Evidence map›Paper›PMID 23593001›Full record

ArticlePLoS pathogens2013

Interferon-inducible mechanism of dendritic cell-mediated HIV-1 dissemination is dependent on Siglec-1/CD169.

Wendy Blay Puryear, Hisashi Akiyama, Suzanne D Geer, Nora P Ramirez, Xinwei Yu, Björn M Reinhard, Suryaram Gummuluru

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers.

0numbers the graph read from it
0cells of the map it votes in
129citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

129 citing papers in PubMed, 169 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Transcription start site heterogeneity controls MDA5 sensing of unspliced HIV-1 RNAs.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Article
  6. Article
  7. CD169 expression of CD14BMC infectious diseases · 2026
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Human CD123Journal of virus eradication · 2025
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

69 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

7 authors at 1 institution in 1 country.

Wendy Blay PuryearDepartment of Microbiology, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Hisashi Akiyama
Suzanne D Geer
Nora P Ramirez
Xinwei Yu
Björn M Reinhard
Suryaram Gummuluru
Boston University · US

Funding

RESEARCH TRAINING IN IMMUNOLOGYT32AI007309 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GUMMULURU, SURYARAM · 1988 to 2024
$7.4M
Mechanism of cell-associated HIV-1 transmissionR01AI064099 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GUMMULURU, SURYARAM · 2005 to 2020
$5.9M
Illuminating Dynamic Receptor Clustering in the Epidermal Growth Factor Receptor Signal Transduction Pathway Using Plasmon CouplingR01CA138509 · NCI · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI Bjoern Markus Reinhard · 2009 to 2026
$5.9M
Characterization of a novel dendritic cell receptor for HIV-1F32AI084558 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI PURYEAR, WENDY BLAY · 2009 to 2010
$100k
NCI NIH HHS CA138509NCI NIH HHS R01 CA138509NIAID NIH HHS 5T32 AI007309-23NIAID NIH HHS AI064099NIAID NIH HHS F32 AI084558NIAID NIH HHS R01 AI064099NIAID NIH HHS T32 AI007309
6 · The paper itself

Abstract

Human immunodeficiency virus type 1 (HIV-1) interactions with myeloid dendritic cells (DCs) can result in virus dissemination to CD4⁺ T cells via a trans infection pathway dependent on virion incorporation of the host cell derived glycosphingolipid (GSL), GM3. The mechanism of DC-mediated trans infection is extremely efficacious and can result in infection of multiple CD4⁺ T cells as these cells make exploratory contacts on the DC surface. While it has long been appreciated that activation of DCs with ligands that induce type I IFN signaling pathway dramatically enhances DC-mediated T cell trans infection, the mechanism by which this occurs has remained unclear until now. Here, we demonstrate that the type I IFN-inducible Siglec-1, CD169, is the DC receptor that captures HIV in a GM3-dependent manner. Selective downregulation of CD169 expression, neutralizing CD169 function, or depletion of GSLs from virions, abrogated DC-mediated HIV-1 capture and trans infection, while exogenous expression of CD169 in receptor-naïve cells rescued GSL-dependent capture and trans infection. HIV-1 particles co-localized with CD169 on DC surface immediately following capture and subsequently within non-lysosomal compartments that redistributed to the DC--T cell infectious synapses upon initiation of T cell contact. Together, these findings describe a novel mechanism of pathogen parasitization of host encoded cellular recognition machinery (GM3--CD169 interaction) for DC-dependent HIV dissemination.

Indexed as

AnimalsCD4-Positive T-LymphocytesCell LineDendritic CellsDown-RegulationG(M3) GangliosideHEK293 CellsHIV-1HIV InfectionsHumansInterferon-alphaMiceRatsRNA InterferenceSialic Acid Binding Ig-like Lectin 1Signal TransductionG(M3) GangliosideInterferon-alphaSialic Acid Binding Ig-like Lectin 1

Identifiers

PMID23593001
PMCPMC3623718
OpenAlexW2044086145

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.