Evidence map›Paper›PMID 17273551›Full record

ArticleThe Journal of clinical investigation2007

An intrinsic host defense against HIV-1 integration?

Paul D Bieniasz

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 43% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. The brain-specific factor FEZ1 is a determinant of neuronal susceptibility to HIV-1 infection.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  7. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Paul D BieniaszAaron Diamond AIDS Research Center and Laboratory of Retrovirology, The Rockefeller University, New York, New York 10016, USA. pbienias@adarc.org
Rockefeller University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HSCs are one of only a few cell types that resist HIV-1 infection despite the presence of HIV-1 receptors. An increasing number of genes have been identified that can reduce the sensitivity of cultured cells to retrovirus infection, and in this issue of the JCI, Zhang et al. identify p21(Waf1/Cip1/Sdi1) (p21) as a gene product that can influence the sensitivity of HSCs to HIV-1 infection (see the related article beginning on page 473). Strikingly, p21 appears to alter the fate of nuclear HIV-1 DNA, promoting the formation of circular viral DNA forms rather than functional proviruses.

Indexed as

Cyclin-Dependent Kinase Inhibitor p21DNA, ViralHematopoietic Stem CellsHIV-1HumansVirus IntegrationVirus ReplicationCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DNA, Viral

Identifiers

PMID17273551
PMCPMC1783824
OpenAlexW2055742583

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.