Evidence map›Paper›PMID 29716624›Full record

ArticleRetrovirology2018

Reconstruction of a replication-competent ancestral murine endogenous retrovirus-L.

Daniel Blanco-Melo, Robert J Gifford, Paul D Bieniasz

Open access · goldAbstract read
In one paragraph

Article in Retrovirology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
4.7field-weighted citation impact, top 6% 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

9 citing papers in PubMed, 21 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

3 authors at 2 institutions in 2 countries.

Daniel Blanco-MeloLaboratory of Retrovirology and Howard Hughes Medical Institute, The Rockefeller University, New York, NY, USA.ORCID 0000-0002-0256-5019
Robert J GiffordMRC-University of Glasgow Centre for Virus Research, Glasgow, UK.
Paul D BieniaszLaboratory of Retrovirology and Howard Hughes Medical Institute, The Rockefeller University, New York, NY, USA. pbieniasz@rockefeller.edu.ORCID 0000-0002-2368-3719
Howard Hughes Medical Institute · USMRC University of Glasgow Centre for Virus Research · GB

Funding

The Center for HIV RNA Studies (CRNA)U54GM103297 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BIENIASZ, PAUL D. · 2017 to 2018
$10.2M
Discovery and Mechanism of Antiretroviral FactorsR37AI064003 · NIAID · ROCKEFELLER UNIVERSITY · PI BIENIASZ, PAUL D. · 2011 to 2020
$4.9M
Howard Hughes Medical Institute Investigator AwardMedical Research Council MC_UU_12014/10Medical Research Council MC_UU_12014/12NIGMS NIH HHS U54 GM103297
6 · The paper itself

Abstract

backgroundAbout 10% of the mouse genome is composed of endogenous retroviruses (ERVs) that represent a molecular fossil record of past retroviral infections. One such retrovirus, murine ERV-L (MuERV-L) is an env-deficient ERV that has undergone episodic proliferation, with the most recent amplification occurring ~ 2 million years ago. MuERV-L related sequences have been co-opted by mice for antiretroviral defense, and possibly as promoters for some genes that regulate totipotency in early mouse embryos. However, MuERV-L sequences present in modern mouse genomes have not been observed to replicate.

resultsHere, we describe the reconstruction of an ancestral MuERV-L (ancML) sequence through paleovirological analyses of MuERV-L elements in the modern mouse genome. The resulting MuERV-L (ancML) sequence was synthesized and a reporter gene embedded. The reconstructed MuERV-L (ancML) could replicate in a manner that is dependent on reverse transcription and generated de novo integrants. Notably, MuERV-L (ancML) exhibited a narrow host range. Interferon-α could reduce MuERV-L (ancML) replication, suggesting the existence of interferon-inducible genes that could inhibit MuERV-L replication. While mouse APOBEC3 was able to restrict the replication of MuERV-L (ancML), inspection of endogenous MuERV-L sequences suggested that the impact of APOBEC3 mediated hypermutation on MuERV-L has been minimal.

conclusionThe reconstruction of an ancestral MuERV-L sequence highlights the potential for the retroviral fossil record to illuminate ancient events and enable studies of the impact of retroviral elements on animal evolution.

Indexed as

Virus ReplicationAmino Acid SequenceAnimalsBase SequenceCell LineCHO CellsComputational BiologyCricetulusCytidine DeaminaseDisease ResistanceEndogenous RetrovirusesEvolution, MolecularHost-Pathogen InteractionsImmunity, InnateMicePhylogenyApobec3 protein, mouseCytidine DeaminaseRNA-Directed DNA Polymerase

Identifiers

PMID29716624
PMCPMC5930517
OpenAlexW2807208842

What Socratic holds

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LicenceCC BY
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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 Socratic graph.