Evidence map›Paper›PMID 28482907›Full record

ReviewRetrovirology2017

A conflict of interest: the evolutionary arms race between mammalian APOBEC3 and lentiviral Vif.

Yusuke Nakano, Hirofumi Aso, Andrew Soper, Eri Yamada, Miyu Moriwaki, Guillermo Juarez-Fernandez, Yoshio Koyanagi, Kei Sato

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Retrovirology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

35 citing papers in PubMed, 52 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Yusuke NakanoLaboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto University, 53 Shogoinkawara-cho, Sakyo-ku, Kyoto, 6068507, Japan.
Hirofumi AsoLaboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto University, 53 Shogoinkawara-cho, Sakyo-ku, Kyoto, 6068507, Japan.
Andrew SoperLaboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto University, 53 Shogoinkawara-cho, Sakyo-ku, Kyoto, 6068507, Japan.
Eri YamadaLaboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto University, 53 Shogoinkawara-cho, Sakyo-ku, Kyoto, 6068507, Japan.
Miyu MoriwakiLaboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto University, 53 Shogoinkawara-cho, Sakyo-ku, Kyoto, 6068507, Japan.
Guillermo Juarez-FernandezLaboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto University, 53 Shogoinkawara-cho, Sakyo-ku, Kyoto, 6068507, Japan.
Yoshio KoyanagiLaboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto University, 53 Shogoinkawara-cho, Sakyo-ku, Kyoto, 6068507, Japan.
Kei SatoLaboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto University, 53 Shogoinkawara-cho, Sakyo-ku, Kyoto, 6068507, Japan. ksato@virus.kyoto-u.ac.jp.ORCID 0000-0003-4431-1380
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3 (APOBEC3) proteins are mammalian-specific cellular deaminases and have a robust ability to restrain lentivirus replication. To antagonize APOBEC3-mediated antiviral action, lentiviruses have acquired viral infectivity factor (Vif) as an accessory gene. Mammalian APOBEC3 proteins inhibit lentiviral replication by enzymatically inserting G-to-A hypermutations in the viral genome, whereas lentiviral Vif proteins degrade host APOBEC3 via the ubiquitin/proteasome-dependent pathway. Recent investigations provide evidence that lentiviral vif genes evolved to combat mammalian APOBEC3 proteins. In corollary, mammalian APOBEC3 genes are under Darwinian selective pressure to escape from antagonism by Vif. Based on these observations, it is widely accepted that lentiviral Vif and mammalian APOBEC3 have co-evolved and this concept is called an "evolutionary arms race." This review provides a comprehensive summary of current knowledge with respect to the evolutionary dynamics occurring at this pivotal host-virus interface.

Indexed as

Evolution, MolecularGenes, vifAnimalsAPOBEC DeaminasesCytidine DeaminaseCytosine DeaminaseHIV-1Host-Pathogen InteractionsHumansLentivirusMammalsSelection, Geneticvif Gene Products, Human Immunodeficiency VirusApobec3 protein, mouseAPOBEC3 proteins, humanAPOBEC DeaminasesCytidine DeaminaseCytosine Deaminasevif Gene Products, Human Immunodeficiency VirusAPOBEC3Evolutionary arms raceLentivirusMammalVif

Identifiers

PMID28482907
PMCPMC5422959
OpenAlexW2613700553

What Socratic 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 Socratic graph.