Evidence map›Paper›PMID 20025530›Full record

ArticleThe Journal of infectious diseases2010

CCR5 deficiency is a risk factor for early clinical manifestations of West Nile virus infection but not for viral transmission.

Jean K Lim, David H McDermott, Andrea Lisco, Gregory A Foster, David Krysztof, Dean Follmann, Susan L Stramer, Philip M Murphy

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 2 pooled it
10.1field-weighted citation impact, top 2% 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

77 citing papers in PubMed, 2 syntheses or guidelines pooled it, 135 citations in OpenAlex.

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17 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Jean K LimMolecular Signaling Section, Laboratory of Molecular Immunology, Laboratory of Cellular and Molecular Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.
David H McDermott
Andrea Lisco
Gregory A Foster
David Krysztof
Dean Follmann
Susan L Stramer
Philip M Murphy
American Red Cross · USEunice Kennedy Shriver National Institute of Child Health and Human Development · USNational Institute of Allergy and Infectious Diseases · US

Funding

Molecular Analysis Of Leukocyte Activation By ChemoattractantsZIAAI000615 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MURPHY, PHILIP · 2009 to 2025
$44.8M
MOLECULAR ANALYSIS OF NEUTROPHIL ACTIVATION BY CHEMOATTRACTANTSZ01AI000615 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI MURPHY, PHILIP · 1991 to 2008
$7.1M
Intramural NIH HHS Z01 AI000615
6 · The paper itself

Abstract

backgroundWest Nile virus (WNV) is a neurotropic flavivirus transmitted to humans by mosquito vectors. Homozygosity for CCR5Delta32, a complete loss-of-function mutation in CC chemokine receptor 5 (CCR5), has been previously associated with severe symptomatic WNV infection in patients who present with clinical disease; however, whether it acts at the level of initial infection or in promoting clinical progression is unknown.

methodsHere, we address this gap in knowledge by comparing CCR5Delta32 distribution among US blood donors identified through a comprehensive blood supply screening program (34,766,863 donations from 2003 through 2008) as either WNV true positive (634 WNV-positive cases) or false positive (422 WNV-negative control participants). All subjects self-reported symptoms occurring during the 2 weeks following blood donation using a standardized questionnaire.

resultsNo difference was observed in CCR5Delta32 homozygous frequency between the WNV-positive cases and WNV-negative control participants. However, CCR5Delta32 homozygosity was associated in cases but not controls with clinical symptoms consistent with WNV infection (P = .002).

conclusionsCCR5 deficiency is not a risk factor for WNV infection per se, but it is a risk factor for both early and late clinical manifestations after infection. Thus, CCR5 may function normally to limit disease due to WNV infection in humans.

Indexed as

Genetic Predisposition to DiseaseAdultBlood DonorsCase-Control StudiesDisease ProgressionFemaleGene FrequencyHumansMaleMiddle AgedMutationOdds RatioReceptors, CCR5United StatesWest Nile FeverReceptors, CCR5

Identifiers

PMID20025530
PMCPMC2934858
OpenAlexW2112731526

What OpenQuestion holds

Textmetadata
LicenceTDM
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.