Evidence map›Paper›PMID 21448280›Full record

ArticlePloS one2011

The base excision repair pathway is required for efficient lentivirus integration.

Kristine E Yoder, Amy Espeseth, Xiao-hong Wang, Qingming Fang, Maria Teresa Russo, R Stephen Lloyd, Daria Hazuda, Robert W Sobol, Richard Fishel

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.0field-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

22 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Association ofFrontiers in genetics · 2022
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Retroviral DNA Integration.Chemical reviews · 2016
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
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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

9 authors at 6 institutions in 2 countries.

Kristine E YoderMolecular Virology, Immunology, and Medical Genetics, Human Cancer Genetics, The Ohio State University Medical Center, The Ohio State University, Columbus, Ohio, United States of America. yoder.176@osu.edu
Amy Espeseth
Xiao-hong Wang
Qingming Fang
Maria Teresa Russo
R Stephen Lloyd
Daria Hazuda
Robert W Sobol
Richard Fishel
Cancer Genetics (United States) · USUnited States Military Academy · USUPMC Hillman Cancer Center · USIstituto Superiore di Sanità · ITOregon Health & Science University · USUniversity of Pittsburgh · US

Funding

Novel approaches to enhance tumor cell cytotoxicity of alkylating agentsR01CA148629 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SOBOL, ROBERT W · 2010 to 2021
$3.4M
DNA Repair Deficiency Associated with Obesity and the Metabolic SyndromeR01DK075974 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI LLOYD, R. STEPHEN · 2009 to 2013
$1.7M
The role of DNA repair in retroviral infectionR21AI082422 · NIAID · OHIO STATE UNIVERSITY · PI FISHEL, RICHARD, YODER, KRISTINE E · 2009 to 2010
$375k
DNA Repair Deficiency Associated with Obesity and the Meatbolic SyndromeR56DK075974 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI LLOYD, R STEPHEN · 2007 to 2007
$115k
NCI NIH HHS CA148629NCI NIH HHS R01 CA148629NIAID NIH HHS AI82422NIAID NIH HHS R21 AI082422NIDDK NIH HHS DK075974NIDDK NIH HHS R01 DK075974NIDDK NIH HHS R56 DK075974
6 · The paper itself

Abstract

An siRNA screen has identified several proteins throughout the base excision repair (BER) pathway of oxidative DNA damage as important for efficient HIV infection. The proteins identified included early repair factors such as the base damage recognition glycosylases OGG1 and MYH and the late repair factor POLß, implicating the entire BER pathway. Murine cells with deletions of the genes Ogg1, Myh, Neil1 and Polß recapitulate the defect of HIV infection in the absence of BER. Defective infection in the absence of BER proteins was also seen with the lentivirus FIV, but not the gammaretrovirus MMLV. BER proteins do not affect HIV infection through its accessory genes nor the central polypurine tract. HIV reverse transcription and nuclear entry appear unaffected by the absence of BER proteins. However, HIV integration to the host chromosome is reduced in the absence of BER proteins. Pre-integration complexes from BER deficient cell lines show reduced integration activity in vitro. Integration activity is restored by addition of recombinant BER protein POLß. Lentiviral infection and integration efficiency appears to depend on the presence of BER proteins.

Indexed as

Active Transport, Cell NucleusAnimalsCell LineCell NucleusCell SurvivalDNA, ComplementaryDNA DamageDNA RepairDNA, ViralGene DeletionHIV InfectionsHumansLentivirusLentivirus InfectionsMiceReverse TranscriptionDNA, ComplementaryDNA, Viral

Identifiers

PMID21448280
PMCPMC3063173
OpenAlexW2102221778

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.