Evidence map›Paper›PMID 24910430›Full record

ArticleCell reports2014

Downmodulation of CCR7 by HIV-1 Vpu results in impaired migration and chemotactic signaling within CD4⁺ T cells.

Peter W Ramirez, Marylinda Famiglietti, Bharatwaj Sowrirajan, Ana Beatriz DePaula-Silva, Christopher Rodesch, Edward Barker, Alberto Bosque, Vicente Planelles

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

46 citing papers in PubMed, 66 citations in OpenAlex.

  1. HIV-1 manipulates CD96 on CD4Science advances · 2025
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  14. CCL19 enhances CD8Journal of gastroenterology · 2021
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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

8 authors at 2 institutions in 2 countries.

Peter W RamirezDivision of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84112, USA.
Marylinda FamigliettiDivision of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84112, USA; School of Medicine, Università Vita-Salute San Raffaele, 20132 Milan, Italy; AIDS Immunopathogenesis Unit, Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, 20132 Milan, Italy.
Bharatwaj SowrirajanDepartment of Immunology/Microbiology, Rush University Medical Center, Chicago, IL 60612, USA.
Ana Beatriz DePaula-SilvaDivision of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84112, USA.
Christopher RodeschDepartment of Core Facilities, University of Utah School of Medicine, Salt Lake City, UT 84112, USA.
Edward BarkerDepartment of Immunology/Microbiology, Rush University Medical Center, Chicago, IL 60612, USA.
Alberto BosqueDivision of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84112, USA.
Vicente PlanellesDivision of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84112, USA. Electronic address: vicente.planelles@path.utah.edu.
University of Utah · USRush University Medical Center · US

Funding

Training Program in Microbial PathogenesisT32AI055434 · NIAID · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI MULVEY, MATTHEW A, PLANELLES, VICENTE · 2004 to 2025
$6.0M
Vpu inhibits NK cell function through down regulation of NTB-AR01AI065361 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI BARKER, EDWARD · 2006 to 2016
$2.9M
An Ex Vivo Model of HIV-1 Latency and Reactivation using Primary Memory CellsR01AI087508 · NIAID · UNIVERSITY OF UTAH · PI PLANELLES, VICENTE · 2010 to 2014
$1.8M
NIAID NIH HHS R01 AI065361NIAID NIH HHS R01 AI087508NIAID NIH HHS T32 AI055434
6 · The paper itself

Abstract

The chemokine receptor CCR7 plays a crucial role in the homing of central memory and naive T cells to peripheral lymphoid organs. Here, we show that the HIV-1 accessory protein Vpu downregulates CCR7 on the surface of CD4(+) T cells. Vpu and CCR7 were found to specifically interact and colocalize within the trans-Golgi network, where CCR7 is retained. Downmodulation of CCR7 did not involve degradation or endocytosis and was strictly dependent on Vpu expression. Stimulation of HIV-1-infected primary CD4(+) T cells with the CCR7 ligand CCL19 resulted in reduced mobilization of Ca(2+), reduced phosphorylation of Erk1/2, and impaired migration toward CCL19. Specific amino acid residues within the transmembrane domain of Vpu that were previously shown to be critical for BST-2 downmodulation (A14, A18, and W22) were also necessary for CCR7 downregulation. These results suggest that BST-2 and CCR7 may be downregulated via similar mechanisms.

Indexed as

CD4-Positive T-LymphocytesCell MovementChemokine CCL19Chemotaxis, LeukocyteDown-RegulationHEK293 CellsHIV-1HIV InfectionsHuman Immunodeficiency Virus ProteinsHumansLigandsReceptors, CCR7Viral Regulatory and Accessory ProteinsViroporin ProteinsCCL19 protein, humanCCR7 protein, humanChemokine CCL19Human Immunodeficiency Virus ProteinsLigandsReceptors, CCR7Viral Regulatory and Accessory ProteinsViroporin Proteinsvpu protein, Human immunodeficiency virus 1

Identifiers

PMID24910430
PMCPMC4080720
OpenAlexW2074767175

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.