Evidence map›Paper›PMID 27732658›Full record

ArticlePLoS pathogens2016

A Single Nucleotide Polymorphism in Human APOBEC3C Enhances Restriction of Lentiviruses.

Cristina J Wittkopp, Madison B Adolph, Lily I Wu, Linda Chelico, Michael Emerman

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
4.1field-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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 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

5 authors at 3 institutions in 2 countries.

Cristina J WittkoppDepartment of Microbiology, University of Washington, Seattle, Washington, United States of America.
Madison B AdolphDepartment of Microbiology and Immunology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.
Lily I WuDivision of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.
Linda ChelicoDepartment of Microbiology and Immunology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.
Michael EmermanDivision of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.
Fred Hutch Cancer Center · USUniversity of Saskatchewan · CAUniversity of Washington · US

Funding

Translational Bioimaging Core Shared ResourceP30CA015704 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Marian Esvelt · 1985 to 2026
$296.4M
VENEREAL DISEASET32AI007140 · NIAID · UNIVERSITY OF WASHINGTON · PI Julia Cook Dombrowski · 1985 to 2026
$19.4M
VPR AND HIV INFECTIONR01AI030927 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI EMERMAN, MICHAEL · 1991 to 2020
$5.3M
NCI NIH HHS P30 CA015704NIAID NIH HHS R01 AI030927NIAID NIH HHS T32 AI007140
6 · The paper itself

Abstract

Humans express seven human APOBEC3 proteins, which can inhibit viruses and endogenous retroelements through cytidine deaminase activity. The seven paralogs differ in the potency of their antiviral effects, as well as in their antiviral targets. One APOBEC3, APOBEC3C, is exceptional as it has been found to only weakly block viruses and endogenous retroelements compared to other APOBEC3s. However, our positive selection analyses suggest that APOBEC3C has played a role in pathogen defense during primate evolution. Here, we describe a single nucleotide polymorphism in human APOBEC3C, a change from serine to isoleucine at position 188 (I188) that confers potent antiviral activity against HIV-1. The gain-of-function APOBEC3C SNP results in increased enzymatic activity and hypermutation of target sequences when tested in vitro, and correlates with increased dimerization of the protein. The I188 is widely distributed in human African populations, and is the ancestral primate allele, but is not found in chimpanzees or gorillas. Thus, while other hominids have lost activity of this antiviral gene, it has been maintained, or re-acquired, as a more active antiviral gene in a subset of humans. Taken together, our results suggest that APOBEC3C is in fact involved in protecting hosts from lentiviruses.

Indexed as

Polymorphism, Single NucleotideAnimalsCytidine DeaminaseGenetic Predisposition to DiseaseHIV InfectionsHumansLentivirus InfectionsPolymerase Chain ReactionPrimatesAPOBEC3C protein, humanCytidine Deaminase

Identifiers

PMID27732658
PMCPMC5061367
OpenAlexW2531886129

What OpenQuestion 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 OpenQuestion graph.