection may in part be genetically determined, and level of expression regulates IFN-α signaling, which in turn may contribute to control of HCV infection.

Indexed as

Gene Expression RegulationSignal TransductionAdultAgedAntiviral AgentsCD56 AntigenFemaleGPI-Linked ProteinsHepacivirusHepatitis C, ChronicHumansInterferon-alphaKiller Cells, NaturalLymphocyte SubsetsMaleMiddle AgedAntiviral AgentsCD56 AntigenFCGR3B protein, humanGPI-Linked ProteinsInterferon-alphaNatural Cytotoxicity Triggering Receptor 3NCAM1 protein, humanNCR3 protein, humanReceptor, Interferon alpha-betaReceptors, IgG

Identifiers

PMID22351942
PMCPMC3295604
OpenAlexW2106358693

What OpenQuestion holds

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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.