Evidence map›Paper›PMID 25080100›Full record

ArticlePLoS pathogens2014

Human APOBEC3 induced mutation of human immunodeficiency virus type-1 contributes to adaptation and evolution in natural infection.

Eun-Young Kim, Ramon Lorenzo-Redondo, Susan J Little, Yoon-Seok Chung, Prabhjeet K Phalora, Irina Maljkovic Berry, John Archer, Sudhir Penugonda, Will Fischer, Douglas D Richman and 3 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

61 citing papers in PubMed, 91 citations in OpenAlex.

  1. Trial
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  14. Recombination patterns in coronaviruses.bioRxiv : the preprint server for biology · 2022
    Article
  15. Article
  16. Review
  17. Article
  18. Host-directed editing of the SARS-CoV-2 genome.Biochemical and biophysical research communications · 2021
    Review
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

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

13 authors at 8 institutions in 2 countries.

Eun-Young KimDivision of Infectious Diseases, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States of America.
Ramon Lorenzo-RedondoDivision of Infectious Diseases, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States of America.
Susan J LittleDivision of Infectious Diseases, University of California San Diego, San Diego, California, United States of America.
Yoon-Seok ChungDivision of Infectious Diseases, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States of America.
Prabhjeet K PhaloraDepartment of Infectious Diseases, King's College London, Guy's Hospital, London, United Kingdom.
Irina Maljkovic BerryDivision of Infectious Diseases, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States of America.
John ArcherFaculty of Life Sciences, University of Manchester, Manchester, United Kingdom.
Sudhir PenugondaDivision of Infectious Diseases, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States of America.
Will FischerLos Alamos National Laboratory, Los Alamos, New Mexico, United States of America.
Douglas D RichmanDivision of Infectious Diseases, University of California San Diego, San Diego, California, United States of America; Veterans Affairs San Diego Healthcare System, San Diego, California, United States of America.
Tanmoy BhattacharyaLos Alamos National Laboratory, Los Alamos, New Mexico, United States of America; Santa Fe Institute, Santa Fe, New Mexico, United States of America.
Michael H MalimDepartment of Infectious Diseases, King's College London, Guy's Hospital, London, United Kingdom.
Steven M WolinskyDivision of Infectious Diseases, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States of America.
Northwestern University · USGuy's Hospital · GBKing's College London · GBLos Alamos National Laboratory · USSanta Fe Institute · USUniversity of California, San Diego · USUniversity of Manchester · GBVA San Diego Healthcare System · US

Funding

MULTICENTER AIDS COHORT STUDYU01AI035039 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI WOLINSKY, STEVEN M · 1993 to 2018
$66.4M
Transmission ProbabilityP01AI074621 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI STRATHDEE, STEFFANIE A. · 2008 to 2012
$23.1M
Primary Infection Resource Consortium (PIRC)R24AI106039 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LITTLE, SUSAN JANET · 2013 to 2021
$23.1M
Southern California Primary Infection ProgramU01AI043638 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RICHMAN, DOUGLAS D · 1998 to 2010
$21.3M
Molecular Virology and Systems Biology Screening CoreP01AI090935 · NIAID · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI KOENIG, RENATE · 2010 to 2014
$20.4M
The APOBEC/Vif Conflict and HIV PathogenesisR01AI070072 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI WOLINSKY, STEVEN M · 2007 to 2011
$2.6M
Medical Research Council G0401570Medical Research Council G1000196Medical Research Council G1001081NIAID NIH HHS P01 AI074621NIAID NIH HHS P01 AI090935NIAID NIH HHS R01 AI070072NIAID NIH HHS U01 AI035039NIAID NIH HHS U01 AI043638
6 · The paper itself

Abstract

Human APOBEC3 proteins are cytidine deaminases that contribute broadly to innate immunity through the control of exogenous retrovirus replication and endogenous retroelement retrotransposition. As an intrinsic antiretroviral defense mechanism, APOBEC3 proteins induce extensive guanosine-to-adenosine (G-to-A) mutagenesis and inhibit synthesis of nascent human immunodeficiency virus-type 1 (HIV-1) cDNA. Human APOBEC3 proteins have additionally been proposed to induce infrequent, potentially non-lethal G-to-A mutations that make subtle contributions to sequence diversification of the viral genome and adaptation though acquisition of beneficial mutations. Using single-cycle HIV-1 infections in culture and highly parallel DNA sequencing, we defined trinucleotide contexts of the edited sites for APOBEC3D, APOBEC3F, APOBEC3G, and APOBEC3H. We then compared these APOBEC3 editing contexts with the patterns of G-to-A mutations in HIV-1 DNA in cells obtained sequentially from ten patients with primary HIV-1 infection. Viral substitutions were highest in the preferred trinucleotide contexts of the edited sites for the APOBEC3 deaminases. Consistent with the effects of immune selection, amino acid changes accumulated at the APOBEC3 editing contexts located within human leukocyte antigen (HLA)-appropriate epitopes that are known or predicted to enable peptide binding. Thus, APOBEC3 activity may induce mutations that influence the genetic diversity and adaptation of the HIV-1 population in natural infection.

Indexed as

Biological EvolutionAdaptation, PhysiologicalAminohydrolasesAPOBEC-3G DeaminaseAPOBEC DeaminasesBase SequenceCytidine DeaminaseCytosine DeaminaseDNA, ViralGenetic VariationGenome, ViralHigh-Throughput Nucleotide SequencingHIV-1HIV InfectionsHumansMolecular Sequence DataAminohydrolasesAPOBEC3D protein, humanAPOBEC3F protein, humanAPOBEC-3G DeaminaseAPOBEC3G protein, humanAPOBEC3H protein, humanAPOBEC3 proteins, humanAPOBEC DeaminasesCytidine DeaminaseCytosine DeaminaseDNA, Viral

Identifiers

PMID25080100
PMCPMC4117599
OpenAlexW1998993816

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.