Evidence map›Paper›PMID 18094161›Full record

ArticleJournal of virology2008

CCR5Delta32 59537-G/A promoter polymorphism is associated with low translational efficiency and the loss of CCR5Delta32 protective effects.

Qingwen Jin, Lokesh Agrawal, L Meyer, R Tubiana, Ioannis Theodorou, Ghalib Alkhatib

Abstract 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. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Lack of Correlation Between the CCR5-Δ32 Mutation and Acute Myeloid Leukemia in Iranian Patients.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2015
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Effects of variant rs346473 in ARHGAP24 gene on disease progression of HBV infection in Han Chinese population.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2011
    Article
  10. The biology of CCR5 and CXCR4.Current opinion in HIV and AIDS · 2009
    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

6 authors.

Qingwen JinDepartment of Microbiology and Immunology, Indiana University School of Medicine, 635 Barnhill Drive, Rm. 420, Indianapolis, IN 46202, USA.
Lokesh Agrawal
L Meyer
R Tubiana
Ioannis Theodorou
Ghalib Alkhatib

Funding

Host Cell Factors and AIDS PathogenesisR01AI052019 · NIAID · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI ALKHATIB, GHALIB ABBAS · 2002 to 2013
$4.0M
NIAID NIH HHS R01 AI052019PHS HHS A152019-01
6 · The paper itself

Abstract

We have recently demonstrated that the CCR5Delta32 protein interacts with CCR5 and CXCR4 and down-modulates their cell surface expression. We have also reported the absence of detectable expression of the truncated CCR5Delta32 protein in four out of six human immunodeficiency virus-infected (HIV(+)) CCR5(-/-) individuals. To explain the defect in protein expression in these samples, we cloned and sequenced the promoter regions of the six HIV(+) individuals. We have identified several polymorphisms in the CCR5Delta32 promoter region, but these polymorphisms were not associated with significant differences in mRNA levels. Coupled in vitro transcription/translation and polyribosome analysis demonstrated a strong association between a variant genotype designated CCR5Delta32 59537-A/A and a low translation efficiency. Protein analysis indicated that the peripheral blood mononuclear cells from two of the HIV(+) CCR5(-/-) individuals carrying the CCR5Delta32 59537-A/A variant expressed trace amounts of CCR5Delta32 protein compared to the individuals carrying the CCR5Delta32 59537-G/G genotype. The results imply that the absence of CCR5Delta32 protein in two HIV(+) individuals is due to a genetic defect in the translation of the protein. Together, these results highlight the importance of the CCR5Delta32 protein as an HIV suppressive factor and provide further insight into the mechanism of the protective effect of the CCR5Delta32 mutation.

Indexed as

Polymorphism, GeneticPromoter Regions, Genetic5' Untranslated RegionsElectrophoresis, Polyacrylamide GelHeLa CellsHIV InfectionsHumansProtein BiosynthesisReceptors, CCR5Reverse Transcriptase Polymerase Chain ReactionRNA, Messenger5' Untranslated RegionsReceptors, CCR5RNA, Messenger

Identifiers

PMID18094161
PMCPMC2258923

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.