Temperate bacterial viruses as double-edged swords in bacterial warfare.

It has been argued that bacterial cells may use their temperate viruses as biological weapons. For instance, a few bacterial cells among a population of lysogenic cells could release the virus and kill susceptible non-lysogenic competitors, while their clone mates would be immune. Because viruses re...

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Autores principales: João Alves Gama, Ana Maria Reis, Iolanda Domingues, Helena Mendes-Soares, Ana Margarida Matos, Francisco Dionisio
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Publicado: Public Library of Science (PLoS) 2013
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spelling oai:doaj.org-article:457577c155f04ce7915077753c5f2efc2021-11-18T07:53:54ZTemperate bacterial viruses as double-edged swords in bacterial warfare.1932-620310.1371/journal.pone.0059043https://doaj.org/article/457577c155f04ce7915077753c5f2efc2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23536852/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203It has been argued that bacterial cells may use their temperate viruses as biological weapons. For instance, a few bacterial cells among a population of lysogenic cells could release the virus and kill susceptible non-lysogenic competitors, while their clone mates would be immune. Because viruses replicate inside their victims upon infection, this process would amplify their number in the arena. Sometimes, however, temperate viruses spare recipient cells from death by establishing themselves in a dormant state inside cells. This phenomenon is called lysogenization and, for some viruses such as the λ virus, the probability of lysogenization increases with the multiplicity of infection. Therefore, the amplification of viruses leads to conflicting predictions about the efficacy of temperate viruses as biological weapons: amplification can increase the relative advantage of clone mates of lysogens but also the likelihood of saving susceptible cells from death, because the probability of lysogenization is higher. To test the usefulness of viruses as biological weapons, we performed competition experiments between lysogenic Escherichia coli cells carrying the λ virus and susceptible λ-free E. coli cells, either in a structured or unstructured habitat. In structured and sometimes in unstructured habitats, the λ virus qualitatively behaved as a "replicating toxin". However, such toxic effect of λ viruses ceased after a few days of competition. This was due to the fact that many of initially susceptible cells became lysogenic. Massive lysogenization of susceptible cells occurred precisely under the conditions where the amplification of the virus was substantial. From then on, these cells and their descendants became immune to the λ virus. In conclusion, if at short term bacterial cells may use temperate viruses as biological weapons, after a few days only the classical view of temperate bacterial viruses as parasitic agents prevails.João Alves GamaAna Maria ReisIolanda DominguesHelena Mendes-SoaresAna Margarida MatosFrancisco DionisioPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 3, p e59043 (2013)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
João Alves Gama
Ana Maria Reis
Iolanda Domingues
Helena Mendes-Soares
Ana Margarida Matos
Francisco Dionisio
Temperate bacterial viruses as double-edged swords in bacterial warfare.
description It has been argued that bacterial cells may use their temperate viruses as biological weapons. For instance, a few bacterial cells among a population of lysogenic cells could release the virus and kill susceptible non-lysogenic competitors, while their clone mates would be immune. Because viruses replicate inside their victims upon infection, this process would amplify their number in the arena. Sometimes, however, temperate viruses spare recipient cells from death by establishing themselves in a dormant state inside cells. This phenomenon is called lysogenization and, for some viruses such as the λ virus, the probability of lysogenization increases with the multiplicity of infection. Therefore, the amplification of viruses leads to conflicting predictions about the efficacy of temperate viruses as biological weapons: amplification can increase the relative advantage of clone mates of lysogens but also the likelihood of saving susceptible cells from death, because the probability of lysogenization is higher. To test the usefulness of viruses as biological weapons, we performed competition experiments between lysogenic Escherichia coli cells carrying the λ virus and susceptible λ-free E. coli cells, either in a structured or unstructured habitat. In structured and sometimes in unstructured habitats, the λ virus qualitatively behaved as a "replicating toxin". However, such toxic effect of λ viruses ceased after a few days of competition. This was due to the fact that many of initially susceptible cells became lysogenic. Massive lysogenization of susceptible cells occurred precisely under the conditions where the amplification of the virus was substantial. From then on, these cells and their descendants became immune to the λ virus. In conclusion, if at short term bacterial cells may use temperate viruses as biological weapons, after a few days only the classical view of temperate bacterial viruses as parasitic agents prevails.
format article
author João Alves Gama
Ana Maria Reis
Iolanda Domingues
Helena Mendes-Soares
Ana Margarida Matos
Francisco Dionisio
author_facet João Alves Gama
Ana Maria Reis
Iolanda Domingues
Helena Mendes-Soares
Ana Margarida Matos
Francisco Dionisio
author_sort João Alves Gama
title Temperate bacterial viruses as double-edged swords in bacterial warfare.
title_short Temperate bacterial viruses as double-edged swords in bacterial warfare.
title_full Temperate bacterial viruses as double-edged swords in bacterial warfare.
title_fullStr Temperate bacterial viruses as double-edged swords in bacterial warfare.
title_full_unstemmed Temperate bacterial viruses as double-edged swords in bacterial warfare.
title_sort temperate bacterial viruses as double-edged swords in bacterial warfare.
publisher Public Library of Science (PLoS)
publishDate 2013
url https://doaj.org/article/457577c155f04ce7915077753c5f2efc
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