Evidence map›Paper›PMID 25700262›Full record

ArticlePloS one2015

Genetic diversity of the KIR/HLA system and susceptibility to hepatitis C virus-related diseases.

Valli De Re, Laura Caggiari, Mariangela De Zorzi, Ombretta Repetto, Anna Linda Zignego, Francesco Izzo, Maria Lina Tornesello, Franco Maria Buonaguro, Alessandra Mangia, Domenico Sansonno and 12 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  19. An immunogenetic view of COVID-19.Genetics and molecular biology · 2021
    Article
  20. Genetic Variants inFrontiers in immunology · 2021
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors at 8 institutions in 1 country.

Valli De ReFacility Bio-proteomica/Dir. Sc, CRO National Cancer Institute, Aviano, Pordenone, Italy.
Laura CaggiariFacility Bio-proteomica/Dir. Sc, CRO National Cancer Institute, Aviano, Pordenone, Italy.
Mariangela De ZorziFacility Bio-proteomica/Dir. Sc, CRO National Cancer Institute, Aviano, Pordenone, Italy.
Ombretta RepettoFacility Bio-proteomica/Dir. Sc, CRO National Cancer Institute, Aviano, Pordenone, Italy.
Anna Linda ZignegoExperimental and Clinical Medicine, University of Florence, Florence, Italy.
Francesco IzzoHepatobiliary Unit, National Cancer Institute "Fondazione Pascale", Naples, Italy.
Maria Lina TorneselloMolecular Biology and Viral Oncology, National Cancer Institute "Fondazione Pascale", Naples, Italy.
Franco Maria BuonaguroMolecular Biology and Viral Oncology, National Cancer Institute "Fondazione Pascale", Naples, Italy.
Alessandra MangiaLiver, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo, Italy.
Domenico SansonnoBiomedical Sciences and Human Oncology, University of Bari Medical School, Bari, Italy.
Vito RacanelliBiomedical Sciences and Human Oncology, University of Bari Medical School, Bari, Italy.
Salvatore De VitaMedical and Biological Sciences, University Hospital Santa Maria della Misericordia, Udine, Italy.
Pietro PioltelliHematology and Transplant Unit, San Gerardo Hospital, University of Milano-Bicocca, Monza, Italy.
Emanuela VaccherMedical Oncology, Centro di riferimento oncologico, Aviano, Pordenone, Italy.
Massimiliano Berretta
Massimiliano BerettaMedical Oncology, Centro di riferimento oncologico, Aviano, Pordenone, Italy.
Cesare MazzaroMedical Oncology, Centro di riferimento oncologico, Aviano, Pordenone, Italy.
Massimo LibraBiomedical Sciences, University of Catania, Catania, Italy.
Andrea GiniEpidemiology and Biostatistics, CRO National Cancer Institute, Aviano, Pordenone, Italy.
Antonella ZucchettoEpidemiology and Biostatistics, CRO National Cancer Institute, Aviano, Pordenone, Italy.
Renato CannizzaroGastroenterology, CRO National Cancer Institute, Aviano, Pordenone, Italy.
Paolo De PaoliFacility Bio-proteomica/Dir. Sc, CRO National Cancer Institute, Aviano, Pordenone, Italy.
Centro di Riferimento Oncologico · ITIstituto Nazionale Tumori IRCCS "Fondazione G. Pascale" · ITUniversity of Bari Aldo Moro · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITOspedale Santa Maria della Misericordia di Udine · ITUniversity of Catania · ITUniversity of Florence · ITUniversity of Milano-Bicocca · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe variability in the association of host innate immune response to Hepatitis C virus (HCV) infection requires ruling out the possible role of host KIR and HLA genotypes in HCV-related disorders: therefore, we therefore explored the relationships between KIR/HLA genotypes and chronic HCV infection (CHC) as they relate to the risk of HCV-related hepatocarcinoma (HCC) or lymphoproliferative disease progression. METHODS AND

findingsWe analyzed data from 396 HCV-positive patients with CHC (n = 125), HCC (118), and lymphoproliferative diseases (153), and 501 HCV-negative patients. All were HIV and HBV negative. KIR-SSO was used to determine the KIR typing. KIR2DL5 and KIR2DS4 variants were performed using PCR and GeneScan analysis. HLA/class-I genotyping was performed using PCR-sequence-based typing. The interaction between the KIR gene and ligand HLA molecules was investigated. Differences in frequencies were estimated using Fisher's exact test, and Cochran-Armitage trend test. The non-random association of KIR alleles was estimated using the linkage disequilibrium test. We found an association of KIR2DS2/KIR2DL2 genes, with the HCV-related lymphoproliferative disorders. Furthermore, individuals with a HLA-Bw6 KIR3DL1+ combination of genes showed higher risk of developing lymphoma than cryoglobulinemia. KIR2DS3 gene was found to be the principal gene associated with chronic HCV infection, while a reduction of HLA-Bw4 + KIR3DS1+ was associated with an increased risk of developing HCC.

conclusionsOur data highlight a role of the innate-system in developing HCV-related disorders and specifically KIR2DS3 and KIR2D genes demonstrated an ability to direct HCV disease progression, and mainly towards lymphoproliferative disorders. Moreover the determination of KIR3D/HLA combination of genes direct the HCV progression towards a lymphoma rather than an hepatic disease. In this contest IFN-α therapy, a standard therapy for HCV-infection and lymphoproliferative diseases, known to be able to transiently enhance the cytotoxicity of NK-cells support the role of NK cells to counterstain HCV-related and lymphoproliferative diseases.

Indexed as

Genetic Predisposition to DiseaseAdultAgedCentromereFemaleGene FrequencyGenetic LociGenotypeHepacivirusHepatitis CHLA AntigensHumansLinkage DisequilibriumMaleMiddle AgedReceptors, KIRHLA AntigensKIR2DS4 protein, humanReceptors, KIRReceptors, KIR2DL5

Identifiers

PMID25700262
PMCPMC4336327
OpenAlexW2022915690

What OpenQuestion holds

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LicenceCC BY
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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.