Evidence map›Paper›PMID 33649317›Full record

ArticleNature communications2021

Chemogenetic ON and OFF switches for RNA virus replication.

E Heilmann, J Kimpel, B Hofer, A Rössler, I Blaas, L Egerer, T Nolden, C Urbiola, H G Kräusslich, G Wollmann and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Scalable control of stem cell fate by riboswitch-regulated RNA viral vector without genomic integration.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
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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

11 authors at 2 institutions in 2 countries.

E HeilmannInstitute of Virology, Medical University of Innsbruck, Innsbruck, Austria.
J KimpelInstitute of Virology, Medical University of Innsbruck, Innsbruck, Austria.
B HoferInstitute of Virology, Medical University of Innsbruck, Innsbruck, Austria.
A RösslerInstitute of Virology, Medical University of Innsbruck, Innsbruck, Austria.
I BlaasInstitute of Virology, Medical University of Innsbruck, Innsbruck, Austria.
L EgererInstitute of Virology, Medical University of Innsbruck, Innsbruck, Austria.
T NoldenInstitute of Virology, Medical University of Innsbruck, Innsbruck, Austria.
C UrbiolaInstitute of Virology, Medical University of Innsbruck, Innsbruck, Austria.
H G KräusslichDepartment of Infectious Diseases, Virology, University Hospital Heidelberg, Heidelberg, Germany.
G WollmannInstitute of Virology, Medical University of Innsbruck, Innsbruck, Austria. guido.wollmann@i-med.ac.at.ORCID 0000-0001-9894-842X
D von LaerInstitute of Virology, Medical University of Innsbruck, Innsbruck, Austria. dorothee.von-Laer@i-med.ac.at.
Innsbruck Medical University · ATHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Therapeutic application of RNA viruses as oncolytic agents or gene vectors requires a tight control of virus activity if toxicity is a concern. Here we present a regulator switch for RNA viruses using a conditional protease approach, in which the function of at least one viral protein essential for transcription and replication is linked to autocatalytical, exogenous human immunodeficiency virus (HIV) protease activity. Virus activity can be en- or disabled by various HIV protease inhibitors. Incorporating the HIV protease dimer in the genome of vesicular stomatitis virus (VSV) into the open reading frame of either the P- or L-protein resulted in an ON switch. Here, virus activity depends on co-application of protease inhibitor in a dose-dependent manner. Conversely, an N-terminal VSV polymerase tag with the HIV protease dimer constitutes an OFF switch, as application of protease inhibitor stops virus activity. This technology may also be applicable to other potentially therapeutic RNA viruses.

Indexed as

AnimalsCell Line, TumorGenome, ViralHIV ProteaseHIV Protease InhibitorsHumansMiceMice, Inbred NODPhosphoproteinsProtein MultimerizationRNA VirusesVesiculovirusVirus ReplicationHIV ProteaseHIV Protease InhibitorsPhosphoproteins

Identifiers

PMID33649317
PMCPMC7921684
OpenAlexW3133717034

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.