scholarly journals The Evolution of Virulence in RNA Viruses under a Competition–Colonization Trade-Off

2010 ◽  
Vol 73 (8) ◽  
pp. 1881-1908 ◽  
Author(s):  
Edgar Delgado-Eckert ◽  
Samuel Ojosnegros ◽  
Niko Beerenwinkel
2012 ◽  
Vol 9 (74) ◽  
pp. 2244-2254 ◽  
Author(s):  
Samuel Ojosnegros ◽  
Edgar Delgado-Eckert ◽  
Niko Beerenwinkel

RNA viruses exist as genetically diverse populations displaying a range of virulence degrees. The evolution of virulence in viral populations is, however, poorly understood. On the basis of the experimental observation of an RNA virus clone in cell culture diversifying into two subpopulations of different virulence, we study the dynamics of mutating virus populations with varying virulence. We introduce a competition–colonization trade-off into standard mathematical models of intra-host viral infection. Colonizers are fast-spreading virulent strains, whereas the competitors are less-virulent variants but more successful within co-infected cells. We observe a two-step dynamics of the population. Early in the infection, the population is dominated by colonizers, which later are outcompeted by competitors. Our simulations suggest the existence of steady state in which all virulence classes coexist but are dominated by the most competitive ones. This equilibrium implies collective virulence attenuation in the population, in contrast to previous models predicting evolution of the population towards increased virulence.


Parasitology ◽  
2007 ◽  
Vol 135 (3) ◽  
pp. 303-308 ◽  
Author(s):  
T. J. LITTLE ◽  
W. CHADWICK ◽  
K. WATT

SUMMARYUnderstanding genetic relationships amongst the life-history traits of parasites is crucial for testing hypotheses on the evolution of virulence. This study therefore examined variation between parasite isolates (the bacterium Pasteuria ramosa) from the crustacean Daphnia magna. From a single wild-caught infected host we obtained 2 P. ramosa isolates that differed substantially in the mortality they caused. Surprisingly, the isolate causing higher early mortality was, on average, less successful at establishing infections and had a slower growth rate within hosts. The observation that within-host replication rate was negatively correlated with mortality could violate a central assumption of the trade-off hypothesis for the evolution of virulence, but we discuss a number of caveats which caution against premature rejection of the trade-off hypothesis. We sought to test if the characteristics of these parasite isolates were constant across host genotypes in a second experiment that included 2 Daphnia host clones. The relative growth rates of the two parasite isolates did indeed depend on the host genotype (although the rank order did not change). We suggest that testing evolutionary hypotheses for virulence may require substantial sampling of both host and parasite genetic variation, and discuss how selection for virulence may change with the epidemiological state of natural populations and how this can promote genetic variation for virulence.


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.


2012 ◽  
Vol 2 (5) ◽  
pp. 556-560 ◽  
Author(s):  
Luis M Márquez ◽  
Marilyn J Roossinck

Evolution ◽  
2003 ◽  
Vol 57 (7) ◽  
pp. 1489 ◽  
Author(s):  
Jean-Baptiste André ◽  
Jean-Baptiste Ferdy ◽  
Bernard Godelle

2006 ◽  
Vol 274 (1607) ◽  
pp. 225-230 ◽  
Author(s):  
Victoria Furió ◽  
Andrés Moya ◽  
Rafael Sanjuán

Mutation rates should be governed by at least three evolutionary factors: the need for beneficial mutations, the benefit of minimizing the mutational load and the cost of replication fidelity. RNA viruses show high mutation rates compared with DNA micro-organisms, and recent findings suggest that the cost of fidelity might play a role in the evolution of increased mutation rates. Here, by analysing previously published data from HIV-1 reverse transcriptase in vitro assays, we show a trade-off between enzymatic accuracy and the maximum rate of polymerization, thus providing a biochemical basis for the fitness cost of fidelity in HIV-1. This trade-off seems to be related to inefficient extension of mispairs, which increases fidelity at the expense of the polymerization rate. Since in RNA viruses fast replication is critical for survival, this could impose a high cost of fidelity and favour the evolution of high mutation rates.


Evolution ◽  
2003 ◽  
Vol 57 (7) ◽  
pp. 1489-1497 ◽  
Author(s):  
Jean-Baptiste André ◽  
Jean-Baptiste Ferdy ◽  
Bernard Godelle

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