Evidence map›Paper›PMID 19165326›Full record

ArticlePLoS genetics2009

Copy number variation of CCL3-like genes affects rate of progression to simian-AIDS in Rhesus Macaques (Macaca mulatta).

Jeremiah D Degenhardt, Paola de Candia, Adrien Chabot, Stuart Schwartz, Les Henderson, Binhua Ling, Meredith Hunter, Zhaoshi Jiang, Robert E Palermo, Michael Katze and 6 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
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  5. Genomic resources for rhesus macaques (Macaca mulatta).Mammalian genome : official journal of the International Mammalian Genome Society · 2022
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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

16 authors at 6 institutions in 2 countries.

Jeremiah D DegenhardtBiological Statistics and Computational Biology, Cornell University, Ithaca, New York, United States of America.
Paola de Candia
Adrien Chabot
Stuart Schwartz
Les Henderson
Binhua Ling
Meredith Hunter
Zhaoshi Jiang
Robert E Palermo
Michael Katze
Evan E Eichler
Mario Ventura
Jeffrey Rogers
Preston Marx
Yoav Gilad
Carlos D Bustamante
University of Chicago · USUniversity of Washington · USTulane University · USCornell University · USTexas Biomedical Research Institute · USUniversity of Bari Aldo Moro · IT

Funding

Natural Selection on Gene Regulation in HumansR01GM077959 · NIGMS · UNIVERSITY OF CHICAGO · PI GILAD, YOAV · 2006 to 2014
$2.9M
NIGMS NIH HHS R01 GM077959
6 · The paper itself

Abstract

Variation in genes underlying host immunity can lead to marked differences in susceptibility to HIV infection among humans. Despite heavy reliance on non-human primates as models for HIV/AIDS, little is known about which host factors are shared and which are unique to a given primate lineage. Here, we investigate whether copy number variation (CNV) at CCL3-like genes (CCL3L), a key genetic host factor for HIV/AIDS susceptibility and cell-mediated immune response in humans, is also a determinant of time until onset of simian-AIDS in rhesus macaques. Using a retrospective study of 57 rhesus macaques experimentally infected with SIVmac, we find that CCL3L CNV explains approximately 18% of the variance in time to simian-AIDS (p<0.001) with lower CCL3L copy number associating with more rapid disease course. We also find that CCL3L copy number varies significantly (p<10(-6)) among rhesus subpopulations, with Indian-origin macaques having, on average, half as many CCL3L gene copies as Chinese-origin macaques. Lastly, we confirm that CCL3L shows variable copy number in humans and chimpanzees and report on CCL3L CNV within and among three additional primate species. On the basis of our findings we suggest that (1) the difference in population level copy number may explain previously reported observations of longer post-infection survivorship of Chinese-origin rhesus macaques, (2) stratification by CCL3L copy number in rhesus SIV vaccine trials will increase power and reduce noise due to non-vaccine-related differences in survival, and (3) CCL3L CNV is an ancestral component of the primate immune response and, therefore, copy number variation has not been driven by HIV or SIV per se.

Indexed as

Gene DosageAnimalsCalibrationChemokine CCL3Disease ProgressionDNA PrimersGenetics, PopulationImmune SystemLikelihood FunctionsMacaca mulattaMicrosatellite RepeatsModels, StatisticalProportional Hazards ModelsReverse Transcriptase Polymerase Chain ReactionSimian Acquired Immunodeficiency SyndromeChemokine CCL3DNA Primers

Identifiers

PMID19165326
PMCPMC2621346
OpenAlexW2016263768

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.