Evidence map›Paper›PMID 27413636›Full record

ArticlePeerJ2016

Virus wars: using one virus to block the spread of another.

Matthew L Paff, Scott L Nuismer, Andrew Ellington, Ian J Molineux, James J Bull

Abstract read
In one paragraph

Article in PeerJ, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. mBio · 2024
    Article
  2. Review
  3. Design and engineering of a transmissible antiviral defense.Journal of biological engineering · 2016
    Article
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.

Matthew L PaffDepartment of Integrative Biology, University of Texas, Austin, TX, United States; The Institute for Cellular and Molecular Biology, University of Texas, Austin, TX, United States.
Scott L NuismerDepartment of Biological Sciences, University of Idaho , Moscow , ID , United States.
Andrew EllingtonDepartment of Molecular Biosciences, University of Texas at Austin, Austin, TX, United States; The Institute for Cellular and Molecular Biology, University of Texas, Austin, TX, United States; Center for Systems, Biology, University of Texas at Austin, Austin, TX, United States.
Ian J MolineuxDepartment of Molecular Biosciences, University of Texas at Austin, Austin, TX, United States; The Institute for Cellular and Molecular Biology, University of Texas, Austin, TX, United States.
James J BullDepartment of Integrative Biology, University of Texas, Austin, TX, United States; The Institute for Cellular and Molecular Biology, University of Texas, Austin, TX, United States; Center for Computational Biology and Bioinformatics, University of Texas, Austin, TX, United States.

Funding

Experimental viral evolution at high mutation rateR01GM057756 · NIGMS · UNIVERSITY OF TEXAS AUSTIN · PI BULL, JAMES J · 1998 to 2013
$2.9M
NIGMS NIH HHS R01 GM057756
6 · The paper itself

Abstract

The failure of traditional interventions to block and cure HIV infections has led to novel proposals that involve treating infections with therapeutic viruses-infectious viruses that specifically inhibit HIV propagation in the host. Early efforts in evaluating these proposals have been limited chiefly to mathematical models of dynamics, for lack of suitable empirical systems. Here we propose, develop and analyze an empirical system of a therapeutic virus that protects a host cell population against a lethal virus. The empirical system uses E. coli bacteria as the host cell population, an RNA phage as the lethal virus and a filamentous phage as the therapeutic virus. Basic dynamic properties are established for each virus alone and then together. Observed dynamics broadly agree with those predicted by a computer simulation model, although some differences are noted. Two cases of dynamics are contrasted, differing in whether the therapeutic virus is introduced before the lethal virus or after the lethal virus. The therapeutic virus increases in both cases but by different mechanisms. With the therapeutic virus introduced first, it spreads infectiously without any appreciable change in host dynamics. With the therapeutic virus introduced second, host abundance is depressed at the time therapy is applied; following an initial period of therapeutic virus spread by infection, the subsequent rise of protection is through reproduction by hosts already protected. This latter outcome is due to inheritance of the therapeutic virus state when the protected cell divides. Overall, the work establishes the feasibility and robustness to details of a viral interference using a therapeutic virus.

Indexed as

BacteriophageGene therapyInfectious vaccineInterventionMathematical modelPopulation dynamicsVaccine alternative

Identifiers

PMID27413636
PMCPMC4933091

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.