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...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Marianne De Paepe, Silvia De Monte, Lydia Robert, Ariel B Lindner, François Taddei
Formato: article
Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2010
Materias:
R
Q
Acceso en línea:https://doaj.org/article/a4ecfe4aff4f403aa34580fd02c57efa
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:a4ecfe4aff4f403aa34580fd02c57efa
record_format dspace
spelling oai:doaj.org-article:a4ecfe4aff4f403aa34580fd02c57efa2021-12-02T20:19:43ZEmergence of variability in isogenic Escherichia coli populations infected by a filamentous virus.1932-620310.1371/journal.pone.0011823https://doaj.org/article/a4ecfe4aff4f403aa34580fd02c57efa2010-07-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20676396/?tool=EBIhttps://doaj.org/toc/1932-6203The 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.Marianne De PaepeSilvia De MonteLydia RobertAriel B LindnerFrançois TaddeiPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 7, p e11823 (2010)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
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.
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.
format article
author Marianne De Paepe
Silvia De Monte
Lydia Robert
Ariel B Lindner
François Taddei
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)
publishDate 2010
url https://doaj.org/article/a4ecfe4aff4f403aa34580fd02c57efa
work_keys_str_mv AT mariannedepaepe emergenceofvariabilityinisogenicescherichiacolipopulationsinfectedbyafilamentousvirus
AT silviademonte emergenceofvariabilityinisogenicescherichiacolipopulationsinfectedbyafilamentousvirus
AT lydiarobert emergenceofvariabilityinisogenicescherichiacolipopulationsinfectedbyafilamentousvirus
AT arielblindner emergenceofvariabilityinisogenicescherichiacolipopulationsinfectedbyafilamentousvirus
AT francoistaddei emergenceofvariabilityinisogenicescherichiacolipopulationsinfectedbyafilamentousvirus
_version_ 1718374181917163520