Evidence map›Paper›PMID 12768008›Full record

ArticleJournal of virology2003

The differential ability of HLA B*5701+ long-term nonprogressors and progressors to restrict human immunodeficiency virus replication is not caused by loss of recognition of autologous viral gag sequences.

Stephen A Migueles, Alisha C Laborico, Hiromi Imamichi, W Lesley Shupert, Cassandra Royce, Mary McLaughlin, Linda Ehler, Julia Metcalf, Shuying Liu, Claire W Hallahan and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
3.6field-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

97 citing papers in PubMed, 157 citations in OpenAlex.

  1. Trial
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  3. HLA-B*14:02-Restricted Env-Specific CD8Journal of virology · 2017
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37 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 1 country.

Stephen A MiguelesLaboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
Alisha C Laborico
Hiromi Imamichi
W Lesley Shupert
Cassandra Royce
Mary McLaughlin
Linda Ehler
Julia Metcalf
Shuying Liu
Claire W Hallahan
Mark Connors
National Institutes of Health · USNational Institute of Allergy and Infectious Diseases · USNational Cancer Institute · US

Funding

Mechanisms Of Immune Mediated Restriction Of HIV Replication In LTNPZIAAI000855 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI CONNORS, MARK · 2009 to 2025
$20.0M
Mechanisms Of Immune Mediated Restriction Of HIV Replication In LTNPZ01AI000855 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI CONNORS, MARK · 1999 to 2008
$2.9M
6 · The paper itself

Abstract

Although the HLA B(*)5701 class I allele is highly overrepresented among human immunodeficiency virus (HIV)-infected long-term nonprogressors (LTNPs), it is also present at the expected frequency (11%) in patients with progressive HIV infection. Whether B57(+) progressors lack restriction of viral replication because of escape from recognition of highly immunodominant B57-restricted gag epitopes by CD8(+) T cells remains unknown. In this report, we investigate the association between restriction of virus replication and recognition of autologous virus sequences in 27 B(*)57(+) patients (10 LTNPs and 17 progressors). Amplification and direct sequencing of single molecules of viral cDNA or proviral DNA revealed low frequencies of genetic variations in these regions of gag. Furthermore, CD8(+) T-cell recognition of autologous viral variants was preserved in most cases. In two patients, responses to autologous viral variants were not demonstrable at one epitope. By using a novel technique to isolate primary CD4(+) T cells expressing autologous viral gene products, it was found that 1 to 13% of CD8(+) T cells were able to respond to these cells by gamma interferon production. In conclusion, escape-conferring mutations occur infrequently within immunodominant B57-restricted gag epitopes and are not the primary mechanism of virus evasion from immune control in B(*)5701(+) HIV-infected patients. Qualitative features of the virus-specific CD8(+) T-cell response not measured by current assays remain the most likely determinants of the differential abilities of HLA B(*)5701(+) LTNPs and progressors to restrict virus replication.

Indexed as

Amino Acid SequenceHIV Long-Term SurvivorsVirus ReplicationAntigen PresentationCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesEpitopes, T-LymphocyteFlow CytometryGene Products, gagHIV-1HIV InfectionsHLA-B AntigensHumansImmunodominant EpitopesMolecular Sequence DataSequence Analysis, DNAEpitopes, T-LymphocyteGene Products, gagHLA-B AntigensImmunodominant EpitopesViral Proteins

Identifiers

PMID12768008
PMCPMC156173
OpenAlexW2010951564

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.