Evidence map›Paper›PMID 20174557›Full record

ArticlePLoS pathogens2010

IFN-alpha-induced upregulation of CCR5 leads to expanded HIV tropism in vivo.

Cheryl A Stoddart, Mary E Keir, Joseph M McCune

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. Article
  3. IFNα induces CCR5 in CD4Communications medicine · 2024
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. HLA-B*57 and IFNL4-related polymorphisms are associated with protection against HIV-1 disease progression in controllers.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2017
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Association between HIV-1 tropism and CCR5 human haplotype E in a Caucasian population.Journal of acquired immune deficiency syndromes (1999) · 2014
    Article
  16. Article
  17. Article
  18. Article
  19. HIV-1 immunopathogenesis in humanized mouse models.Cellular & molecular immunology · 2012
    Review
  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

3 authors at 2 institutions in 1 country.

Cheryl A StoddartDivision of Experimental Medicine, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, San Francisco, California, USA. cheryl.stoddart@ucsf.edu
Mary E Keir
Joseph M McCune
San Francisco General Hospital · USUniversity of California, San Francisco · US

Funding

NIH Director's Pioneer Award (RMI)DP1OD000329 · OD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MCCUNE, JOSEPH M · 2004 to 2008
$4.2M
FLOW CYTOMETRY STUDY OF T CELL RESPONSES TO HIV VACCINESR01AI047062 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MCCUNE, JOSEPH M · 2000 to 2007
$3.6M
Thymic Function in Adults With HIV-1 DiseaseU01AI043864 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MCCUNE, JOSEPH M · 2003 to 2007
$3.0M
TISSUE-BASED SMALL ANIMAL MODEL FOR HIV DRUG DISCOVERYN01AI005418 · NIAID · J. DAVID GLADSTONE INSTITUTES · PI STODDART, CHERYL · 2000 to 2000
$971k
NIAID NIH HHS N01 AI005418NIAID NIH HHS N01-AI-05418NIAID NIH HHS N01 AI070002NIAID NIH HHS R01 AI047062NIAID NIH HHS R37 AI47062NIAID NIH HHS U01 AI043864NIAID NIH HHS U01 AI43864NIH HHS DP1 OD000329NIH HHS DPI OD00329
6 · The paper itself

Abstract

Chronic immune activation and inflammation (e.g., as manifest by production of type I interferons) are major determinants of disease progression in primate lentivirus infections. To investigate the impact of such activation on intrathymic T-cell production, we studied infection of the human thymus implants of SCID-hu Thy/Liv mice with X4 and R5 HIV. X4 HIV was observed to infect CD3(-)CD4(+)CD8(-)CXCR4(+)CCR5(-) intrathymic T-cell progenitors (ITTP) and to abrogate thymopoiesis. R5 HIV, by contrast, first established a nonpathogenic infection of thymic macrophages and then, after many weeks, began to replicate in ITTP. We demonstrate here that the tropism of R5 HIV is expanded and pathogenicity enhanced by upregulation of CCR5 on these key T-cell progenitors. Such CCR5 induction was mediated by interferon-alpha (IFN-alpha) in both thymic organ cultures and in SCID-hu mice, and antibody neutralization of IFN-alpha in R5 HIV-infected SCID-hu mice inhibited both CCR5 upregulation and infection of the T-cell progenitors. These observations suggest a mechanism by which IFN-alpha production may paradoxically expand the tropism of R5 HIV and, in so doing, accelerate disease progression.

Indexed as

AnimalsCell SeparationDisease ProgressionFlow CytometryHematopoietic Stem CellsHIVHIV InfectionsHumansInterferon-alphaMiceMice, SCIDReceptors, CCR5Thymus GlandT-LymphocytesUp-RegulationViral TropismInterferon-alphaReceptors, CCR5

Identifiers

PMID20174557
PMCPMC2824759
OpenAlexW2043006217

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.