Evidence map›Paper›PMID 18216107›Full record

ArticleJournal of virology2008

Analysis of the evolutionary forces in an immunodominant CD8 epitope in hepatitis C virus at a population level.

Christoph Neumann-Haefelin, David N Frick, Jing Jing Wang, Oliver G Pybus, Shadi Salloum, Gagandeep S Narula, Anna Eckart, Andrea Biezynski, Thomas Eiermann, Paul Klenerman and 5 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 62 citations in OpenAlex.

  1. Frontiers in microbiology · 2024
    Article
  2. CD8Frontiers in immunology · 2022
    Article
  3. Review
  4. CD8Journal of clinical medicine · 2021
    Review
  5. Adaptive Immune Response against Hepatitis C Virus.International journal of molecular sciences · 2020
    Review
  6. Article
  7. Article
  8. Review
  9. Differential escape of HCV from CD8Journal of viral hepatitis · 2019
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

15 authors at 5 institutions in 3 countries.

Christoph Neumann-HaefelinDepartment of Medicine II, University of Freiburg, Hugstetter Str. 55, 79106 Freiburg, Germany.
David N Frick
Jing Jing Wang
Oliver G Pybus
Shadi Salloum
Gagandeep S Narula
Anna Eckart
Andrea Biezynski
Thomas Eiermann
Paul Klenerman
Sergei Viazov
Michael Roggendorf
Robert Thimme
Markus Reiser
Jörg Timm
New York Medical College · USUniversity of Freiburg · DEParacelsus-Kliniken · DEUniversität Hamburg · DEUniversity of Oxford · GB

Funding

Enzymatic Differences Among Hepatitis C Virus GenotypesR01AI052395 · NIAID · NEW YORK MEDICAL COLLEGE · PI FRICK, DAVID N · 2003 to 2007
$1.5M
NIAID NIH HHS AI052395NIAID NIH HHS R01 AI052395Wellcome Trust
6 · The paper itself

Abstract

Failure of the adaptive immune response to control infection with the hepatitis C virus (HCV) can result from mutational escape in targeted T-cell epitopes. Recent studies suggest that T-cell immune pressure is an important factor in the evolution of the nonstructural proteins in HCV. The aim of this study was to characterize the forces that contribute to viral evolution in an HLA-A*01-restricted epitope in HCV NS3. This epitope represents a potentially attractive target for vaccination strategies since it is conserved across all genotypes. In our cohort of subjects with chronic HCV infection (genotype 1b or 3a), it is a frequently recognized CD8 epitope in HLA-A*01-positive subjects. Viral sequence data reveal that an escape variant is the dominant residue in both genotypes. The predominant Y1444F substitution seemingly impairs binding to the HLA-A*01 molecule, which may have an important impact on the ability to prime a functional CD8 response upon infection. Interestingly, a case of evolution toward the prototype sequence was observed during chronic infection, possibly because the helicase activity of the protein containing the Y1444F substitution is reduced compared to the prototype sequence. Comparison of HCV sequences from Asia and Europe suggests that the frequency of the HLA-A*01 allele in a population may influence the frequency of the escape variant in circulating strains. These data suggest a complex interaction of multiple forces shaping the evolution of HCV in which immune pressure both within the individual and also at the population level in addition to functional constraints are important contributing factors.

Indexed as

Evolution, MolecularAdenosine TriphosphateAdultAgedAmino Acid SubstitutionAsiaDEAD-box RNA HelicasesDNA HelicasesEpitopes, T-LymphocyteEuropeFemaleHepacivirusHepatitis C, ChronicHLA-A1 AntigenHLA-A AntigensHumansAdenosine TriphosphateDEAD-box RNA HelicasesDNA HelicasesEpitopes, T-LymphocyteHLA-A1 AntigenHLA-A AntigensNS3 protein, hepatitis C virusNucleoside-TriphosphataseRNA, ViralSerine EndopeptidasesViral Nonstructural ProteinsViral Proteases

Identifiers

PMID18216107
PMCPMC2268453
OpenAlexW2117665565

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.