Evidence map›Paper›PMID 25760631›Full record

ArticlePLoS pathogens2015

CD169-mediated trafficking of HIV to plasma membrane invaginations in dendritic cells attenuates efficacy of anti-gp120 broadly neutralizing antibodies.

Hisashi Akiyama, Nora-Guadalupe Pina Ramirez, Manasa V Gudheti, Suryaram Gummuluru

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

57 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Exploring CD169Vaccines · 2025
    Review
  6. Article
  7. Cytoskeletal Vimentin Directs Cell-Cell Transmission of Hepatitis C Virus.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  8. Article
  9. Review
  10. Antigen Presenting Cell-Mediated HIV-1Medical research archives · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Hisashi AkiyamaDepartment of Microbiology, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Nora-Guadalupe Pina RamirezDepartment of Microbiology, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Manasa V GudhetiBruker Nano Surfaces, Salt Lake City, Utah, United States of America.
Suryaram GummuluruDepartment of Microbiology, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Boston University · USBruker (United States) · US

Funding

Mechanism of cell-associated HIV-1 transmissionR01AI064099 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GUMMULURU, SURYARAM · 2005 to 2020
$5.9M
NIAID NIH HHS AI064099NIAID NIH HHS R01 AI064099
6 · The paper itself

Abstract

Myeloid dendritic cells (DCs) can capture HIV-1 via the receptor CD169/Siglec-1 that binds to the ganglioside, GM3, in the virus particle membrane. In turn, HIV-1 particles captured by CD169, an I-type lectin, whose expression on DCs is enhanced upon maturation with LPS, are protected from degradation in CD169+ virus-containing compartments (VCCs) and disseminated to CD4⁺ T cells, a mechanism of DC-mediated HIV-1 trans-infection. In this study, we describe the mechanism of VCC formation and its role in immune evasion mechanisms of HIV-1. We find HIV-1-induced formation of VCCs is restricted to myeloid cells, and that the cytoplasmic tail of CD169 is dispensable for HIV-1 trafficking and retention within VCCs and subsequent trans-infection to CD4⁺ T cells. Interestingly, introduction of a di-aromatic endocytic motif in the cytoplasmic tail of CD169 that results in endocytosis of HIV-1 particles, suppressed CD169-mediated HIV-1 trans-infection. Furthermore, super-resolution microscopy revealed close association of CD169 and HIV-1 particles in surface-accessible but deep plasma membrane invaginations. Intriguingly, HIV-1 particles in deep VCCs were inefficiently accessed by anti-gp120 broadly neutralizing antibodies, VRC01 and NIH45-46 G54W, and thus were less susceptible to neutralization. Our study suggests that HIV-1 capture by CD169 can provide virus evasion from both innate (phagocytosis) and adaptive immune responses.

Indexed as

Antibodies, NeutralizingCell MembraneDendritic CellsElectrophoresis, Polyacrylamide GelHIV-1HIV Envelope Protein gp120HIV InfectionsHumansImmune EvasionMicroscopy, ElectronSialic Acid Binding Ig-like Lectin 1Virus IntegrationAntibodies, NeutralizingHIV Envelope Protein gp120Sialic Acid Binding Ig-like Lectin 1SIGLEC1 protein, human

Identifiers

PMID25760631
PMCPMC4356592
OpenAlexW1981160943

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.