Evidence map›Paper›PMID 9294127›Full record

ArticleThe Journal of clinical investigation1997

Heterozygosity for a defective gene for CC chemokine receptor 5 is not the sole determinant for the immunologic and virologic phenotype of HIV-infected long-term nonprogressors.

O J Cohen, M Vaccarezza, G K Lam, B F Baird, K Wildt, P M Murphy, P A Zimmerman, T B Nutman, C H Fox, S Hoover and 16 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
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  9. HLA B*5701 is highly associated with restriction of virus replication in a subgroup of HIV-infected long term nonprogressors.Proceedings of the National Academy of Sciences of the United States of America · 2000
    Article
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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

26 authors at 7 institutions in 1 country.

O J CohenLaboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA.
M Vaccarezza
G K Lam
B F Baird
K Wildt
P M Murphy
P A Zimmerman
T B Nutman
C H Fox
S Hoover
J Adelsberger
M Baseler
J Arthos
R T Davey
R L Dewar
J Metcalf
D J Schwartzentruber
J M Orenstein
S Buchbinder
A J Saah
R Detels
J Phair
C Rinaldo
J B Margolick
G Pantaleo
A S Fauci
National Institutes of Health · USJohns Hopkins University · USGeorge Washington University · USNorthwestern University · USSan Francisco AIDS Foundation · USUniversity of California, Los Angeles · USUniversity of Pittsburgh · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HIV-1-infected long-term nonprogressors are a heterogeneous group of individuals with regard to immunologic and virologic markers of HIV-1 disease. CC chemokine receptor 5 (CCR5) has recently been identified as an important coreceptor for HIV-1 entry into CD4+ T cells. A mutant allele of CCR5 confers a high degree of resistance to HIV-1 infection in homozygous individuals and partial protection against HIV disease progression in heterozygotes. The frequency of CCR5 heterozygotes is increased among HIV-1- infected long-term nonprogressors compared with progressors; however, the host defense mechanisms responsible for nonprogression in CCR5 heterozygotes are unknown. We hypothesized that nonprogressors who were heterozygous for the mutant CCR5 gene might define a subgroup of nonprogressors with higher CD4+ T cell counts and lower viral load compared with CCR5 wild-type nonprogressors. However, in a cohort of 33 HIV-1-infected long-term nonprogressors, those who were heterozygous for the mutant CCR5 gene were indistinguishable from CCR5 wild-type nonprogressors with regard to all measured immunologic and virologic parameters. Although epidemiologic data support a role for the mutant CCR5 allele in the determination of the state of long-term nonprogression in some HIV-1- infected individuals, it is not the only determinant. Furthermore, long-term nonprogressors with the wild-type CCR5 genotype are indistinguishable from heterozygotes from an immunologic and virologic standpoint.

Indexed as

MutationAdultCD4-Positive T-LymphocytesChemokine CCL4Chemokine CCL5Disease-Free SurvivalDisease ProgressionFemaleHeterozygoteHIV-1HIV InfectionsHomozygoteHumansImmunohistochemistryIn Situ HybridizationLymph NodesChemokine CCL4Chemokine CCL5Macrophage Inflammatory ProteinsReceptors, CCR5Receptors, Complement 3d

Identifiers

PMID9294127
PMCPMC508340
OpenAlexW2036795887

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.