Evidence map›Paper›PMID 10438841›Full record

ArticleJournal of virology1999

Envelope-dependent restriction of human immunodeficiency virus type 1 spreading in CD4(+) T lymphocytes: R5 but not X4 viruses replicate in the absence of T-cell receptor restimulation.

E Vicenzi, P P Bordignon, P Biswas, A Brambilla, C Bovolenta, M Cota, F Sinigaglia, G Poli

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Viral hijacking of G-protein-coupled-receptor signalling networks.Nature reviews. Molecular cell biology · 2004
    Review
  15. Article
  16. Cell surface CCR5 density determines the postentry efficiency of R5 HIV-1 infection.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  17. Naive CD4 T cells inhibit CD28-costimulated R5 HIV replication in memory CD4 T cells.Proceedings of the National Academy of Sciences of the United States of America · 2001
    Article
  18. Article
  19. Article
  20. Selective inhibition of HIV replication in primary macrophages but not T lymphocytes by macrophage-derived chemokine.Proceedings of the National Academy of Sciences of the United States of America · 2000
    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

8 authors at 1 institution in 1 country.

E VicenziAIDS Immunopathogenesis Unit, DIBIT, San Raffaele Scientific Institute, 20132 Milan, Italy. vicenzi.elisa@hsr.it
P P Bordignon
P Biswas
A Brambilla
C Bovolenta
M Cota
F Sinigaglia
G Poli
Roche (Italy) · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human immunodeficiency virus (HIV) replicates in activated CD4(+) T lymphocytes. However, only CD4(+) Th2 and Th0, but not Th1, CD4(+) T-cell clones have been reported to efficiently support HIV-1 replication. This dichotomous pattern was further investigated in the present study in Th1, Th2, or Th0 cell lines derived from umbilical human cord blood and in T-cell clones obtained from the peripheral blood mononuclear cells (PBMC) of healthy adults. Both primary and laboratory-adapted HIV-1 strains with CCR5 as the exclusive entry coreceptor (R5 viruses) efficiently replicated in Th1, Th2, and Th0 cells. In sharp contrast, CXCR4-dependent (X4) viruses poorly replicated in both polarized and unpolarized CD4(+) T cells, including adults' PBMC infected several days after mitogenic stimulation. Unlike the X4 HIV-1(NL4-3), a chimera in which the env gene had been replaced with that of the R5 HIV-1(NL(AD8)), efficiently replicated in both Th1 and Th2 cells. This X4-dependent restriction of HIV replication was not explained by either the absence of functional CXCR4 on the cell surface or by the inefficient viral entry and reverse transcription. T-cell receptor stimulation by anti-CD3 monoclonal antibodies fully rescued X4 HIV-1 replication in both Th1 and Th2 cells, whereas it did not alter the extent and kinetics of R5 HIV-1 spreading. Thus, R5 HIVs show a replicative advantage in comparison to X4 viruses in their ability to efficiently propagate among suboptimally activated T lymphocytes, regardless of their polarized or unpolarized functional profiles. This observation may help to explain the absolute predominance of R5 HIVs over X4 viruses observed after viral transmission and during early-stage disease.

Indexed as

Virus ReplicationAdultAntibodies, MonoclonalCD3 ComplexCD4-Positive T-LymphocytesCells, CulturedChemokine CXCL12Chemokines, CXCHematopoietic Stem CellsHIV-1HIV Envelope Protein gp120HumansReceptors, CCR5Receptors, CXCR4Th1 CellsTh2 CellsAntibodies, MonoclonalCD3 ComplexChemokine CXCL12Chemokines, CXCCXCL12 protein, humanHIV Envelope Protein gp120Receptors, CCR5Receptors, CXCR4

Identifiers

PMID10438841
PMCPMC104278
OpenAlexW1932864759

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.