Evidence map›Paper›PMID 15280458›Full record

ArticleJournal of virology2004

Diverse hepatitis C virus glycoproteins mediate viral infection in a CD81-dependent manner.

J A McKeating, L Q Zhang, C Logvinoff, M Flint, J Zhang, J Yu, D Butera, D D Ho, L B Dustin, C M Rice and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
9.4field-weighted citation impact, top 1% 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

77 citing papers in PubMed, 166 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. The Multifaceted Roles of Autophagy in Flavivirus-Host Interactions.International journal of molecular sciences · 2018
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Immunopathogenesis of Hepatitis C Virus Infection.Gastroenterology clinics of North America · 2015
    Review
  18. Article
  19. Article
  20. Article

17 more citing papers are in PubMed but not listed here.

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

11 authors at 3 institutions in 2 countries.

J A McKeatingCenter for the Study of Hepatitis C, The Rockefeller University, 1230 York Ave., New York, NY 10021, USA. mckeatj@rockefeller.edu
L Q Zhang
C Logvinoff
M Flint
J Zhang
J Yu
D Butera
D D Ho
L B Dustin
C M Rice
P Balfe
Rockefeller University · USAaron Diamond AIDS Research Center · USColumbia University · US

Funding

Structure and function of the HCV RNA replicaseR01CA057973 · NCI · WASHINGTON UNIVERSITY · PI RICE, CHARLES M · 1992 to 2013
$4.7M
Immune complexes: Origins and effects in HCV infectionR01AI060561 · NIAID · UNIVERSITY OF OXFORD · PI DUSTIN, LYNN B · 2003 to 2015
$3.9M
NCI NIH HHS CA57973NCI NIH HHS R01 CA057973NIAID NIH HHS N01 AI040034NIAID NIH HHS R01 AI060561
6 · The paper itself

Abstract

We recently reported that retroviral pseudotypes bearing the hepatitis C virus (HCV) strain H and Con1 glycoproteins, genotype 1a and 1b, respectively, require CD81 as a coreceptor for virus-cell entry and infection. Soluble truncated E2 cloned from a number of diverse HCV genotypes fail to interact with CD81, suggesting that viruses of diverse origin may utilize different receptors and display altered cell tropism. We have used the pseudotyping system to study the tropism of viruses bearing diverse HCV glycoproteins. Viruses bearing these glycoproteins showed a 150-fold range in infectivity for hepatoma cells and failed to infect lymphoid cells. The level of glycoprotein incorporation into particles varied considerably between strains, generally reflecting the E2 expression level within transfected cells. However, differences in glycoprotein incorporation were not associated with virus infectivity, suggesting that infectivity is not limited by the absolute level of glycoprotein. All HCV pseudotypes failed to infect HepG2 cells and yet infected the same cells after transduction to express human CD81, confirming the critical role of CD81 in HCV infection. Interestingly, these HCV pseudotypes differed in their ability to infect HepG2 cells expressing a panel of CD81 variants, suggesting subtle differences in the interaction of CD81 residues with diverse viral glycoproteins. Our current model of HCV infection suggests that CD81, together with additional unknown liver specific receptor(s), mediate the virus-cell entry process.

Indexed as

Amino Acid SequenceAnimalsAntigens, CDCell LineCell Line, TumorCells, CulturedHepacivirusHepatocytesHIV-1HumansLiverLymphocytesMiceMolecular Sequence DataOrgan SpecificityTetraspanin 28Antigens, CDCD81 protein, humanCd81 protein, mouseE1 protein, Hepatitis C virusglycoprotein E2, Hepatitis C virusTetraspanin 28Viral Envelope Proteins

Identifiers

PMID15280458
PMCPMC479078
OpenAlexW2108494941

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.