Emergence of variability in isogenic Escherichia coli populations infected by a filamentous virus.

The spread of epidemics not only depends on the average number of parasites produced per host, but also on the existence of highly infectious individuals. It is widely accepted that infectiousness depends on genetic and environmental determinants. However, even in clonal populations of host and viru...

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Main Authors: Marianne De Paepe, Silvia De Monte, Lydia Robert, Ariel B Lindner, François Taddei
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2010-07-01
Series:PLoS ONE
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20676396/?tool=EBI
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spelling doaj-a4ecfe4aff4f403aa34580fd02c57efa2021-03-04T02:23:14ZengPublic Library of Science (PLoS)PLoS ONE1932-62032010-07-0157e1182310.1371/journal.pone.0011823Emergence of variability in isogenic Escherichia coli populations infected by a filamentous virus.Marianne De PaepeSilvia De MonteLydia RobertAriel B LindnerFrançois TaddeiThe spread of epidemics not only depends on the average number of parasites produced per host, but also on the existence of highly infectious individuals. It is widely accepted that infectiousness depends on genetic and environmental determinants. However, even in clonal populations of host and viruses growing in homogeneous conditions, high variability can exist. Here we show that Escherichia coli cells commonly display high differentials in viral burst size, and address the kinetics of emergence of such variability with the non-lytic filamentous virus M13. By single-cell imaging of a virally-encoded fluorescent reporter, we monitor the viral charge distribution in infected bacterial populations at different time following infection. A mathematical model assuming autocatalytic virus replication and inheritance of bacterial growth rates quantitatively reproduces the experimental distributions, demonstrating that deterministic amplification of small host inhomogeneities is a mechanism sufficient to explain large and highly skewed distributions. This mechanism of amplification is general and may occur whenever a parasite has an initial phase of exponential growth within its host. Moreover, it naturally reproduces the shift towards higher virulence when the host is experimenting poor conditions, as observed commonly in host-parasite systems.https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20676396/?tool=EBI
collection DOAJ
language English
format Article
sources DOAJ
author Marianne De Paepe
Silvia De Monte
Lydia Robert
Ariel B Lindner
François Taddei
spellingShingle Marianne De Paepe
Silvia De Monte
Lydia Robert
Ariel B Lindner
François Taddei
Emergence of variability in isogenic Escherichia coli populations infected by a filamentous virus.
PLoS ONE
author_facet Marianne De Paepe
Silvia De Monte
Lydia Robert
Ariel B Lindner
François Taddei
author_sort Marianne De Paepe
title Emergence of variability in isogenic Escherichia coli populations infected by a filamentous virus.
title_short Emergence of variability in isogenic Escherichia coli populations infected by a filamentous virus.
title_full Emergence of variability in isogenic Escherichia coli populations infected by a filamentous virus.
title_fullStr Emergence of variability in isogenic Escherichia coli populations infected by a filamentous virus.
title_full_unstemmed Emergence of variability in isogenic Escherichia coli populations infected by a filamentous virus.
title_sort emergence of variability in isogenic escherichia coli populations infected by a filamentous virus.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2010-07-01
description The spread of epidemics not only depends on the average number of parasites produced per host, but also on the existence of highly infectious individuals. It is widely accepted that infectiousness depends on genetic and environmental determinants. However, even in clonal populations of host and viruses growing in homogeneous conditions, high variability can exist. Here we show that Escherichia coli cells commonly display high differentials in viral burst size, and address the kinetics of emergence of such variability with the non-lytic filamentous virus M13. By single-cell imaging of a virally-encoded fluorescent reporter, we monitor the viral charge distribution in infected bacterial populations at different time following infection. A mathematical model assuming autocatalytic virus replication and inheritance of bacterial growth rates quantitatively reproduces the experimental distributions, demonstrating that deterministic amplification of small host inhomogeneities is a mechanism sufficient to explain large and highly skewed distributions. This mechanism of amplification is general and may occur whenever a parasite has an initial phase of exponential growth within its host. Moreover, it naturally reproduces the shift towards higher virulence when the host is experimenting poor conditions, as observed commonly in host-parasite systems.
url https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20676396/?tool=EBI
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