Evidence map›Paper›PMID 15308706›Full record

ArticleJournal of virology2004

Analysis of human immunodeficiency virus type 1 transcriptional elongation in resting CD4+ T cells in vivo.

Kara G Lassen, Justin R Bailey, Robert F Siliciano

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

107 citing papers in PubMed, 150 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Review
  5. Article
  6. Observational
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. HIV-1 latency reversal agent boosting is not limited by opioid use.medRxiv : the preprint server for health sciences · 2024
    Article
  13. Article
  14. Review
  15. Premature transcription termination complex proteins PCF11 and WDR82 silence HIV-1 expression in latently infected cells.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

47 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Kara G LassenDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Justin R Bailey
Robert F Siliciano
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

LATENT VIRAL RESERVOIRS IN HIV1 INFECTIONR01AI043222 · NIAID · JOHNS HOPKINS UNIVERSITY · PI SILICIANO, ROBERT F · 1998 to 2013
$3.5M
NIAID NIH HHS AI43222NIAID NIH HHS R01 AI043222
6 · The paper itself

Abstract

A stable latent reservoir for human immunodeficiency virus type 1 (HIV-1) in resting memory CD4+ T cells presents a barrier to eradication of the infection even in patients on highly active antiretroviral therapy. Potential mechanisms for latency include inaccessibility of the integrated viral genome, absence of key host transcription factors, premature termination of HIV-1 RNAs, and abnormal splicing patterns. To differentiate among these mechanisms, we isolated extremely pure populations of resting CD4+ T cells from patients on highly active antiretroviral therapy. These cells did not produce virus but retained the capacity to do so if appropriately stimulated. Products of HIV-1 transcription were examined in purified resting CD4+ T cells. Although short, prematurely terminated HIV-1 transcripts have been suggested as a marker for latently infected cells, the production of short transcripts had not been previously demonstrated in purified populations of resting CD4+ T cells. By separating RNA into polyadenylated and nonpolyadenylated fractions, we showed that resting CD4+ T cells from patients on highly active antiretroviral therapy produce abortive transcripts that lack a poly(A) tail and that terminate prior to nucleotide 181. Short transcripts dominated the pool of total HIV-1 transcripts in resting CD4+ T cells. Processive, polyadenylated HIV-1 mRNAs were also present at a low level. Both unspliced and multiply spliced forms were found. Taken together, these results show that the nonproductive nature of the infection in resting CD4+ T cells from patients on highly active antiretroviral therapy is not due to absolute blocks at the level of either transcriptional initiation or elongation but rather relative inefficiencies at multiple steps.

Indexed as

Cell CycleGene Expression Regulation, ViralAnti-HIV AgentsAntiretroviral Therapy, Highly ActiveCD4-Positive T-LymphocytesCell DivisionCells, CulturedCell SeparationExonsGenome, ViralHIV-1HumansRNA SplicingRNA, ViralTranscription, GeneticVirus LatencyAnti-HIV AgentsRNA, Viral

Identifiers

PMID15308706
PMCPMC506937
OpenAlexW2126183658

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.