Evidence map›Paper›PMID 18838615›Full record

ArticleBlood2009

Hepatitis C virus association with peripheral blood B lymphocytes potentiates viral infection of liver-derived hepatoma cells.

Zania Stamataki, Claire Shannon-Lowe, Jean Shaw, David Mutimer, Alan B Rickinson, John Gordon, David H Adams, Peter Balfe, Jane A McKeating

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
  2. Review
  3. Antibody Responses in Hepatitis C Infection.Cold Spring Harbor perspectives in medicine · 2021
    Review
  4. Review
  5. Observational
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Engineering Antibodies for the Treatment of Infectious Diseases.Advances in experimental medicine and biology · 2017
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. In vitro systems for the study of hepatitis C virus infection.International journal of hepatology · 2012
    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

9 authors at 3 institutions in 1 country.

Zania StamatakiHepatitis C Virus Research Group, Division of Immunity and Infection, Institute for Cancer Studies, UK
Claire Shannon-Lowe
Jean Shaw
David Mutimer
Alan B Rickinson
John Gordon
David H Adams
Peter Balfe
Jane A McKeating
Cancer Research UK · GBNational Health Service · GBQueen Elizabeth Hospital · GB

Funding

Functional analysis of hepatitis C virus glycoproteinsR01AI050798 · NIAID · UNIVERSITY OF BIRMINGHAM · PI MCKEATING, JANE A. · 2004 to 2008
$1.3M
Medical Research Council G0400802Medical Research Council G0801976NIAID NIH HHS AI40034-14NIAID NIH HHS AI50798NIAID NIH HHS N01 AI040034NIAID NIH HHS R01 AI050798Wellcome Trust
6 · The paper itself

Abstract

Hepatitis C virus (HCV) primarily replicates within the liver, leading to hepatitis, fibrosis, and hepatocellular carcinoma. Infection is also associated with B-cell abnormalities, suggesting an association of the virus with B cells. The infectious JFH-1 strain of HCV can bind primary and immortalized B cells but fails to establish productive infection. However, B cell-associated virus readily infects hepatoma cells, showing an enhanced infectivity compared with extracellular virus. B cells express the viral receptors CD81, SR-BI, and the C-type lectins DC-SIGN and L-SIGN. Antibodies specific for SR-BI and DC-SIGN/L-SIGN reduced B-cell transinfection, supporting a role for these molecules in B-cell association with HCV. Stimulation of B cells with CD40 ligand and interleukin-4 promoted their ability to transinfect hepatoma cells. B cell-associated virus is resistant to trypsin proteolysis and HCV-specific neutralizing antibodies, consistent with particle internalization. HCV promoted the adhesion of primary B cells to Huh-7 hepatomas, providing a mechanism for B-cell retention in the infected liver. In summary, B cells may provide a vehicle for HCV to persist and transmit to the liver.

Indexed as

AnimalsBlotting, WesternB-LymphocytesCarcinoma, HepatocellularFlow CytometryHepacivirusHepatitis CHumansLiver NeoplasmsReceptors, VirusReverse Transcriptase Polymerase Chain ReactionReceptors, Virus

Identifiers

PMID18838615
PMCPMC2628366
OpenAlexW2085614123

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.