Evidence map›Paper›PMID 10196258›Full record

ArticleJournal of virology1999

Shared usage of the chemokine receptor CXCR4 by primary and laboratory-adapted strains of feline immunodeficiency virus.

J Richardson, G Pancino, R Merat, T Leste-Lasserre, A Moraillon, J Schneider-Mergener, M Alizon, P Sonigo, N Heveker

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 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
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  6. Article
  7. CXCR3 activation by lentivirus infection suppresses neuronal autophagy: neuroprotective effects of antiretroviral therapy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Feline immunodeficiency virus neuropathogenesis: from cats to calcium.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2007
    Review
  13. Article
  14. Article
  15. Article
  16. Article
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  18. Review
  19. 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

9 authors at 3 institutions in 2 countries.

J RichardsonGénétique des Virus (ICGM-CNRS UPR 0415), and Génétique Moléculaire Génétique Virale (INRA), Ecole Nationale Vétérinaire d'Alfort, 94704 Maisons-Alfort, France.
G Pancino
R Merat
T Leste-Lasserre
A Moraillon
J Schneider-Mergener
M Alizon
P Sonigo
N Heveker
Inserm · FRCharité - Universitätsmedizin Berlin · DEÉcole Nationale Vétérinaire d'Alfort · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Strains of the feline immunodeficiency virus (FIV) presently under investigation exhibit distinct patterns of in vitro tropism. In particular, the adaptation of FIV for propagation in Crandell feline kidney (CrFK) cells results in the selection of strains capable of forming syncytia with cell lines of diverse species origin. The infection of CrFK cells by CrFK-adapted strains appears to require the chemokine receptor CXCR4 and is inhibited by its natural ligand, stromal cell-derived factor 1alpha (SDF-1alpha). Here we found that inhibitors of CXCR4-mediated infection by human immunodeficiency virus type I (HIV-1), such as the bicyclam AMD3100 and short peptides derived from the amino-terminal region of SDF-1alpha, also blocked infection of CrFK by FIV. Nevertheless, we observed differences in the ranking order of the peptides as inhibitors of FIV and HIV-1 and showed that such differences are related to the species origin of CXCR4 and not that of the viral envelope. These results suggest that, although the envelope glycoproteins of FIV and HIV-1 are substantially divergent, FIV and HIV-1 interact with CXCR4 in a highly similar manner. We have also addressed the role of CXCR4 in the life cycle of primary isolates of FIV. Various CXCR4 ligands inhibited infection of feline peripheral blood mononuclear cells (PBMC) by primary FIV isolates in a concentration-dependent manner. These ligands also blocked the viral transduction of feline PBMC by pseudotyped viral particles when infection was mediated by the envelope glycoprotein of a primary FIV isolate but not by the G protein of vesicular stomatitis virus, indicating that they act at an envelope-mediated step and presumably at viral entry. These findings strongly suggest that primary and CrFK-adapted strains of FIV, despite disparate in vitro tropisms, share usage of CXCR4.

Indexed as

Adaptation, BiologicalAnimalsAnti-HIV AgentsCatsCell Line, TransformedChemokine CXCL12Chemokines, CXCConcanavalin AHeLa CellsHumansImmunodeficiency Virus, FelineLigandsLymphocyte ActivationLymphocytesMiceMitogensAnti-HIV AgentsChemokine CXCL12Chemokines, CXCConcanavalin ACXCL12 protein, humanCxcl12 protein, mouseLigandsMitogensReceptors, CXCR4

Identifiers

PMID10196258
PMCPMC104141
OpenAlexW1834162491

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.