Evidence map›Paper›PMID 20162731›Full record

ArticleHepatology (Baltimore, Md.)2010

Hepatitis C virus core protein interacts with fibrinogen-beta and attenuates cytokine stimulated acute-phase response.

Malika Ait-Goughoulte, Arup Banerjee, Keith Meyer, Budhaditya Mazumdar, Kousuke Saito, Ratna B Ray, Ranjit Ray

Open access · bronzeAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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  8. Review
  9. Article
  10. Cyclophilin A as a New Therapeutic Target for Hepatitis C Virus-induced Hepatocellular Carcinoma.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2013
    Review
  11. Article
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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 1 institution in 1 country.

Malika Ait-GoughoulteDepartment of Internal Medicine, Saint Louis University, St Louis, MO 63104, USA.
Arup Banerjee
Keith Meyer
Budhaditya Mazumdar
Kousuke Saito
Ratna B Ray
Ranjit Ray
Saint Louis University · US

Funding

Virology and Smallpox VaccinationsU54AI057160 · NIAID · WASHINGTON UNIVERSITY · PI RAY, RANJIT · 2003 to 2013
$80.9M
Mechanisms of Liver Disease Progression by Hepatitis C VirusR01DK080812 · NIDDK · SAINT LOUIS UNIVERSITY · PI RAY, RANJIT · 2009 to 2013
$1.6M
Developing an in vitro system for HCV propagationR21AI065535 · NIAID · SAINT LOUIS UNIVERSITY · PI RAY, RATNA B. · 2008 to 2009
$369k
NIAID NIH HHS R21 AI065535NIAID NIH HHS U54 AI057160NIAID NIH HHS U54AI057160NIDDK NIH HHS DK080812NIDDK NIH HHS R01 DK080812
6 · The paper itself

Abstract

unlabelledFibrinogen-beta (FBG-beta), an important acute-phase protein (APP), is generated by the liver as a target for inflammatory mediators. Here we identified FBG-beta as a hepatitis C virus (HCV) core interacting protein by screening a human liver complementary DNA (cDNA) library using mammalian two-hybrid analysis. An association between FBG-beta and HCV core protein was verified by confocal microscopy and coimmunoprecipitation from the transfected human hepatocyte (Huh-7) cell line. HCV core or genomic RNA transfected Huh-7 cells modestly increased FBG-beta protein expression when compared to the basal level in control hepatocytes. Transfection of HCV core or full-length (FL) gene into Huh-7 cells up-regulated basal FBG-beta promoter activity. Exogenous addition of IL-6 stimulates FBG-beta promoter activity in hepatocytes. However, ectopic expression of HCV core or FL in hepatocytes inhibited IL-6-stimulated FBG-beta promoter activation. Inhibition of endogenous FBG-beta expression following introduction of small interfering RNA (siRNA) into cells displayed a gain of function of promoter regulation by HCV core protein. Further studies suggested that HCV core gene expression in stable transfectants of Huh-7 cells resulted in a basal up-regulation of FBG-beta and other APPs. However, treatment with cytokines, interleukin-6 (IL-6), or tumor necrosis factor-alpha repressed FBG-beta and other acute-phase response (APR) genes.

conclusionOur results reveal that the core/FBG-beta interaction may act as a regulatory feedback, allowing repression of IL-6-stimulated APR genes. Together, these data suggested a network of interactions between HCV core and the hepatic APR genes, and may contribute to impaired innate immunity for viral persistence.

Indexed as

Acute-Phase ReactionCell LineFibrinogenHepacivirusHepatocytesHumansInterleukin-6Protein Interaction MappingProtein SubunitsTumor Necrosis Factor-alphaTwo-Hybrid System TechniquesViral Core ProteinsFibrinogenInterleukin-6nucleocapsid protein, Hepatitis C virusProtein SubunitsTumor Necrosis Factor-alphaViral Core Proteins

Identifiers

PMID20162731
PMCPMC5837823
OpenAlexW2087460294

What OpenQuestion holds

Textmetadata
LicenceTDM
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.