Evidence map›Paper›PMID 16970603›Full record

ArticleJournal of viral hepatitis2006

Transient immunological control during acute hepatitis C virus infection: ex vivo analysis of helper T-cell responses.

A Ulsenheimer, M Lucas, N P Seth, J Tilman Gerlach, N H Gruener, A Loughry, G R Pape, K W Wucherpfennig, H M Diepolder, P Klenerman

Open access · greenAbstract read
In one paragraph

Article in Journal of viral hepatitis, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

  1. Trial
  2. Review
  3. Evidence of CD4Scientific reports · 2018
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. MHC class II tetramers.Journal of immunology (Baltimore, Md. : 1950) · 2012
    Review
  9. Article
  10. Adaptive immunity to the hepatitis C virus.Advances in virus research · 2010
    Review
  11. Improving the diagnosis of acute hepatitis C virus infection with expanded viral load criteria.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2009
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. CD4+ T cell responses in hepatitis C virus infection.World journal of gastroenterology · 2007
    Review
  17. Article
  18. Review
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

10 authors at 3 institutions in 3 countries.

A UlsenheimerInstitute for Immunology, University of Munich, Munich, Germany. axel@ulsenheimer.de
M Lucas
N P Seth
J Tilman Gerlach
N H Gruener
A Loughry
G R Pape
K W Wucherpfennig
H M Diepolder
P Klenerman
Medawar Building for Pathogen Research · GBDana-Farber Cancer Institute · USUniversity of Hohenheim · DE

Funding

TCR recognition of MHC class II peptide compexes in multiple sclerosisP01AI045757 · NIAID · DANA-FARBER CANCER INSTITUTE · PI KUCHROO, VIJAY K., LOVE, JOHN CHRISTOPHER · 1999 to 2017
$22.8M
NIAID NIH HHS AI45757NIAID NIH HHS P01 AI045757Wellcome Trust
6 · The paper itself

Abstract

Hepatitis C virus (HCV) readily sets up persistence after acute infection. Cellular immune responses are thought to play a major role in control of the virus. Failure of CD4+ T-cell responses in acute disease is associated with viral persistence but the dynamics of this are poorly understood. We aimed to assess such responses using a novel set of Class II tetrameric complexes (tetramers) to study helper T-cells ex vivo in acute disease. We analysed the HCV-specific CD4+ T-cell response in a patient with acute hepatitis c infection. We were able to track the virus-specific CD4+ T-cells directly ex vivo with HLA DR4 tetramers. Proliferative responses were absent initially, recovered as viral load dropped and were lost again during relapse. Longitudinal tetramer analyses showed expanded populations of antiviral CD4+ T-cells throughout acute infection despite lack of proliferation. A pattern of transient CD4+ T-cell proliferative responses as HCV is partially controlled is observed. Failure to control virus is associated with emergence of 'dysfunctional' CD4+ T-cell populations. Failure to control HCV in acute disease may relate to the capacity to sustain efficient immune responses as virus attempts to 'bounce back' after partial control.

Indexed as

Acute DiseaseAntigens, ViralAntiviral AgentsHepatitis CHLA-DR AntigensHLA-DRB1 ChainsHumansInterferon-alphaLymphocyte ActivationRibavirinT-Lymphocytes, Helper-InducerT-Lymphocyte SubsetsAntigens, ViralAntiviral AgentsHLA-DR AntigensHLA-DRB1 ChainsInterferon-alphaRibavirin

Identifiers

PMID16970603
PMCPMC4515975
OpenAlexW2037161720

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.