Evidence map›Paper›PMID 18566437›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Transcriptome analysis reveals human cytomegalovirus reprograms monocyte differentiation toward an M1 macrophage.

Gary Chan, Elizabeth R Bivins-Smith, M Shane Smith, Patrick M Smith, Andrew D Yurochko

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.

0numbers the graph read from it
0cells of the map it votes in
113citing 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

113 citing papers in PubMed.

  1. Mechanisms and Determinants of CMV Reactivation in Kidney Transplantation.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Macrophage fate: to kill or not to kill?Infection and immunity · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. Hematopoietic stem cells and betaherpesvirus latency.Frontiers in cellular and infection microbiology · 2023
    Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Helicobacter pylori outer membrane vesicles induce expression and secretion of oncostatin M in AGS gastric cancer cells.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2021
    Article
  18. CD34Journal of virology · 2021
    Article
  19. Review
  20. Article

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

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

5 authors.

Gary ChanDepartment of Microbiology and Immunology, Center for Molecular and Tumor Virology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA.
Elizabeth R Bivins-Smith
M Shane Smith
Patrick M Smith
Andrew D Yurochko

Funding

RECRUITMENT YEAR FOR PI#5P20RR018724 · NCRR · LOUISIANA STATE UNIV HSC SHREVEPORT · PI KIM, SEONG K · 2003 to 2011
$16.1M
Analysis of HCMV Infection of Monocytes and MacrophagesR01AI056077 · NIAID · LOUISIANA STATE UNIV HSC SHREVEPORT · PI YUROCHKO, ANDREW D · 2004 to 2020
$4.7M
COBRE Center for Molecular and Tumor VirologyP20GM103433 · NIGMS · LOUISIANA STATE UNIV HSC SHREVEPORT · PI O'CALLAGHAN, DENNIS JOHN · 2012 to 2012
$1.9M
NCRR NIH HHS P20 RR018724NIAID NIH HHS R01 AI056077NIGMS NIH HHS P20 GM103433
6 · The paper itself

Abstract

Monocytes are primary targets for human CMV (HCMV) infection and are proposed to be responsible for hematogenous dissemination of the virus. Monocytes acquire different functional traits during polarization to the classical proinflammatory M1 macrophage or the alternative antiinflammatory M2 macrophage. We hypothesized that HCMV induced a proinflammatory M1 macrophage following infection to promote viral dissemination because, biologically, a proinflammatory state provides the tools to drive infected monocytes from the blood into the tissue. To test this hypothesis of monocyte conversion from a normal quiescent phenotype to an inflammatory phenotype, we used Affymetrix Microarray to acquire a transcriptional profile of infected monocytes at a time point our data emphasized is a key temporal regulatory point following infection. We found that HCMV significantly up-regulated 583 (5.2%) of the total genes and down-regulated 621 (5.5%) of the total genes>or=1.5-fold at 4 h postinfection. Further ontology analysis revealed that genes implicated in classical M1 macrophage activation were stimulated by HCMV infection. We found that 65% of genes strictly associated with M1 polarization were up-regulated, while only 4% of genes solely associated with M2 polarization were up-regulated. Analysis of the monocyte chemokinome at the transcriptional level showed that 44% of M1 and 33% of M2 macrophage chemokines were up-regulated. Proteomic analysis using chemokine Ab arrays confirmed the secretion of these chemotactic proteins from HCMV-infected monocytes. Overall, the results identify that the HCMV-infected monocyte transcriptome displayed a unique M1/M2 polarization signature that was skewed toward the classical M1 activation phenotype.

Indexed as

Cell DifferentiationCytomegalovirusCell AdhesionCell Adhesion MoleculesCells, CulturedCytokinesGene Expression ProfilingHumansMacrophagesMonocytesPhenotypePhosphatidic AcidsTranscription, GeneticUp-RegulationUridine1-palmitoyl-2-oleoyl-phosphatidyl-uridineCell Adhesion MoleculesCytokinesPhosphatidic AcidsUridine

Identifiers

PMID18566437
PMCPMC2614917

What OpenQuestion holds

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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.