Evidence map›Paper›PMID 10974030›Full record

ArticleThe Journal of experimental medicine2000

B cells of HIV-1-infected patients bind virions through CD21-complement interactions and transmit infectious virus to activated T cells.

S Moir, A Malaspina, Y Li, T W Chun, T Lowe, J Adelsberger, M Baseler, L A Ehler, S Liu, R T Davey and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
3.7field-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

84 citing papers in PubMed, 195 citations in OpenAlex.

  1. Trial
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  5. Article
  6. Review
  7. Review
  8. Review
  9. Antigen Presenting Cell-Mediated HIV-1Medical research archives · 2023
    Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. In the Crosshairs: RNA Viruses OR Complement?Frontiers in immunology · 2020
    Review
  16. Early ART in Acute HIV-1 Infection: Impact on the B-Cell Compartment.Frontiers in cellular and infection microbiology · 2020
    Article
  17. Article
  18. Review
  19. Article
  20. Article

24 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

12 authors at 3 institutions in 1 country.

S MoirLaboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. smoir@niaid.nih.gov
A Malaspina
Y Li
T W Chun
T Lowe
J Adelsberger
M Baseler
L A Ehler
S Liu
R T Davey
J A Mican
A S Fauci
National Institutes of Health · USNational Cancer Institute · USBioScience Laboratories (United States) · US

Funding

Role of B Lymphocytes In HIV Infection And PathogenesisZIAAI000825 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MOIR, SUSAN · 2009 to 2025
$24.5M
Immunologic And Virologic Approaches To HIV-1 TherapeuticsZIAAI000865 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DAVEY, RICHARD · 2009 to 2019
$8.8M
Immunologic/Virologic Approaches To HIV-1 TherapeuticsZ01AI000865 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI DAVEY, RICHARD · 2000 to 2008
$4.6M
Role Of B Lymphocytes In HIV Infection And PathogenesisZ01AI000825 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI FAUCI, ANTHONY S. · 1998 to 2008
$1.5M
6 · The paper itself

Abstract

The impact of HIV-associated immunopathogenesis on B cells has been largely associated with indirect consequences of viral replication. This study demonstrates that HIV interacts directly with B cells in both lymphoid tissues and peripheral blood. B cells isolated from lymph node and peripheral blood mononuclear cells (PBMCs) of 4 and 23 chronically infected patients, respectively, demonstrated similar capacities to pass virus to activated HIV-negative PBMCs when compared with CD4(+) cells from the same patients. However, in contrast to T cells, virus associated with B cells was surface bound, as shown by its sensitivity to pronase and the staining pattern revealed by in situ amplification of HIV-1 RNA. Cell sorting and ligand displacing approaches established that CD21 was the HIV-binding receptor on B cells, and that this association was mediated through complement-opsonized virus. These B cells were also found to express significantly lower levels of CD21 compared with HIV-negative individuals, suggesting a direct perturbing effect of HIV on B cells. These findings suggest that B cells, although they themselves are not readily infected by HIV, are similar to follicular dendritic cells in their capacity to serve as extracellular reservoirs for HIV-1. Furthermore, B cells possess the added capability of circulating in peripheral blood and migrating through tissues where they can potentially interact with and pass virus to T cells.

Indexed as

Lymphocyte ActivationAcquired Immunodeficiency SyndromeAntibodies, MonoclonalB-LymphocytesChronic DiseaseComplement C3HIV-1HumansReceptors, Complement 3dRNA, ViralT-LymphocytesVirionAntibodies, MonoclonalComplement C3Receptors, Complement 3dRNA, Viral

Identifiers

PMID10974030
PMCPMC2193277
OpenAlexW2101353031

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.