Evidence map›Paper›PMID 19299650›Full record

ArticleBlood2009

Desensitization to type I interferon in HIV-1 infection correlates with markers of immune activation and disease progression.

Gareth A D Hardy, Scott F Sieg, Benigno Rodriguez, Wei Jiang, Robert Asaad, Michael M Lederman, Clifford V Harding

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

35 citing papers in PubMed, 46 citations in OpenAlex.

  1. Trial
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  8. Dynamics of trophoblast differentiation in peri-implantation-stage human embryos.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  9. Article
  10. Review
  11. Review
  12. Interferon-The Journal of pharmacology and experimental therapeutics · 2018
    Article
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  15. Review
  16. Nuclear import sequence identification in hOAS3 protein.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016
    Article
  17. Article
  18. Article
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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

7 authors at 3 institutions in 1 country.

Gareth A D HardyDepartment of Pathology, Case Western Reserve University and University Hospitals Case Medical Center, Cleveland, OH 44106-7288, USA.
Scott F Sieg
Benigno Rodriguez
Wei Jiang
Robert Asaad
Michael M Lederman
Clifford V Harding
Case Western Reserve University · USInfectious Disease Consultants · USUniversity Hospitals Case Medical Center · US

Funding

WG3: HIV, Co-infections and Co-morbiditiesP30AI036219 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI Sharon L. Hillier, JONATHAN KARN · 1994 to 2026
$50.0M
Regulation of macrophages by Mycobacterium tuberculosisR01AI034343 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI HARDING, CLIFFORD V · 1994 to 2017
$6.2M
CLASS II MHC TRANSPORT AND FUNCTIONR01AI035726 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI HARDING, CLIFFORD V · 1994 to 2010
$3.0M
M. tuberculosis lipoprotein-TLR2 interactionsR01AI069085 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI HARDING, CLIFFORD V · 2007 to 2011
$1.9M
NIAID NIH HHS AI034343NIAID NIH HHS AI035726NIAID NIH HHS AI036219NIAID NIH HHS AI069085NIAID NIH HHS P30 AI036219NIAID NIH HHS R01 AI034343NIAID NIH HHS R01 AI035726NIAID NIH HHS R01 AI069085
6 · The paper itself

Abstract

Type I interferon (IFNalpha/beta) plays a complex role in HIV-1 infection and has been proposed alternately to have roles in either disease protection or progression. Although IFNalpha/beta plays crucial roles in regulating monocytes and dendritic cells, responsiveness of these cells to IFNalpha/beta in HIV-1 infection is poorly understood. We report significant defects in IFNalpha/beta receptor (IFNalpha/betaR) expression, IFNalpha signaling, and IFNalpha-induced gene expression in monocytes from HIV-1-infected subjects. IFNalpha/betaR expression correlated directly with CD4+ T-cell count and inversely with HIV-1 RNA level and expression of CD38 by memory (CD45RO+) CD8+ T cells, a measure of pathologic immune activation in HIV-1 infection associated with disease progression. In addition, monocytes from HIV-1-infected persons showed diminished responses to IFNalpha, including decreased induction of phosphorylated STAT1 and the classical interferon-stimulated gene produces MxA and OAS. These IFNalpha responses were decreased regardless of IFNalpha/betaR expression, suggesting that regulation of intracellular signaling may contribute to unresponsiveness to IFNalpha/beta in HIV-1 disease. Defective monocyte responses to IFNalpha/beta may play an important role in the pathogenesis of HIV-1 infection, and decreased IFNalpha/betaR expression may serve as a novel marker of disease progression.

Indexed as

HIV-1Immunity, ActiveAdultAntiviral AgentsBiomarkersCase-Control StudiesCross-Sectional StudiesDisease ProgressionDrug Resistance, ViralFemaleHIV InfectionsHumansInterferon Type IMaleMiddle AgedMonocytesAntiviral AgentsBiomarkersInterferon Type IReceptors, Interferon

Identifiers

PMID19299650
PMCPMC2689050
OpenAlexW2016318435

What OpenQuestion holds

Textmetadata
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.