Evidence map›Paper›PMID 28331087›Full record

ArticleJournal of virology2017

Feline Immunodeficiency Virus Evolutionarily Acquires Two Proteins, Vif and Protease, Capable of Antagonizing Feline APOBEC3.

Rokusuke Yoshikawa, Junko S Takeuchi, Eri Yamada, Yusuke Nakano, Naoko Misawa, Yuichi Kimura, Fengrong Ren, Takayuki Miyazawa, Yoshio Koyanagi, Kei Sato

Open access · hybridAbstract read
In one paragraph

Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

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  17. First Nearly Complete Genome Sequence ofGenome announcements · 2017
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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

10 authors at 2 institutions in 1 country.

Rokusuke YoshikawaLaboratory of Viral Pathogenesis, Institute for Virus Research, Kyoto University, Kyoto, Japan.
Junko S TakeuchiLaboratory of Viral Pathogenesis, Institute for Virus Research, Kyoto University, Kyoto, Japan.
Eri YamadaLaboratory of Viral Pathogenesis, Institute for Virus Research, Kyoto University, Kyoto, Japan.
Yusuke NakanoLaboratory of Viral Pathogenesis, Institute for Virus Research, Kyoto University, Kyoto, Japan.
Naoko MisawaLaboratory of Viral Pathogenesis, Institute for Virus Research, Kyoto University, Kyoto, Japan.
Yuichi KimuraLaboratory of Viral Pathogenesis, Institute for Virus Research, Kyoto University, Kyoto, Japan.
Fengrong RenDepartment of Bioinformatics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Takayuki MiyazawaLaboratory of Signal Transduction, Institute for Virus Research, Kyoto University, Kyoto, Japan.
Yoshio KoyanagiLaboratory of Viral Pathogenesis, Institute for Virus Research, Kyoto University, Kyoto, Japan.
Kei SatoLaboratory of Viral Pathogenesis, Institute for Virus Research, Kyoto University, Kyoto, Japan ksato@virus.kyoto-u.ac.jp.ORCID http://orcid.org/0000-0003-4431-1380
Kyoto University · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interplay between viral and host proteins has been well studied to elucidate virus-host interactions and their relevance to virulence. Mammalian genes encode apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3) proteins, which act as intrinsic restriction factors against lentiviruses. To overcome APOBEC3-mediated antiviral actions, lentiviruses have evolutionarily acquired an accessory protein, viral infectivity factor (Vif), and Vif degrades host APOBEC3 proteins via a ubiquitin/proteasome-dependent pathway. Although the Vif-APOBEC3 interaction and its evolutionary significance, particularly those of primate lentiviruses (including HIV) and primates (including humans), have been well investigated, those of nonprimate lentiviruses and nonprimates are poorly understood. Moreover, the factors that determine lentiviral pathogenicity remain unclear. Here, we focus on feline immunodeficiency virus (FIV), a pathogenic lentivirus in domestic cats, and the interaction between FIV Vif and feline APOBEC3 in terms of viral virulence and evolution. We reveal the significantly reduced diversity of FIV subtype B compared to that of other subtypes, which may associate with the low pathogenicity of this subtype. We also demonstrate that FIV subtype B Vif is less active with regard to feline APOBEC3 degradation. More intriguingly, we further reveal that FIV protease cleaves feline APOBEC3 in released virions. Taken together, our findings provide evidence that a lentivirus encodes two types of anti-APOBEC3 factors, Vif and viral protease.

Indexed as

AnimalsAPOBEC DeaminasesAspartic Acid EndopeptidasesCatsEvolution, MolecularGene Products, vifHost-Pathogen InteractionsImmunodeficiency Virus, FelineVirulenceAPOBEC DeaminasesAspartic Acid EndopeptidasesFIV proteaseGene Products, vifAPOBEC3evolutionary arms raceFIVlentivirusproteaseVif

Identifiers

PMID28331087
PMCPMC5432859
OpenAlexW2600376068

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.