Evidence map›Paper›PMID 21873218›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

CD4+ T cells from elite suppressors are more susceptible to HIV-1 but produce fewer virions than cells from chronic progressors.

Karen A O'Connell, S Alireza Rabi, Robert F Siliciano, Joel N Blankson

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.4field-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

30 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. CD8Frontiers in microbiology · 2021
    Article
  6. Article
  7. Article
  8. Analysis ofJournal of virus eradication · 2018
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Identification of miRNA-mRNA crosstalk in CD4Journal of translational medicine · 2017
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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 at 1 institution in 1 country.

Karen A O'ConnellDepartment of Medicine and The Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
S Alireza Rabi
Robert F Siliciano
Joel N Blankson
Howard Hughes Medical Institute · US

Funding

CD8+ T cell mediated inhibition of HIV-1 replication in Elite SuppressorsR01AI080328 · NIAID · JOHNS HOPKINS UNIVERSITY · PI BLANKSON, JOEL N · 2009 to 2012
$1.3M
Howard Hughes Medical InstituteNIAID NIH HHS R01 AI080328
6 · The paper itself

Abstract

Elite suppressors/controllers (ES) are HIV-1-infected individuals who maintain stable CD4(+) T-cell counts and viral loads of <50 copies/mL without antiretroviral therapy. Research has predominantly focused on immune factors contributing to the control of viral replication in these patients. A more fundamental question, however, is whether there are differences in the nature of CD4(+) T-cell infection in ES compared with viremic patients. Here, we compare chronic progressor (CP), ES, and uninfected donors in terms of three aspects of CD4(+) T-cell infection: cellular susceptibility to infection, death of infected cells, and production of virus from infected cells. Using multiple methods of infection and both single-cycle and replication-competent virus, we show that unmanipulated CD4(+) T-cell populations from ES are actually more susceptible to HIV-1 infection than those populations from CP. Depletion of highly susceptible cells in CP may contribute to this difference. Using 7AAD and AnnexinV staining, we show that infected cells die more rapidly than uninfected cells, but the increased death of infected cells from CP and ES is proportional. Finally, using an assay for measuring virus production, we show that virus production by cells from CP is high compared with virus production by cells from ES or uninfected donors. This higher virus production is linked to cellular activation levels. These data identify fundamental differences in chronic infection of ES and CP that likely contribute to differential HIV-1 disease progression.

Indexed as

Disease ProgressionCD4-Positive T-LymphocytesCell DeathChronic DiseaseCohort StudiesDisease SusceptibilityHIV-1HIV InfectionsHumansImmunologic MemoryLymphocyte ActivationTissue DonorsVirion

Identifiers

PMID21873218
PMCPMC3174588
OpenAlexW2030265247

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.