Evidence map›Paper›PMID 18987152›Full record

ArticleJournal of virology2009

Differential expression of the CXCR3 ligands in chronic hepatitis C virus (HCV) infection and their modulation by HCV in vitro.

Karla J Helbig, Andrew Ruszkiewicz, Robert E Lanford, Mark D Berzsenyi, Hugh A Harley, Shaun R McColl, Michael R Beard

Abstract read
In one paragraph

Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 72 citations in OpenAlex.

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  14. The role of chemokines in hepatitis C virus-mediated liver disease.International journal of molecular sciences · 2014
    Review
  15. Article
  16. Review
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  18. Article
  19. HIV and co-infections.Immunological reviews · 2013
    Review
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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

7 authors at 5 institutions in 2 countries.

Karla J HelbigInfectious Diseases Laboratories, Institute of Medical and Veterinary Science, Adelaide 5000,South Australia.
Andrew Ruszkiewicz
Robert E Lanford
Mark D Berzsenyi
Hugh A Harley
Shaun R McColl
Michael R Beard
University of Adelaide · AURoyal Adelaide Hospital · AUSouth Australia Pathology · AUTexas Biomedical Research Institute · USThe Alfred Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To investigate chemokine expression networks in chronic hepatitis C virus (HCV) infection, we used microarray analysis to determine chemokine expression in human infection and in chimpanzees experimentally infected with HCV. The CXCR3 chemokine family was highly expressed in both human and chimpanzee infection. CXCL10 was the only CXCR3 chemokine elevated in the serum, suggesting that it may neutralize any CXCR3 chemokine gradient established between the periphery and liver by CXCL11 and CXCL9. Thus, CXCR3 chemokines may not be responsible for recruitment of T lymphocytes but may play a role in positioning these cells within the liver. The importance of the CXCR3 chemokines, in particular CXCL11, was highlighted by replicating HCV (JFH-1) to selectively upregulate its expression in response to gamma interferon (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha). This selective upregulation was confirmed at the transcriptional level by using the CXCL11 promoter driving the luciferase reporter gene. This synergistic increase in expression was not a result of HCV protein expression but the nonspecific innate response to double-stranded RNA (dsRNA), as both in vitro-transcribed HCV RNA and the dsRNA analogue poly(I:C) increased CXCL11 expression and promoter activity. Furthermore, we show that CXCL11 is an IRF3 (interferon regulatory factor 3) response gene whose expression is selectively enhanced by IFN-gamma and TNF-alpha. In conclusion, the CXCR3 chemokines are the most significantly expressed chemokines in chronic hepatitis C and most likely play a role in positioning T cells in the liver. Furthermore, HCV can selectively increase CXCL11 expression in response to IFN-gamma and TNF-alpha stimulation that may play a role in the pathogenesis of HCV-related liver disease.

Indexed as

AnimalsCells, CulturedChemokine CXCL10Chemokine CXCL11Chemokine CXCL9Gene Expression ProfilingGenes, ReporterHepacivirusHepatitis C, ChronicHumansInterferon-gammaLiverLuciferasesOligonucleotide Array Sequence AnalysisPan troglodytesTumor Necrosis Factor-alphaChemokine CXCL10Chemokine CXCL11Chemokine CXCL9Interferon-gammaLuciferasesTumor Necrosis Factor-alpha

Identifiers

PMID18987152
PMCPMC2612358
OpenAlexW2165643360

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.