Evidence map›Paper›PMID 25048949›Full record

ArticleVirology journal2014

The CD8 antiviral factor (CAF) can suppress HIV-1 transcription from the long terminal repeat (LTR) promoter in the absence of elements upstream of the CATATAA box.

Varsha Shridhar, Yue Chen, Phalguni Gupta

Open access · goldAbstract read
In one paragraph

Article in Virology journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. The CD8Microbiology and molecular biology reviews : MMBR · 2021
    Review
  3. Article
  4. Canonical Wnts Mediate CD8Journal of immunology (Baltimore, Md. : 1950) · 2020
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Discovery of another anti-HIV protein in the search for the CD8+ cell anti-HIV Factor.Proceedings of the National Academy of Sciences of the United States of America · 2015
    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

3 authors at 1 institution in 1 country.

Varsha Shridhar
Yue Chen
Phalguni GuptaPittsburgh Retrovirology Laboratory, Department of Infectious Diseases and Microbiology, University of Pittsburgh Graduate School of Public Health, 426, Parran Hall, 130, DeSoto Street, Pittsburgh 15261, USA. pgupta1@pitt.edu.
University of Pittsburgh · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe CD8 Antiviral Factor (CAF) suppresses viral transcription from the HIV-1 Long Terminal Repeat (LTR) promoter in a non-cytolytic manner. However, the region on the LTR upon which CAF acts is unknown. Our objective was to determine the region on the LTR upon which CAF acts to suppress HIV-1 transcription.

methodsSerial deletions of the LTR from the 5' end and inactivating point mutations were made.

resultsSerial deletions of the LTR from the 5' end indicated the importance of a short ~120 bp segment, containing the 3 SpI sites, CATA box (used by HIV-1 instead of the TATA box) and TAR region, in the suppressive process. Introduction of deletions or inactivating point mutations in the SpI sites or deletion of the TAR region did not abolish CAF-mediated transcriptional suppression. Yet, CAF-mediated transcriptional suppression was still retained in the HIV-1 CATA-TAR segment.

conclusionCAF is able to suppress transcription from the LTR lacking all the elements upstream of the CATA box. Our results suggest that the HIV-1 CATA box may be responsible for CAF-mediated suppression of transcription from the HIV-1 LTR.

Indexed as

Gene Expression Regulation, ViralHIV Long Terminal RepeatPromoter Regions, GeneticTranscription, GeneticBinding SitesCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell LineGene ExpressionGenes, ReporterHIV-1HIV InfectionsHumansNucleic Acid ConformationProtein BindingProteinsProteinsRNA, MessengerTranscription Factors

Identifiers

PMID25048949
PMCPMC4223764
OpenAlexW2014046910

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.