Evidence map›Paper›PMID 16378982›Full record

ArticleJournal of virology2006

Naïve and memory cell turnover as drivers of CCR5-to-CXCR4 tropism switch in human immunodeficiency virus type 1: implications for therapy.

Ruy M Ribeiro, Mette D Hazenberg, Alan S Perelson, Miles P Davenport

Abstract read
In one paragraph

Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
–field-weighted citation impact
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

40 citing papers in PubMed.

  1. Review
  2. Article
  3. Discoveries and developments of CXCR4-targeted HIV-1 entry inhibitors.Experimental biology and medicine (Maywood, N.J.) · 2020
    Review
  4. Disparate impact on CD4 T cell count by two distinct HIV-1 phylogenetic clusters from the same clade.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  5. Modeling the immune response to HIV infection.Current opinion in systems biology · 2018
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

4 authors.

Ruy M RibeiroTheoretical Biology and Biophysics, Los Alamos National Laboratory, Los Alamos, NM 87545, USA.
Mette D Hazenberg
Alan S Perelson
Miles P Davenport

Funding

UNM COBRE: THEORETICAL STUDY OF SPECIFICITY OF RNA SILENCING MECHANISMP20RR018754 · NCRR · UNIVERSITY OF NEW MEXICO · PI LOKER, ERIC SAMUEL · 2003 to 2011
$16.7M
MODELING VIRAL AND T LYMPHOCYTE DYNAMICSR01RR006555 · NCRR · UNIVERSITY OF CALIF-LOS ALAMOS NAT LAB · PI PERELSON, ALAN S · 1991 to 2011
$3.9M
Immune System Modeling/HIVR01AI028433 · NIAID · UNIVERSITY OF CALIF-LOS ALAMOS NAT LAB · PI PERELSON, ALAN S · 1990 to 2021
$3.7M
Immune System Modeling/HIVR37AI028433 · NIAID · UNIVERSITY OF CALIF-LOS ALAMOS NAT LAB · PI PERELSON, ALAN S · 2002 to 2011
$2.4M
NCRR NIH HHS P20 RR018754NCRR NIH HHS R01 RR006555NCRR NIH HHS RR06555NCRR NIH HHS RR18754-02NIAID NIH HHS AI28433NIAID NIH HHS R01 AI028433NIAID NIH HHS R37 AI028433
6 · The paper itself

Abstract

Early human immunodeficiency virus infection is characterized by the predominance of CCR5-tropic (R5) virus. However, in many individuals CXCR4-tropic (X4) virus appears in late infection. The reasons for this phenotypic switch are unclear. The patterns of chemokine receptor expression suggest that X4 and R5 viruses have a preferential tropism for naïve and memory T cells, respectively. Since memory cells divide approximately 10 times as often as naïve cells in uninfected individuals, a tropism for memory cells in early infection may provide an advantage. However, with disease progression both naïve and memory cell division frequencies increase, and at low CD4 counts, the naïve cell division frequency approaches that of memory cells. This may provide a basis for the phenotypic switch from R5 to X4 virus observed in late infection. We show that a model of infection using observed values for cell turnover supports this mechanism. The phenotypic switch from R5 to X4 virus occurs at low CD4 counts and is accompanied by a rapid rise in viral load and drop in CD4 count. Thus, low CD4 counts are both a cause and an effect of X4 virus dominance. We also investigate the effects of different antiviral strategies. Surprisingly, these results suggest that both conventional antiretroviral regimens and CCR5 receptor-blocking drugs will promote R5 virus over X4 virus.

Indexed as

Models, ImmunologicalAnti-HIV AgentsCCR5 Receptor AntagonistsCD4 Lymphocyte CountCD4-Positive T-LymphocytesCell DivisionHIV-1HIV InfectionsHumansImmunologic MemoryReceptors, CCR5Receptors, CXCR4Time FactorsVirus ReplicationAnti-HIV AgentsCCR5 Receptor AntagonistsReceptors, CCR5Receptors, CXCR4

Identifiers

PMID16378982
PMCPMC1346847

What OpenQuestion holds

Textmetadata
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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.