Evidence map›Paper›PMID 25987741›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

Novel Human Cytomegalovirus Viral Chemokines, vCXCL-1s, Display Functional Selectivity for Neutrophil Signaling and Function.

Jinho Heo, Pranay Dogra, Tom J Masi, Elisabeth A Pitt, Petra de Kruijf, Martine J Smit, Tim E Sparer

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  15. Review
  16. Review
  17. Chemokine Subversion by Human Herpesviruses.Journal of innate immunity · 2018
    Review
  18. Chemokines encoded by herpesviruses.Journal of leukocyte biology · 2017
    Review
  19. Article
  20. Article
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

7 authors at 3 institutions in 2 countries.

Jinho HeoDepartment of Microbiology, The University of Tennessee, Knoxville, TN 37996; and.
Pranay DograDepartment of Microbiology, The University of Tennessee, Knoxville, TN 37996; and.
Tom J MasiDepartment of Microbiology, The University of Tennessee, Knoxville, TN 37996; and.
Elisabeth A PittDepartment of Microbiology, The University of Tennessee, Knoxville, TN 37996; and.
Petra de KruijfDivision of Medicinal Chemistry, VU University Amsterdam, 1081 HV Amsterdam, the Netherlands.
Martine J SmitDivision of Medicinal Chemistry, VU University Amsterdam, 1081 HV Amsterdam, the Netherlands.
Tim E SparerDepartment of Microbiology, The University of Tennessee, Knoxville, TN 37996; and tsparer@utk.edu.
University of Tennessee at Knoxville · USAmsterdam Neuroscience · NLVrije Universiteit Amsterdam · NL

Funding

Viral Chemokine Alteration of Neutrophil FunctionsR01AI071042 · NIAID · UNIVERSITY OF TENNESSEE KNOXVILLE · PI SPARER, TIMOTHY E · 2008 to 2012
$1.6M
NIAID NIH HHS R01 AI071042PHS HHS 1R01A1071042-01A2
6 · The paper itself

Abstract

Human CMV (HCMV) uses members of the hematopoietic system including neutrophils for dissemination throughout the body. HCMV encodes a viral chemokine, vCXCL-1, that is postulated to attract neutrophils for dissemination within the host. The gene encoding vCXCL-1, UL146, is one of the most variable genes in the HCMV genome. Why HCMV has evolved this hypervariability and how this affects the virus' dissemination and pathogenesis is unknown. Because the vCXCL-1 hypervariability maps to important binding and activation domains, we hypothesized that vCXCL-1s differentially activate neutrophils, which could contribute to HCMV dissemination, pathogenesis, or both. To test whether these viral chemokines affect neutrophil function, we generated vCXCL-1 proteins from 11 different clades from clinical isolates from infants infected congenitally with HCMV. All vCXCL-1s were able to induce calcium flux at a concentration of 100 nM and integrin expression on human peripheral blood neutrophils, despite differences in affinity for the CXCR1 and CXCR2 receptors. In fact, their affinity for CXCR1 or CXCR2 did not correlate directly with chemotaxis, G protein-dependent and independent (β-arrestin-2) activation, or secondary chemokine (CCL22) expression. Our data suggest that vCXCL-1 polymorphisms affect the binding affinity, receptor usage, and differential peripheral blood neutrophil activation that could contribute to HCMV dissemination and pathogenesis.

Indexed as

AnimalsArrestinsbeta-Arrestin 2beta-ArrestinsCalciumChemokine CCL22Chemokines, CXCCytomegalovirusCytomegalovirus InfectionsGene Expression RegulationGenetic VariationHEK293 CellsHL-60 CellsHost-Pathogen InteractionsHumansInfantARRB2 protein, humanArrestinsbeta-Arrestin 2beta-ArrestinsCalciumCCL22 protein, humanChemokine CCL22Chemokines, CXCReceptors, Interleukin-8AReceptors, Interleukin-8BRecombinant Proteinsviral chemokine CXC-1, CytomegalovirusViral Proteins

Identifiers

PMID25987741
PMCPMC4475499
OpenAlexW1877691250

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.