Evidence map›Paper›PMID 19279442›Full record

ArticleAIDS (London, England)2009

Combinatorial content of CCL3L and CCL4L gene copy numbers influence HIV-AIDS susceptibility in Ukrainian children.

Ludmila Shostakovich-Koretskaya, Gabriel Catano, Zoya A Chykarenko, Weijing He, German Gornalusse, Srinivas Mummidi, Racquel Sanchez, Matthew J Dolan, Seema S Ahuja, Robert A Clark and 2 more

Open access · greenAbstract readMulticenter Study
In one paragraph

Article in AIDS (London, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. BeyondFrontiers in genetics · 2026
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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

12 authors at 4 institutions in 2 countries.

Ludmila Shostakovich-KoretskayaDepartment of General Pediatrics and Pediatric Infectious Diseases, Dnepropetrovsk State Medical Academy, Dnepropetrovsk, Ukraine.
Gabriel Catano
Zoya A Chykarenko
Weijing He
German Gornalusse
Srinivas Mummidi
Racquel Sanchez
Matthew J Dolan
Seema S Ahuja
Robert A Clark
Hemant Kulkarni
Sunil K Ahuja
United States Department of Veterans Affairs · USThe University of Texas Health Science Center at Houston · USDnipropetrovsk State Medical Academy · UASan Antonio Military Medical Center · US

Funding

Host Genetic Determinants of HIV PathogenesisR37AI046326 · NIAID · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI AHUJA, SUNIL K · 2005 to 2014
$7.8M
HOST GENETIC DETERMINANTS OF HIV PATHOGENESISR01AI046326 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI AHUJA, SUNIL K · 2000 to 2004
$2.8M
NIAID NIH HHS R01 AI046326NIAID NIH HHS R37 AI046326PHS HHS R37046326
6 · The paper itself

Abstract

objectiveCCL3L and CCL4L genes encode HIV-suppressive chemokines, colocalize on chromosome 17q12 and have copy number variation. Copy number variation of CCL3L associates with HIV-AIDS susceptibility. Here, we determined the influence of the combinatorial content of distinct CCL3L and CCL4L genes on HIV-AIDS susceptibility.

methodsBy designing gene-specific assays, the association between doses of all CCL3L or CCL4L genes or their individual duplicated components (CCL3La/b and CCL4La/b) with HIV-AIDS susceptibility was determined in 298 perinatally exposed Ukrainian children.

resultsThe odds of transmission was increased in children with less than two copies of CCL3L or CCL4L, compared with those with at least two copies, and 10-fold higher when both mother and offspring had less than two CCL3L or CCL4L copies, compared with mother-child pairs with at least two copies. The extent of the pair-wise correlations between CCL3La, CCL3Lb, CCL4La and CCL4Lb copy number varied extensively, with an inverse correlation between CCL4L genes that transcribe a classical chemokine (CCL4La) versus aberrantly-spliced transcripts (CCL4Lb). Children possessing only CCL4Lb progressed four times faster to AIDS than those with only CCL4La. A lower content of CCL3L and CCL4L genes that transcribe classical chemokines was associated with enhanced HIV-AIDS susceptibility.

conclusionTransmission risk is greatest when mother and offspring both have low CCL3L or CCL4L gene doses. The impact on HIV-AIDS susceptibility of the chemokine gene-rich locus on 17q12 is dependent on the balance between the doses of genes conferring protective (CCL3La and CCL4La) versus detrimental (CCL4Lb) effects. Hence, the combinatorial genomic content of distinct genes within a copy number variable region may determine disease susceptibility.

Indexed as

Gene DosageHIV-1Acquired Immunodeficiency SyndromeChemokine CCL3Chemokine CCL4Disease ProgressionFemaleGenetic Predisposition to DiseaseHIV InfectionsHumansInfant, NewbornInfectious Disease Transmission, VerticalPolymerase Chain ReactionPregnancyPregnancy ComplicationsTerminology as TopicChemokine CCL3Chemokine CCL4

Identifiers

PMID19279442
PMCPMC2929972
OpenAlexW2008152684

What OpenQuestion holds

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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.