Evidence map›Paper›PMID 30085096›Full record

ArticleNucleic acids research2018

HIV-1 Vpr and p21 restrict LINE-1 mobility.

Koudai Kawano, Aurélien J Doucet, Mikinori Ueno, Ryusho Kariya, Wenfeng An, Flavia Marzetta, Misao Kuroki, Priscilla Turelli, Sayaka Sukegawa, Seiji Okada and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.1field-weighted citation impact, top 7% 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

14 citing papers in PubMed, 27 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

13 authors at 5 institutions in 4 countries.

Koudai KawanoCenter for AIDS Research, Kumamoto University, Kumamoto 860-0811, Japan.
Aurélien J DoucetInstitute for Research on Cancer and Aging, Nice (IRCAN), INSERM U1081, CNRS UMR 7284, Université de Nice-Sophia-Antipolis, Faculté de Médecine, 06107 Nice Cedex 2, France.
Mikinori UenoCenter for AIDS Research, Kumamoto University, Kumamoto 860-0811, Japan.
Ryusho KariyaCenter for AIDS Research, Kumamoto University, Kumamoto 860-0811, Japan.
Wenfeng AnDepartment of Pharmaceutical Sciences, South Dakota State University, Brookings, SD 57007, USA.
Flavia MarzettaSchool of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, Lausanne CH-1015, Switzerland.
Misao KurokiCenter for AIDS Research, Kumamoto University, Kumamoto 860-0811, Japan.
Priscilla TurelliSchool of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, Lausanne CH-1015, Switzerland.
Sayaka SukegawaNational Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-0460, USA.
Seiji OkadaCenter for AIDS Research, Kumamoto University, Kumamoto 860-0811, Japan.
Klaus StrebelNational Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-0460, USA.
Didier TronoSchool of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, Lausanne CH-1015, Switzerland.
Yasuo AriumiCenter for AIDS Research, Kumamoto University, Kumamoto 860-0811, Japan.
Kumamoto University · JPÉcole Polytechnique Fédérale de Lausanne · CHNational Institutes of Health · USCentre National de la Recherche Scientifique · FRSouth Dakota State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long interspersed element-1 (LINE-1, L1) composes ∼17% of the human genome. However, genetic interactions between L1 and human immunodeficiency virus type 1 (HIV-1) remain poorly understood. In this study, we found that HIV-1 suppresses L1 retrotransposition. Notably, HIV-1 Vpr strongly inhibited retrotransposition without inhibiting L1 promoter activity. Since Vpr is known to regulate host cell cycle, we examined the possibility whether Vpr suppresses L1 retrotransposition in a cell cycle dependent manner. We showed that the inhibitory effect of a mutant Vpr (H71R), which is unable to arrest the cell cycle, was significantly relieved compared with that of wild-type Vpr, suggesting that Vpr suppresses L1 mobility in a cell cycle dependent manner. Furthermore, a host cell cycle regulator p21Waf1 strongly suppressed L1 retrotransposition. The N-terminal kinase inhibitory domain (KID) of p21 was required for this inhibitory effect. Another KID-containing host cell cycle regulator p27Kip1 also strongly suppressed L1 retrotransposition. We showed that Vpr and p21 coimmunoprecipitated with L1 ORF2p and they suppressed the L1 reverse transcriptase activity in LEAP assay, suggesting that Vpr and p21 inhibit ORF2p-mediated reverse transcription. Altogether, our results suggest that viral and host cell cycle regulatory machinery limit L1 mobility in cultured cells.

Indexed as

Cell CycleCell LineCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27EndonucleasesGenes, ReporterGenes, vprHIV-1HumansLong Interspersed Nucleotide ElementsProtein DomainsProteinsRNA-Directed DNA PolymeraseRNA InterferenceTranscription, GeneticVirionCDKN1A protein, humanCDKN1B protein, humanCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27EndonucleasesORF1 protein, humanORF2 protein, humanProteinsRNA-Directed DNA Polymerasevpr Gene Products, Human Immunodeficiency Virusvpr protein, Human immunodeficiency virus 1

Identifiers

PMID30085096
PMCPMC6144823
OpenAlexW2886231163

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.