Evidence map›Paper›PMID 17475639›Full record

ArticleJournal of virology2007

Primary cell model for activation-inducible human immunodeficiency virus.

Bryan Burke, Helen J Brown, Matthew D Marsden, Gregory Bristol, Dimitrios N Vatakis, Jerome A Zack

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

26 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Finding a cure for human immunodeficiency virus-1 infection.Infectious disease clinics of North America · 2014
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Towards an HIV cure: a global scientific strategy.Nature reviews. Immunology · 2012
    Review
  12. Article
  13. Article
  14. HIV latency in the humanized BLT mouse.Journal of virology · 2012
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  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

6 authors at 2 institutions in 2 countries.

Bryan BurkeDepartment of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90095-1678, USA.
Helen J Brown
Matthew D Marsden
Gregory Bristol
Dimitrios N Vatakis
Jerome A Zack
Laboratory of Molecular Genetics · PLUniversity of California, Los Angeles · US

Funding

Virology CoreP30AI028697 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ANTON, PETER A · 1991 to 2018
$39.9M
NIAID NIH HHS P30 AI028697
6 · The paper itself

Abstract

Quiescent T lymphocytes containing latent human immunodeficiency virus (HIV) provide a long-lived viral reservoir. This reservoir may be the source of active infection that is reinitiated following the cessation of antiretroviral therapy. Therefore, it is important to understand the mechanisms involved in latent infection to develop new strategies to eliminate the latent HIV reservoir. We have previously demonstrated that latently infected quiescent lymphocytes can be generated during thymopoiesis in vivo in the SCID-hu mouse system. However, there is still a pressing need for an in vitro model of HIV latency in primary human cells. Here, we present a novel in vitro model that recapitulates key aspects of dormant HIV infection. Using an enhanced green fluorescent protein-luciferase fusion protein-containing reporter virus, we have generated a stable infection in primary human CD4(+) CD8(+) thymocytes in the absence of viral gene expression. T-cell activation induces a >200-fold induction of reporter activity. The induced reporter activity originates from a fully reverse-transcribed and integrated genome. We further demonstrate that this model can be useful to study long terminal repeat regulation, as previously characterized NF-kappaB response element mutations decrease the activation of viral gene expression. This model can therefore be used to study intricate molecular aspects of activation-inducible HIV infection in primary cells.

Indexed as

Models, BiologicalVirus ActivationBase SequenceCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesDNA PrimersElectrophoretic Mobility Shift AssayFlow CytometryHIVNF-kappa BDNA PrimersNF-kappa B

Identifiers

PMID17475639
PMCPMC1933352
OpenAlexW2139984318

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.