Evidence map›Paper›PMID 24498008›Full record

ArticlePloS one2014

Variation of human immunodeficiency virus type-1 reverse transcriptase within the simian immunodeficiency virus genome of RT-SHIV.

Debra A Wadford, Robert C Kauffman, Jesse D Deere, Scott T Aoki, Richard A Stanton, Joanne Higgins, Koen K A Van Rompay, Andradi Villalobos, James H Nettles, Raymond F Schinazi and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 51% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. 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

12 authors at 3 institutions in 1 country.

Debra A WadfordCenter for Comparative Medicine, University of California Davis, Davis, California, United States of America.
Robert C KauffmanCenter for Comparative Medicine, University of California Davis, Davis, California, United States of America.
Jesse D DeereCenter for Comparative Medicine, University of California Davis, Davis, California, United States of America.
Scott T AokiCenter for Comparative Medicine, University of California Davis, Davis, California, United States of America.
Richard A StantonChildren's Center for Drug Discovery (CDD), Departments of Pediatrics and Biomedical Informatics, Emory University School of Medicine, Atlanta, Georgia, United States of America.
Joanne HigginsCenter for Comparative Medicine, University of California Davis, Davis, California, United States of America.
Koen K A Van RompayCalifornia National Primate Research Center, University of California Davis, Davis, California, United States of America.
Andradi VillalobosCenter for Comparative Medicine, University of California Davis, Davis, California, United States of America.
James H NettlesChildren's Center for Drug Discovery (CDD), Departments of Pediatrics and Biomedical Informatics, Emory University School of Medicine, Atlanta, Georgia, United States of America.
Raymond F SchinaziEmory University School of Medicine, Veterans Affairs Medical Center, Decatur, Georgia, United States of America.
Niels C PedersenDepartment of Medicine and Epidemiology, School of Veterinary Medicine, University of California Davis, Davis, California, United States of America.
Thomas W NorthCenter for Comparative Medicine, University of California Davis, Davis, California, United States of America ; Department of Molecular Biosciences, School of Veterinary Medicine, University of California Davis, Davis, California, United States of America.
University of California, Davis · USChildren's Center · USEmory University · US

Funding

ZONA PELLUCIDA PEPTIDES AS IMMUNOCONTRACEPTIVE ANTIGENSP51RR000169 · NCRR · UNIVERSITY OF CALIFORNIA DAVIS · PI HYDE, DALLAS MELVIN · 1985 to 2011
$126.2M
Roles of N-TEF and P-TEBb in HIV LatencyP01AI058708 · NIAID · J. DAVID GLADSTONE INSTITUTES · PI NORTH, THOMAS W · 2004 to 2009
$11.6M
UC Davis Biology ProgramR25GM056765 · NIGMS · UNIVERSITY OF CALIFORNIA DAVIS · PI GOMES, ALDRIN V. · 1998 to 2019
$9.7M
SIV MODEL FOR MULTIDRUG RESISTANCE TO AIDS THERAPYR01RR013967 · NCRR · UNIVERSITY OF CALIFORNIA DAVIS · PI NORTH, THOMAS W · 1999 to 2002
$1.2M
RT-SHIV MODEL FOR RESISTANCE TO AIDS THERAPYR01AI047070 · NIAID · UNIVERSITY OF CALIFORNIA DAVIS · PI NORTH, THOMAS W · 2000 to 2002
$1.1M
NCRR NIH HHS P51 RR000169NCRR NIH HHS P51RR000169NCRR NIH HHS RR13967NIAID NIH HHS P01 AI058708NIAID NIH HHS R01 AI47070NIGMS NIH HHS R25 GM056765NIGMS NIH HHS R25 GM 56765
6 · The paper itself

Abstract

RT-SHIV is a chimera of simian immunodeficiency virus (SIV) containing the reverse transcriptase (RT)-encoding region of human immunodeficiency virus type 1 (HIV-1) within the backbone of SIVmac239. It has been used in a non-human primate model for studies of non-nucleoside RT inhibitors (NNRTI) and highly active antiretroviral therapy (HAART). We and others have identified several mutations that arise in the "foreign" HIV-1 RT of RT-SHIV during in vivo replication. In this study we catalogued amino acid substitutions in the HIV-1 RT and in regions of the SIV backbone with which RT interacts that emerged 30 weeks post-infection from seven RT-SHIV-infected rhesus macaques. The virus set points varied from relatively high virus load, moderate virus load, to undetectable virus load. The G196R substitution in RT was detected from 6 of 7 animals at week 4 post-infection and remained in virus from 4 of 6 animals at week 30. Virus from four high virus load animals showed several common mutations within RT, including L74V or V75L, G196R, L214F, and K275R. The foreign RT from high virus load isolates exhibited as much variation as that of the highly variable envelope surface glycoprotein, and 10-fold higher than that of the native RT of SIVmac239. Isolates from moderate virus load animals showed much less variation in the foreign RT than the high virus load isolates. No variation was found in SIVmac239 genes known to interact with RT. Our results demonstrate substantial adaptation of the foreign HIV-1 RT in RT-SHIV-infected macaques, which most likely reflects selective pressure upon the foreign RT to attain optimal activity within the context of the chimeric RT-SHIV and the rhesus macaque host.

Indexed as

MutationAmino Acid SubstitutionAnimalsAntiretroviral Therapy, Highly ActiveCells, CulturedFemaleGenome, ViralHIV Reverse TranscriptaseHost-Pathogen InteractionsHumansMacaca mulattaMaleModels, MolecularProtein Structure, TertiaryRecombinant Fusion ProteinsReverse Transcriptase InhibitorsHIV Reverse TranscriptaseRecombinant Fusion ProteinsReverse Transcriptase InhibitorsRNA-Directed DNA PolymeraseRNA, ViralViral Proteins

Identifiers

PMID24498008
PMCPMC3909041
OpenAlexW2016082374

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.