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

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 chief...

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Autores principales: Paff, Matthew L., Nuismer, Scott L., Ellington, Andrew, Molineux, Ian J., Bull, James J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: PeerJ Inc. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4933091/
https://www.ncbi.nlm.nih.gov/pubmed/27413636
http://dx.doi.org/10.7717/peerj.2166
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author Paff, Matthew L.
Nuismer, Scott L.
Ellington, Andrew
Molineux, Ian J.
Bull, James J.
author_facet Paff, Matthew L.
Nuismer, Scott L.
Ellington, Andrew
Molineux, Ian J.
Bull, James J.
author_sort Paff, Matthew L.
collection PubMed
description 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.
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spelling pubmed-49330912016-07-13 Virus wars: using one virus to block the spread of another Paff, Matthew L. Nuismer, Scott L. Ellington, Andrew Molineux, Ian J. Bull, James J. PeerJ Biotechnology 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. PeerJ Inc. 2016-06-29 /pmc/articles/PMC4933091/ /pubmed/27413636 http://dx.doi.org/10.7717/peerj.2166 Text en ©2016 Paff et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited.
spellingShingle Biotechnology
Paff, Matthew L.
Nuismer, Scott L.
Ellington, Andrew
Molineux, Ian J.
Bull, James J.
Virus wars: using one virus to block the spread of another
title Virus wars: using one virus to block the spread of another
title_full Virus wars: using one virus to block the spread of another
title_fullStr Virus wars: using one virus to block the spread of another
title_full_unstemmed Virus wars: using one virus to block the spread of another
title_short Virus wars: using one virus to block the spread of another
title_sort virus wars: using one virus to block the spread of another
topic Biotechnology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4933091/
https://www.ncbi.nlm.nih.gov/pubmed/27413636
http://dx.doi.org/10.7717/peerj.2166
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