Evidence map›Paper›PMID 22577869›Full record

ArticleEuropean journal of medical research2012

Cytokine/chemokine patterns connect host and viral characteristics with clinics during chronic hepatitis C.

Antonios Katsounas, Martin Trippler, Shyam Kottilil, Richard A Lempicki, Guido Gerken, Joerg F Schlaak

Abstract read
In one paragraph

Article in European journal of medical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
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.

Antonios KatsounasDepartment of Gastroenterology and Hepatology, University Hospital of Essen, Germany. antonios.katsounas@uk-essen.de
Martin Trippler
Shyam Kottilil
Richard A Lempicki
Guido Gerken
Joerg F Schlaak

Funding

Therapeutic Strategies for the Management of HCV/HIV co- infectionZIAAI000390 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI FAUCI, ANTHONY S. · 2009 to 2014
$4.2M
PHS HHS HHSN261200800001E
6 · The paper itself

Abstract

backgroundIn chronic hepatitis C virus (HCV) infection, liver tissue pathology and HCV genotype are important determinants of clinical and/or treatment-related outcome. Although consistent epidemiological and/or molecular-biological clues derived from different studies on single virus-host interactions are meanwhile published, the in vivo transcriptional responses and cellular pathways affected in >1 key aspects of the disease or treatment process are far from being understood.

methodsMicroarray analysis was performed in peripheral whole blood (PB) samples from 36 therapy-naïve HCV-infected patients with known liver histology. Linear regression analysis identified gene expression profiles significantly correlating (P < 0.015) with ≥1 out of 7 variables: sustained viral response (SVR), viral non-response (NR), end of treatment viral response (ETR), viral breakthrough (VB), HCV genotype (Gt. 1 vs. Gt. 2/3), stage of hepatic fibrosis [St. 0/1 vs. St. 2/3/4] and grade of hepatic inflammation (Gr. 0/1 vs. Gr. 2/3/4). Correlation values across all seven contrasts were considered for hierarchical clustering (HCL).

resultsA total of 1,697 genes showed ≥1 significant correlation results and genes involved in cell differentiation (183), immune response (53), and apoptosis (170) were leading fractions. HCL grouped the genes into six major clusters. Functional annotation analysis using DAVID (http://david.abcc.ncifcrf.gov) revealed that expression profiles that best linked these variables were highly enriched in cytokine/chemokine activity (Fisher-exact P < 0.0001) and specific biological module-centric algorithms finally led our focus on four out of fifty-three immune response genes: SMAD family member 3 (SMAD3), interleukin 1 receptor accessory protein (IL1RAP), tumor necrosis factor receptor superfamily member 1A (TNFRSF1A), and chemokine 'C-C motif' receptor 5 (CCR5). Of those, TNFRSF1A and CCR5 showed significant correlation with two out of seven variables based on microarray and/or quantitative real-time polymerase chain reaction (qRT-PCR) data.

conclusionWe identified molecular targets of the innate and adaptive immune system and validated their transcriptional specificity in vivo suggesting significant involvement in two unique outcomes during HCV treatment.

Indexed as

AlgorithmsAntiviral AgentsApoptosisChemokinesCytokinesFollow-Up StudiesGenes, ViralGenotypeHepacivirusHepatitis C, ChronicHumansInflammationInterferon-alphaLinear ModelsLiverOligonucleotide Array Sequence AnalysisAntiviral AgentsChemokinesCytokinesInterferon-alphaReceptors, CCR5Receptors, Tumor Necrosis Factor, Type IRNA, ViralSmad3 ProteinSMAD3 protein, humanTNFRSF1A protein, human

Identifiers

PMID22577869
PMCPMC3489717

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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.