Evidence map›Paper›PMID 23152537›Full record

ArticleJournal of virology2013

Suppression of HIV-1 infection by APOBEC3 proteins in primary human CD4(+) T cells is associated with inhibition of processive reverse transcription as well as excessive cytidine deamination.

Kieran Gillick, Darja Pollpeter, Prabhjeet Phalora, Eun-Young Kim, Steven M Wolinsky, Michael H Malim

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

80 citing papers in PubMed, 115 citations in OpenAlex.

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  2. Journal of virology · 2025
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  13. The von Hippel-Lindau Cullin-RING E3 ubiquitin ligase regulates APOBEC3 cytidine deaminases.Translational research : the journal of laboratory and clinical medicine · 2021
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  14. Review
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20 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

6 authors at 2 institutions in 2 countries.

Kieran GillickDepartment of Infectious Diseases, King's College London, London, United Kingdom.
Darja Pollpeter
Prabhjeet Phalora
Eun-Young Kim
Steven M Wolinsky
Michael H Malim
King's College London · GBNorthwestern University · US

Funding

Vif Antagonism: Lead Discovery and SAR - Project 1P01MH100942 · NIMH · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI STEVENSON, MARIO · 2013 to 2017
$6.0M
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 AI070072NIAID NIH HHS R01 AI070072NIMH NIH HHS P01 MH100942
6 · The paper itself

Abstract

The Vif protein of human immunodeficiency virus type 1 (HIV-1) promotes viral replication by downregulation of the cell-encoded, antiviral APOBEC3 proteins. These proteins exert their suppressive effects through the inhibition of viral reverse transcription as well as the induction of cytidine deamination within nascent viral cDNA. Importantly, these two effects have not been characterized in detail in human CD4(+) T cells, leading to controversies over their possible contributions to viral inhibition in the natural cell targets of HIV-1 replication. Here we use wild-type and Vif-deficient viruses derived from the CD4(+) T cells of multiple donors to examine the consequences of APOBEC3 protein function at natural levels of expression. We demonstrate that APOBEC3 proteins impart a profound deficiency to reverse transcription from the initial stages of cDNA synthesis, as well as excessive cytidine deamination (hypermutation) of the DNAs that are synthesized. Experiments using viruses from transfected cells and a novel method for mapping the 3' termini of cDNAs indicate that the inhibition of reverse transcription is not limited to a few specific sites, arguing that APOBEC3 proteins impede enzymatic processivity. Detailed analyses of mutation spectra in viral cDNA strongly imply that one particular APOBEC3 protein, APOBEC3G, provides the bulk of the antiviral phenotype in CD4(+) T cells, with the effects of APOBEC3F and APOBEC3D being less significant. Taken together, we conclude that the dual mechanisms of action of APOBEC3 proteins combine to deliver more effective restriction of HIV-1 than either function would by itself.

Indexed as

Reverse TranscriptionAPOBEC-3G DeaminaseCD4-Positive T-LymphocytesCells, CulturedCytidineCytidine DeaminaseCytosine DeaminaseDeaminationGene DeletionHIV-1Humansvif Gene Products, Human Immunodeficiency VirusVirulence FactorsAPOBEC3D protein, humanAPOBEC3F protein, humanAPOBEC-3G DeaminaseAPOBEC3G protein, humanCytidineCytidine DeaminaseCytosine Deaminasevif Gene Products, Human Immunodeficiency Virusvif protein, Human immunodeficiency virus 1Virulence Factors

Identifiers

PMID23152537
PMCPMC3554184
OpenAlexW2141014320

What OpenQuestion holds

Textmetadata
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.