Evidence map›Paper›PMID 20523911›Full record

ArticleViruses2010

The Role of Nucleotide Excision by Reverse Transcriptase in HIV Drug Resistance.

Antonio J Acosta-Hoyos, Walter A Scott

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

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  13. Structural basis of HIV-1 resistance to AZT by excision.Nature structural & molecular biology · 2010
    Article
  14. 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

2 authors at 1 institution in 1 country.

Antonio J Acosta-HoyosDepartment of Biochemistry and Molecular Biology, University of Miami Miller School of Medicine, P.O. Box 016129, Miami, FL 33101-6129, USA; AAcosta3@med.miami.edu (A.J.A.-H.).
Walter A Scott
University of Miami · US

Funding

University of Miami Developmental Center for AIDS Research (D-CFAR)P30AI073961 · NIAID · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI ALLAN E RODRIGUEZ · 2007 to 2026
$33.8M
Biochemical Mechanisms of Drug Resistance in HIV RTR01AI039973 · NIAID · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI ZHANG, YANBIN · 1997 to 2012
$4.5M
NIAID NIH HHS P30 AI073961NIAID NIH HHS R01 AI039973
6 · The paper itself

Abstract

Nucleoside reverse transcriptase (RT) inhibitors of HIV block viral replication through the ability of HIV RT to incorporate chain-terminating nucleotide analogs during viral DNA synthesis. Once incorporated, the chain-terminating residue must be removed before DNA synthesis can continue. Removal can be accomplished by the excision activity of HIV RT, which catalyzes the transfer of the 3'-terminal residue on the blocked DNA chain to an acceptor substrate, probably ATP in most infected cells. Mutations of RT that enhance excision activity are the most common cause of resistance to 3'-azido-3'-deoxythymidine (AZT) and exhibit low-level cross-resistance to most other nucleoside RT inhibitors. The resistance to AZT is suppressed by a number of additional mutations in RT, most of which were identified because they conferred resistance to other RT inhibitors. Here we review current understanding of the biochemical mechanisms responsible for increased or decreased excision activity due to these mutations.

Identifiers

PMID20523911
PMCPMC2879589
OpenAlexW1975040883

What OpenQuestion holds

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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.