evolution of virulence
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2021 ◽  
Vol 7 (12) ◽  
Author(s):  
Lijuan Luo ◽  
Hong Wang ◽  
Michael J. Payne ◽  
Chelsea Liang ◽  
Li Bai ◽  
...  

Escherichia albertii is a recently recognized species in the genus Escherichia that causes diarrhoea. The population structure, genetic diversity and genomic features have not been fully examined. Here, 169 E. albertii isolates from different sources and regions in China were sequenced and combined with 312 publicly available genomes (from additional 14 countries) for genomic analyses. The E. albertii population was divided into two clades and eight lineages, with lineage 3 (L3), L5 and L8 more common in China. Clinical isolates were observed in all clades/lineages. Virulence genes were found to be distributed differently among lineages: subtypes of the intimin encoding gene eae and the cytolethal distending toxin gene cdtB were lineage associated, and the second type three secretion system (ETT2) island was truncated in L3 and L6. Seven new eae subtypes and one new cdtB subtype (cdtB-VI) were identified. Alarmingly, 85.9 % of the Chinese E. albertii isolates were predicted to be multidrug-resistant (MDR) with 35.9 % harbouring genes capable of conferring resistance to 10 to 14 different drug classes. The majority of the MDR isolates were of poultry source from China and belonged to four sequence types (STs) [ST4638, ST4479, ST4633 and ST4488]. Thirty-four plasmids with some carrying MDR and virulence genes, and 130 prophages were identified from 17 complete E. albertii genomes. The 130 intact prophages were clustered into five groups, with group five prophages harbouring more virulence genes. We further identified three E. albertii specific genes as markers for the identification of this species. Our findings provided fundamental insights into the population structure, virulence variation and drug resistance of E. albertii .


2021 ◽  
Author(s):  
Graham R Northrup ◽  
Steven R Parratt ◽  
Carly Rozins ◽  
Anna-Liisa Laine ◽  
Mike Boots

AbstractEvolutionary theory has typically focused on pairwise interactions, such as those between hosts and parasites, with relatively little work on more complex interactions including hyperparasites: parasites of parasites. Hyperparasites are common in nature, with the chestnut blight fungus virus CHV-1 a well-known natural example, but also notably include the phages of important human bacterial diseases. Theory on hyperparasitism has mostly focused on their impact on the evolution of virulence of their parasite host and relatively little is known about evolutionary trajectories of hyperparasites themselves. Our general modeling framework highlights the central role the that ability of a hyperparasite to be transmitted with its parasite plays in their evolution. Hyperparasites which transmit with their parasite hosts (hitchhike) will be selected for lower virulence, trending towards hypermutualism or hypercommensalism and select against causing a reduction in parasite virulence (hypovirulence). We examine the impact on the evolution of hyperparasite systems a of a wide range of host and parasite traits showing, for example, that high parasite virulence selects for higher hyperparasite virulence feeding back into selection for hypovirulence in the parasite. Our results have implications for hyperparasite research, both as biocontrol agents and for understanding of how hyperparasites shape community ecology and evolution.


2021 ◽  
Vol 1 ◽  
pp. 1-None
Author(s):  
David Monnin ◽  
Natacha Kremer ◽  
Caroline Michaud ◽  
Manon Villa ◽  
Hélène Henri ◽  
...  

2021 ◽  
Author(s):  
David A Kennedy

Why would a pathogen evolve to kill its hosts when killing a host ends a pathogen's own opportunity for transmission? A vast body of scientific literature has attempted to answer this question using "trade-off theory," which posits that host mortality persists due to its cost being balanced by benefits of other traits that correlate with host mortality. The most commonly invoked trade-off is the mortality-transmission trade-off, where increasingly harmful pathogens are assumed to transmit at higher rates from hosts while the hosts are alive, but the pathogens truncate their infectious period by killing their hosts. Here I show that costs of mortality are too small to plausibly constrain the evolution of disease severity except in systems where survival is rare. I alternatively propose that disease severity can be much more readily constrained by a cost of behavioral change due to the detection of infection, whereby increasingly harmful pathogens have increasing likelihood of detection and behavioral change following detection, thereby limiting opportunities for transmission. Using a mathematical model, I show the conditions under which detection can limit disease severity. Ultimately, this argument may explain why empirical support for trade-off theory has been limited and mixed.


2021 ◽  
Vol 501 (1) ◽  
pp. 444-448
Author(s):  
E. S. Medvedeva ◽  
A. A. Mouzykantov ◽  
V. V. Kostenko ◽  
N. B. Baranova ◽  
M. I. Markelova ◽  
...  

2021 ◽  
pp. 353-388
Author(s):  
Paul Schmid-Hempel

Virulence (i.e. reduction of host fitness) results from the parasite–host interaction. It can be an unselected side effect or the result of short-sighted evolution. The evolutionary theory of virulence predicts virulence by the fitness advantages for the parasite. Thereby, trade-offs among virulence level and host recovery or transmission rates are critical. This process can lead to lower, higher, or intermediate virulence, depending on conditions. Vertical transmission generally selects for lower virulence, whereas co-infection tends to increase virulence levels, also depending on genetic relatedness among the parasites. The sensitivity framework more generally addresses virulence levels in different systems; in this context, manipulation by parasites can result in significant virulence effects, especially when avoiding clearance and when effects are delayed. Different vaccination mechanisms can modify the evolution of virulence. Besides, virulence can evolve within hosts; for example, adaptation to a particular host type with serial passage attenuates virulence on other hosts.


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