Spatial determinants of viral infections
Publikation: Bog/antologi/afhandling/rapport › Ph.d.-afhandling › Forskning
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Spatial determinants of viral infections. / Eriksen, Rasmus Skytte.
Niels Bohr Institute, Faculty of Science, University of Copenhagen, 2020. 205 s.Publikation: Bog/antologi/afhandling/rapport › Ph.d.-afhandling › Forskning
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TY - BOOK
T1 - Spatial determinants of viral infections
AU - Eriksen, Rasmus Skytte
PY - 2020
Y1 - 2020
N2 - Bacteria and their virus predator, the bacteriophage, are the most abundant organisms on earth, and their interaction has led to several discoveries for over a century. It is therefore quite remarkable that we do not fully understand how the bacteria can survive the viciousness of the (bacterio)phage. In this thesis, I discuss how two different aspects of bacterial life, spatial structure and bacterial cooperation, may influence the interaction between bacteria and the phages.I use a mixture of mathematical modelling and laboratory experiments to showhow spatial structure, both on long and short length scale, drastically changes the bacteria's exposure to the phages. These spatial effects counter-acts the phages ability to prey on the bacteria and may help explain how bacteria moderates the phage killing. On long length-scales, spatial organization works by partially restricting the phage proliferation to the local area and thereby reduce their interactions with bacteria far away. Furthermore, bacteria are often arranged in small clusters such as biofilm, microcolonies, or chains of connected bacteria. These small-scale structures have a large impact on how the phages prey on the bacteria: By aggregating in small clusters, the bacteria leave large swaths of space empty, and phages take longer to find the bacteria. However, once the bacteria are found, there are fresh hosts in the immediate vicinity. The tight clustering of bacteria means some bacteria shield others from the phages and are hit by disproportionately many phages. In general, when more than one phage hits a bacterium, the excess phages are effectively "wasted" since thebacterium dies with even one infection. These high numbers of wasted phages mean fewer phages leave the bacterial cluster to find new hosts. In some special cases, these "superinfections" are known to drastically alter the phage strategy by delaying the killing of the host by a process called lysis inhibition, or by going into a dormant state called lysogeny, which protects the bacterium from subsequent phage infections.A consequence of evolution is that bacteria often live in diverse ecosystems along several other bacterial strains who are related but with substantial genetic differences caused by mutations. The well-known phrase \survival of the fittest" highlights the ever-present competition between such co-existing bacteria which tends to favour the survival of only a single species. However, it is known that a widespread bacterial defence system, the restriction-modiffcation (RM) system, can limit this competition in favour of emergent cooperation. This cooperation allows the bacteria to collectively drive the population of the phage predator down and allow several bacterial strains to stably co-exist. By accounting for a trade-off between cost and efficacy of these defence systems, as well as the fact that several bacterial strains often contain the same RM systems, I show that the diversity of these ecosystems can be higher stilland, in some cases, be so without suppressing the phage population to low levels.
AB - Bacteria and their virus predator, the bacteriophage, are the most abundant organisms on earth, and their interaction has led to several discoveries for over a century. It is therefore quite remarkable that we do not fully understand how the bacteria can survive the viciousness of the (bacterio)phage. In this thesis, I discuss how two different aspects of bacterial life, spatial structure and bacterial cooperation, may influence the interaction between bacteria and the phages.I use a mixture of mathematical modelling and laboratory experiments to showhow spatial structure, both on long and short length scale, drastically changes the bacteria's exposure to the phages. These spatial effects counter-acts the phages ability to prey on the bacteria and may help explain how bacteria moderates the phage killing. On long length-scales, spatial organization works by partially restricting the phage proliferation to the local area and thereby reduce their interactions with bacteria far away. Furthermore, bacteria are often arranged in small clusters such as biofilm, microcolonies, or chains of connected bacteria. These small-scale structures have a large impact on how the phages prey on the bacteria: By aggregating in small clusters, the bacteria leave large swaths of space empty, and phages take longer to find the bacteria. However, once the bacteria are found, there are fresh hosts in the immediate vicinity. The tight clustering of bacteria means some bacteria shield others from the phages and are hit by disproportionately many phages. In general, when more than one phage hits a bacterium, the excess phages are effectively "wasted" since thebacterium dies with even one infection. These high numbers of wasted phages mean fewer phages leave the bacterial cluster to find new hosts. In some special cases, these "superinfections" are known to drastically alter the phage strategy by delaying the killing of the host by a process called lysis inhibition, or by going into a dormant state called lysogeny, which protects the bacterium from subsequent phage infections.A consequence of evolution is that bacteria often live in diverse ecosystems along several other bacterial strains who are related but with substantial genetic differences caused by mutations. The well-known phrase \survival of the fittest" highlights the ever-present competition between such co-existing bacteria which tends to favour the survival of only a single species. However, it is known that a widespread bacterial defence system, the restriction-modiffcation (RM) system, can limit this competition in favour of emergent cooperation. This cooperation allows the bacteria to collectively drive the population of the phage predator down and allow several bacterial strains to stably co-exist. By accounting for a trade-off between cost and efficacy of these defence systems, as well as the fact that several bacterial strains often contain the same RM systems, I show that the diversity of these ecosystems can be higher stilland, in some cases, be so without suppressing the phage population to low levels.
M3 - Ph.D. thesis
BT - Spatial determinants of viral infections
PB - Niels Bohr Institute, Faculty of Science, University of Copenhagen
ER -
ID: 252770260